Vegetable Diseases PDF

Vegetable
Diseases
A Colour Handbook
Steven T. Koike
Plant Pathology Farm Advisor, Monterey County, University of California Cooperative Extension
Peter Gladders
Plant Pathologist, ADAS Boxworth, Cambridge, UK
Albert O. Paulus
Plant Pathology Department, University of California, Riverside
MANSON
PUBLISHING
Steven Koike dedicates this book to Margaret, Evan, and Andrew Koike
Copyright © 2007 Manson Publishing Ltd
ISBN-10: 1-84076-075-3
ISBN-13: 978-1-84076-075-0
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Plant Protection Handbooks Series

Alford: Pests of Fruit Crops – A Colour Handbook
Alford: Pests of Ornamental Trees, Shrubs and Flowers – A Colour Atlas
Biddle/Cattlin: Pests, Diseases and Disorders of Peas and Bean – A Colour Handbook
Blancard: Cucurbit Diseases – A Colour Atlas
Blancard: Tomato Diseases – A Colour Atlas
Blancard/Lot/Maisonneuve: Diseases of Lettuce and Related Salad Crops – A Colour Atlas
Bridge/Starr: Plant Nematodes of Agricultural Importance – A Colour Handbook
Fletcher/Gaze: Mushroom Pest and Disease Control – A Colour Handbook
Helyer et al: Biological Control in Plant Protection – A Colour Handbook
Koike/Gladders/Paulus: Vegetable Diseases – A Colour Handbook
Murray et al: Diseases of Small Grain Cereal Crops – A Colour Handbook
Wale/Platt/Cattlin: Pests and Diseases of Potatoes – A Colour Handbook
Williams: Weed Seedlings – A Colour Atlas
Contents
Preface. . . . . . . . . . . . . . . . . . . . . . . . . 8 PART 2 APIACEAE (parsley family)
Acknowledgements. . . . . . . . . . . . . 9 Diseases of vegetable crops APIUM GRAVEOLENS (celery)
Bacterial diseases
PART 1 ALLIACEAE (onion family) Aster yellows phytoplasma
Introduction to vegetable Bacterial diseases Aster yellows . . . . . . . . . . . . . . . . . 80
crops and diseases Pseudomonas syringae pv. porri Pseudomonas syringae pv. apii
Bacterial blight . . . . . . . . . . . . . . . . 54 Bacterial leaf spot . . . . . . . . . . . . . . 82
VEGETABLE PRODUCTION Fungal diseases Fungal diseases
The increasing importance Alternaria porri, Cercospora apii
of vegetables. . . . . . . . . . . . . . . . . . 12 Stemphylium vesicarium Early blight. . . . . . . . . . . . . . . . . . . 83
Vegetable commodities . . . . . . . . . . . . 13 Purple blotch . . . . . . . . . . . . . . . . . 56 Fusarium oxysporum f. sp. apii
Technological advances. . . . . . . . . . . . 14 Aspergillus niger Fusarium yellows . . . . . . . . . . . . . . 85
Challenges in vegetable production . . . 15 Black mold . . . . . . . . . . . . . . . . . . . 58 Phoma apiicola
The challenge of vegetable diseases . . . 16 Botryotinia squamosa Phoma crown and root rot . . . . . . . 86
Botrytis leaf blight, Botrytis blast. . 59 Pythium spp.
Botrytis allii Damping-off, Pythium root rot . . . 87
CAUSES OF DISEASE Neck rot . . . . . . . . . . . . . . . . . . . . . 61 Sclerotinia sclerotiorum
Diseases caused by biotic agents . . . . . 18 Fusarium culmorum, F. oxysporum, Pink rot. . . . . . . . . . . . . . . . . . . . . . 88
Bacteria . . . . . . . . . . . . . . . . . . . . . . . . 18 F. proliferatum Septoria apiicola
Viruses. . . . . . . . . . . . . . . . . . . . . . . . . 20 Fusarium basal plate rot . . . . . . . . . 63 Late blight . . . . . . . . . . . . . . . . . . . 90
Fungi . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Mycosphaerella allii, M. allii-cepae Thanatephorus cucumeris
Fungus-like pathogens. . . . . . . . . . . . . 24 Cladosporium leaf blotch. . . . . . . . 64 Crater spot . . . . . . . . . . . . . . . . . . . 91
Disorders caused by abiotic factors Penicillium hirsutum Viral diseases
and physiological conditions. . . . . . 24 Penicillium mold, blue mold. . . . . . 66 Celery mosaic virus
Peronospora destructor Celery mosaic . . . . . . . . . . . . . . . . . 92
Downy mildew. . . . . . . . . . . . . . . . 67 Cucumber mosaic virus
DIAGNOSING DISEASE
Phoma terrestris Cucumber mosaic . . . . . . . . . . . . . 93
The importance of timely, Pink root . . . . . . . . . . . . . . . . . . . . 69
accurate diagnoses . . . . . . . . . . . . . 31 Abiotic disorders
Phytophthora porri
Overall strategy . . . . . . . . . . . . . . . . . . 31 Blackheart . . . . . . . . . . . . . . . . . . . . . . 94
White tip . . . . . . . . . . . . . . . . . . . . 70
Asking the right questions . . . . . . . . . . 31 Puccinia allii
Questions about the healthy plant . . . . 32 Rust . . . . . . . . . . . . . . . . . . . . . . . . 72 DAUCUS CAROTA (carrot)
Questions about the unhealthy plant . 32 Sclerotium cepivorum Bacterial diseases
Questions about possible White rot . . . . . . . . . . . . . . . . . . . . 74 Xanthomonas campestrsi pv. carotae
agents and factors . . . . . . . . . . . . . . 33 Urocystis cepulae Bacterial leaf blight. . . . . . . . . . . . . 95
Questions about the surrounding Smut. . . . . . . . . . . . . . . . . . . . . . . . 77 Fungal diseases
environment, growing conditions, Viral diseases Alternaria dauci
production practices . . . . . . . . . . . . 33 Garlic yellow stripe virus, Alternaria leaf blight. . . . . . . . . . . . 96
Conducting the examination . . . . . . . . 35 Garlic yellow streak virus, Alternaria radicina
Incorporating laboratory tests . . . . . . . 35 Leek yellow stripe virus, Black rot. . . . . . . . . . . . . . . . . . . . . 98
Diagnosing virus diseases . . . . . . . . . . 36 Garlic mosaic . . . . . . . . . . . . . . . . . 78 Athelia arachnoidea
Digitally assisted diagnosis . . . . . . . . . 36 Onion yellow dwarf virus Crater rot . . . . . . . . . . . . . . . . . . . 100
Compiling information Onion yellow dwarf . . . . . . . . . . . . 79 Athelia rolfsii
and drawing a conclusion . . . . . . . . 36 Southern blight. . . . . . . . . . . . . . . 101
Cercospora carotae
Cercospora leaf blight . . . . . . . . . 102
CONTROLLING DISEASE
Erysiphe heraclei,
Criteria for commercial control of Leveillula spp.
vegetable diseases . . . . . . . . . . . . . . 38 Powdery mildew . . . . . . . . . . . . . 103
Disease control options . . . . . . . . . . . .38 Helicobasidium brebissonii
Other aspects of disease management .49 Violet root rot. . . . . . . . . . . . . . . . 105
4 V EGETABLE D ISEASES – A C OLOUR H ANDBOOK
Mycocentrospora acerina ASPARAGUS OFFICINALIS BRASSICACEAE

Licorice rot. . . . . . . . . . . . . . . . . . 107 (Asparagus ) (mustard family)
Pythium violae, P. sulcatum Fungal diseases Bacterial diseases
Cavity spot. . . . . . . . . . . . . . . . . . 108
Cercospora asparagi Erwinia spp., Pseudomonas spp.
Sclerotinia minor, S. sclerotiorum Cercospora blight. . . . . . . . . . . . . 129 Bacterial head/spear rot
White mold, cottony rot,
Fusarium oxysporum f.sp. asparagi, of broccoli . . . . . . . . . . . . . . . . . . 155
watery soft rot . . . . . . . . . . . . . . . 111
F. proliferatum Pseudomonas syringae pv. alisalensis
Streptomyces scabies Fusarium crown and root rot . . . . 130 Bacterial blight . . . . . . . . . . . . . . . 157
Scab . . . . . . . . . . . . . . . . . . . . . . . 112
Helicobasidium brebissonii, Pseudomonas syringae pv. maculicola
Thanatephorus cucumeris Zopfia rhizophila Bacterial leaf spot . . . . . . . . . . . . . 158
Crown and root rot . . . . . . . . . . . 113 Root rots . . . . . . . . . . . . . . . . . . . 132 Xanthomonas campestris pv.
Thielaviopsis basicola, Phytophthora megasperma, campestris
Chalaropsis thielaviodes Phytophthora spp. Black rot. . . . . . . . . . . . . . . . . . . . 159
Black mold . . . . . . . . . . . . . . . . . . 114 Phytophthora spear and
Uromyces graminis, U. lineolatus Fungal diseases
crown rot . . . . . . . . . . . . . . . . . . . 133
Rust . . . . . . . . . . . . . . . . . . . . . . . 115 Albugo candida
Pleospora herbarum White rust, white blister . . . . . . . . 162
Viral diseases Purple spot . . . . . . . . . . . . . . . . . . 134
Alternaria brassicae,A. brassicicola
Carrot red leaf virus, Puccinia asparagi Alternaria leaf spot/head rot,
Carrot mottle virus Rust . . . . . . . . . . . . . . . . . . . . . . . 135 dark leaf spot . . . . . . . . . . . . . . . . 164
Carrot motley dwarf . . . . . . . . . . 116 Viral diseases Botrytis cinerea
Asparagus virus 1, 2, 3, Gray mold . . . . . . . . . . . . . . . . . . 167
PASTINACA SATIVA (parsnip) Tobacco streak virus. . . . . . . . . . . 137 Erysiphe cruciferarum
Fungal diseases Powdery mildew . . . . . . . . . . . . . 168
Erysiphe heraclei BETA VULGARIS (beet) Fusarium oxysporum
Powdery mildew . . . . . . . . . . . . . 118 f. sp. conglutinans,
Itersonilia perplexans, I. pastinaceae
Fungal diseases F. oxysporum f. sp. raphani
Itersonilia canker, Aphanomyces cochlioides Fusarium wilt, Fusarium yellows. . 169
black canker. . . . . . . . . . . . . . . . . 118 Damping-off, black root rot. . . . . 138
Leptosphaeria maculans, L. biglobosa
Phloeospora heraclei Cercospora beticola Black leg,
Phloeospora leaf spot . . . . . . . . . . 120 Cercospora leaf spot. . . . . . . . . . . 140 Phoma leaf spot and canker . . . . . 171
Phoma complanata Erysiphe betae Mycosphaerella brassicicola
Phoma canker . . . . . . . . . . . . . . . 121 Powdery mildew . . . . . . . . . . . . . 141 Ring spot . . . . . . . . . . . . . . . . . . . 174
Plasmopara umbelliferarum Peronospora farinosa f. sp. betae Mycosphaerella capsellae
Downy mildew. . . . . . . . . . . . . . . 122 Downy mildew. . . . . . . . . . . . . . . 142 White leaf spot . . . . . . . . . . . . . . . 176
Ramularia pastinacae Pleospora bjoerlingii Peronospora parasitica
Ramularia leaf spot . . . . . . . . . . . 123 Black leg . . . . . . . . . . . . . . . . . . . . 143 Downy mildew. . . . . . . . . . . . . . . 178
Viral diseases Ramularia beticola Plasmodiophora brassicae
Ramularia leaf spot . . . . . . . . . . . 145 Clubroot . . . . . . . . . . . . . . . . . . . 181
Parsnip yellow fleck virus
Parsnip yellow fleck . . . . . . . . . . . 124 Streptomyces spp. Phytophthora brassicae
Scab . . . . . . . . . . . . . . . . . . . . . . . 146 Phytophthora storage rot . . . . . . . 186
Uromyces betae Phytophthora megasperma
PETROSELINUM CRISPUM (parsley)
Rust . . . . . . . . . . . . . . . . . . . . . . . 147 Phytophthora root rot . . . . . . . . . 184
Fungal diseases
Viral diseases Pyrenopeziza brassicae
Erysiphe heraclei,
Beet curly top virus Light leaf spot. . . . . . . . . . . . . . . . 185
Leveillula lanuginosa
Beet curly top . . . . . . . . . . . . . . . . 148 Sclerotinia minor, S. sclerotiorum
Powdery mildew . . . . . . . . . . . . . 126
Beet leaf curl virus White mold, Sclerotinia stem rot,
Phytophthora spp., Pythium spp.
Beet leaf curl . . . . . . . . . . . . . . . . . 149 watery soft rot . . . . . . . . . . . . . . . 189
Root rot . . . . . . . . . . . . . . . . . . . . 126
Beet mild yellowing virus Thanatephorus cucumeris
Sclerotinia sclerotiorum
Beet mild yellowing . . . . . . . . . . . 150 Rhizoctonia diseases:
White mold . . . . . . . . . . . . . . . . . 127
Beet mosaic virus damping-off, wirestem,
Septoria petroselini bottom/root rot . . . . . . . . . . . . . . 191
Beet mosaic . . . . . . . . . . . . . . . . . 151
Septoria blight . . . . . . . . . . . . . . . 128
Beet necrotic yellow vein virus Verticillium dahliae,V. longisporum
Beet necrotic yellow vein, Verticillium wilt . . . . . . . . . . . . . . 196
Rhizomania . . . . . . . . . . . . . . . . . 151 Viral diseases
Beet pseudo-yellows virus Beet western yellows virus
Beet pseudo-yellows . . . . . . . . . . . 152 Beet western yellows . . . . . . . . . . 194
Beet western yellows virus Cauliflower mosaic virus
Beet western yellows . . . . . . . . . . 153 Cauliflower mosaic . . . . . . . . . . . 197
Beet yellows virus Turnip mosaic virus
Beet yellows . . . . . . . . . . . . . . . . . 154 Turnip mosaic . . . . . . . . . . . . . . . 198
C ONTENTS 5
CAPSICUM (pepper) CUCURBITACEAE FABACEAE (pea family)

Bacterial diseases (gourd family) PHASEOLUS SPECIES (beans)
Xanthomonas campestris Bacterial diseases Bacterial diseases
pv. vesicatoria Acidovorax avenae subsp. citrulli Pseudomonas syringae
Bacterial spot . . . . . . . . . . . . . . . . 199 Bacterial fruit blotch. . . . . . . . . . . 220 pv. phaseolicola
Fungal diseases Erwinia tracheiphila Halo blight . . . . . . . . . . . . . . . . . . 252
Athelia rolfsii Bacterial wilt . . . . . . . . . . . . . . . . 222 Xanthomonas campestris
Southern blight. . . . . . . . . . . . . . . 201 Pseudomonas syringae pv. lachrymans pv. phaseoli
Botrytis cinerea Angular leaf spot . . . . . . . . . . . . . 224 Common bacterial blight . . . . . . . 254
Gray mold . . . . . . . . . . . . . . . . . . 202 Serratia marcescens Fungal diseases
Colletotrichum capsici, C. coccodes, Cucurbit yellow vine disease . . . . 225 Aphanomyces euteiches,
C. gloeosporioides Fungal diseases Fusarium oxysporum f. sp. phaseoli,
Anthracnose. . . . . . . . . . . . . . . . . 204 Acremonium cucurbitacearum, Phoma medicaginis var. pinodella,
Leveillula taurica Fusarium spp., Phytophthora spp., Pythium spp., Rhizoctonia solani,
Powdery mildew . . . . . . . . . . . . . 205 Pythium spp., Rhizoctonia solani, Thielaviopsis basicola
Rhizopycnis vagum Root/foot rot complex . . . . . . . . . 256
Phytophthora capsici,
P. nicotianae var. parasitica Damping-off, root rots. . . . . . . . . 226 Botrytis cinerea
Phytophthora blight/ Gray mold . . . . . . . . . . . . . . . . . . 258
Cladosporium cucumerinum
root and crown rots . . . . . . . . . 206 Scab . . . . . . . . . . . . . . . . . . . . . . . 228 Erysiphe polygoni
Phytophthora spp., Pythium spp., Powdery mildew . . . . . . . . . . . . . 259
Didymella bryoniae
Rhizoctonia solani Gummy stem blight, black rot . . . 230 Fusarium oxysporum f. sp. phaseoli
Damping-off, Pythium root rot . . 208 Fusarium wilt,
Erysiphe cichoracearum, Sphaerotheca
Sclerotinia minor, S. sclerotiorum Fusarium yellows . . . . . . . . . . . . . 260
fuliginea, Leveillula taurica
White mold, Sclerotinia rot . . . . . 210 Powdery mildew . . . . . . . . . . . . . 232 Glomerella lindemuthiana
Stemphylium solani, S. lycopersici Anthracnose. . . . . . . . . . . . . . . . . 260
Fusarium oxysporum f. sp. cucumerinum,
Gray leaf spot. . . . . . . . . . . . . . . . 211 f. sp. melonis, f. sp. niveum, Sclerotinia sclerotiorum,
Verticillium dahliae f. sp. radicis-cucumerinum S. trifoliorum, S. minor
Verticillium wilt . . . . . . . . . . . . . . 212 Fusarium wilt, White mold, Sclerotinia rot . . . . . 262
Fusarium root/stem rot. . . . . . . . . 234 Uromyces appendiculatus
Viral diseases Rust . . . . . . . . . . . . . . . . . . . . . . . 265
Beet curly top virus Fusarium solani f. sp. cucurbitae
Beet curly top . . . . . . . . . . . . . . . . 214 Fusarium crown and foot rot . . . . 236 Viral diseases
Cucumber mosaic virus Glomerella lagenarium Bean common mosaic virus
Cucumber mosaic . . . . . . . . . . . . 218 Anthracnose. . . . . . . . . . . . . . . . . 238 Bean common mosaic . . . . . . . . . 267
Macrophomina phaseolina Bean yellow mosaic virus
Pepper mild mottle virus
Charcoal rot. . . . . . . . . . . . . . . . . 240 Bean yellow mosaic . . . . . . . . . . . 268
Pepper mild mottle . . . . . . . . . . 219
Monosporascus cannonballus
Potato virus Y
Monosporascus root rot PISUM SATIVUM (pea)
Potato virus Y . . . . . . . . . . . . . . 215 and vine decline . . . . . . . . . . . . . . 241
Sinaloa tomato leaf curl virus Bacterial diseases
Phytophthora capsici
Sinaloa tomato leaf curl . . . . . . 217 Phytophthora crown and root rot 243 Pseudomonas syringae pv. pisi
Tobacco etch virus Bacterial blight . . . . . . . . . . . . . . . 269
Pseudoperonospora cubensis
Tobacco etch . . . . . . . . . . . . . . . . 217 Downy mildew. . . . . . . . . . . . . . . 244 Fungal diseases
Tobacco mosaic virus, Verticillium dahliae Aphanomyces euteiches
Tomato mosaic viruses Verticillium wilt . . . . . . . . . . . . . . 246 Aphanomyces root rot,
Tobacco mosaic, tomato mosaic . 218 common root rot . . . . . . . . . . . . . 270
Viral diseases
Tomato spotted wilt virus Aphanomyces euteiches,
Tomato spotted wilt . . . . . . . . . . . 218 Cucumber mosaic virus Fusarium solani f. sp. pisi,
Cucumber mosaic . . . . . . . . . . . . 247 Phoma medicaginis var. pinodella,
Papaya ringspot virus type W Pythium spp., Rhizoctonia solani,
Papaya ringspot . . . . . . . . . . . . . . 248 Thielaviopsis basicola
Squash leaf curl virus Foot rot complex . . . . . . . . . . . . . 272
Squash leaf curl . . . . . . . . . . . . . . 248 Ascochyta pisi
Squash mosaic virus Leaf and pod spot. . . . . . . . . . . . . 274
Squash mosaic . . . . . . . . . . . . . . . 249 Botrytis cinerea
Tobacco ringspot virus Gray mold . . . . . . . . . . . . . . . . . . 275
Tobacco ringspot . . . . . . . . . . . . . 249 Erysiphe pisi
Watermelon mosaic virus Powdery mildew . . . . . . . . . . . . . 276
Watermelon mosaic virus . . . . . . . 250 Fusarium oxysporum f. sp. pisi
Zucchini yellow mosaic virus Fusarium wilt . . . . . . . . . . . . . . . . 277
Zucchini yellow mosaic . . . . . . . . 250
6 V EGETABLE D ISEASES – A C OLOUR H ANDBOOK
Mycosphaerella pinodes LACTUCA SATIVA (lettuce) SOLANUM

Ascochyta blight. . . . . . . . . . . . . . 278 LYCOPERSICUM (tomato)
Bacterial diseases
Peronospora viciae Bacterial diseases
Aster yellows phytoplasma
Downy mildew. . . . . . . . . . . . . . . 280
Aster yellows . . . . . . . . . . . . . . . . 296 Clavibacter michiganensis
Pythium spp. subsp. michiganensis
Pseudomonas cichorii
Pythium root rot, damping off . . . 282 Bacterial canker . . . . . . . . . . . . . . 327
Varnish spot . . . . . . . . . . . . . . . . . 298
Sclerotinia minor, S. sclerotiorum, Pseudomonas syringae pv. tomato
Rhizomonas suberifaciens
S. trifoliorum Bacterial speck . . . . . . . . . . . . . . . 330
Corky root . . . . . . . . . . . . . . . . . . 299
White mold, Sclerotinia rot . . . . . 283
Xanthomonas campestris pv. vitians Xanthomonas campestris
Viral diseases Bacterial leaf spot . . . . . . . . . . . . . 301 pv. vesicatoria
Bean leaf roll virus Bacterial spot . . . . . . . . . . . . . . . . 332
Bean leaf roll . . . . . . . . . . . . . . . . 283
Fungal diseases
Bremia lactucae Pseudomonas corrugata
Pea early browning virus Tomato pith necrosis . . . . . . . . . . 334
Downy mildew . . . . . . . . . . . . . . 302
Pea early browning. . . . . . . . . . . . 284
Botrytis cinerea Fungal diseases
Pea enation mosaic virus Alternaria alternata
Gray mold . . . . . . . . . . . . . . . . . . 304
Pea enation mosaic. . . . . . . . . . . . 285 Black mold . . . . . . . . . . . . . . . . . . 336
Fusarium oxysporum f. sp. lactucae
Pea seedborne mosaic virus Alternaria alternata f. sp. lycopersici
Fusarium wilt . . . . . . . . . . . . . . . . 306
Pea seedborne mosaic. . . . . . . . . . 286 Alternaria stem canker . . . . . . . . . 337
Golovinomyces cichoracearum
Pea streak virus Alternaria solani
Powdery mildew . . . . . . . . . . . . . 307
Pea streak . . . . . . . . . . . . . . . . . . . 286 Early blight. . . . . . . . . . . . . . . . . . 338
Microdocium panattonianum
Anthracnose, ring spot . . . . . . . . . 308 Athelia rolfsii
VICIA FABA (broad bean) Phoma exigua Southern blight. . . . . . . . . . . . . . . 340
Fungal diseases Phoma basal rot . . . . . . . . . . . . . . 310 Botrytis cinerea
Aphanomyces euteiches, Rhizoctonia solani Gray mold . . . . . . . . . . . . . . . . . . 341
Fusarium spp., Pythium spp., Bottom rot . . . . . . . . . . . . . . . . . . 311 Colletotrichum coccodes,
Phytophthora megasperma, Sclerotinia minor, S. sclerotiorum C. gloeosporioides, C. dematium
Rhizoctonia solani Lettuce drop . . . . . . . . . . . . . . . . . 313 Anthracnose. . . . . . . . . . . . . . . . . 343
Fusarium and other root rots . . . . 287 Fusarium oxysporum f. sp. lycopersici
Verticillium dahliae
Botrytis fabae, B. cinerea Verticillium wilt . . . . . . . . . . . . . . 315 Fusarium wilt . . . . . . . . . . . . . . . . 344
Chocolate spot . . . . . . . . . . . . . . . 288 Fusarium oxysporum
Didymella fabae
Viral diseases
f. sp. radicis-lycopersici
Leaf and pod spot. . . . . . . . . . . . . 290 Beet western yellows virus Fusarium crown and root rot . . . . 346
Beet western yellows. . . . . . . . . . . 317
Peronospora viciae Leveillula taurica,
Downy mildew. . . . . . . . . . . . . . . 291 Lettuce mosaic virus Oidium lycopersici,
Lettuce mosaic . . . . . . . . . . . . . . . 318 O. neolycopersici
Sclerotinia minor, S. sclerotiorum,
S. trifoliorum Lettuce necrotic stunt virus Powdery mildew . . . . . . . . . . . . . 348
White mold, Sclerotinia rot . . . . . 292 Lettuce dieback . . . . . . . . . . . . . . 320 Phytophthora capsici, P. cryptogea,
Uromyces vicia-fabae Mirafiori lettuce virus P. drechsleri, P. parasitica
Rust . . . . . . . . . . . . . . . . . . . . . . . 293 Lettuce big vein . . . . . . . . . . . . . . 321 Phytophthora root rot . . . . . . . . . 350
Tomato spotted wilt virus Phytophthora infestans
Viral diseases
Tomato spotted wilt . . . . . . . . . . . 323 Late blight . . . . . . . . . . . . . . . . . . 352
Broad bean stain virus,
Broad bean true mosaic virus Turnip mosaic virus Phytophthora spp., Pythium spp.,
Broad bean stain, Turnip mosaic . . . . . . . . . . . . . . . 324 Rhizoctonia solani
broad bean true mosaic . . . . . . . . 295 Abiotic disorders Damping-off, fruit rots. . . . . . . . . 355
Ammonium toxicity . . . . . . . . . . . . . 325 Pyrenochaeta lycopersici
Tipburn . . . . . . . . . . . . . . . . . . . . . . . 326 Corky root rot . . . . . . . . . . . . . . . 356
Sclerotinia minor, S. sclerotiorum
White mold, Sclerotinia rot . . . . . 358
Verticillium wilt . . . . . . . . . . . . . . 360
Viral diseases
Alfalfa mosaic virus
Alfalfa mosaic . . . . . . . . . . . . . . . 361
Beet curly top virus
Beet curly top . . . . . . . . . . . . . . . . 362
Cucumber mosaic virus
Cucumber mosaic . . . . . . . . . . . . 363
Potato virus Y
Potato virus Y. . . . . . . . . . . . . . . . 363
C ONTENTS 7
Tobacco mosaic virus, SPECIALTY AND
Tomato mosaic virus HERB CROPS
Tobacco mosaic, tomato mosaic . 364
Amoracia rusticana
Tomato spotted wilt virus Horseradish . . . . . . . . . . . . . . . . . 383
Tomato spotted wilt . . . . . . . . . . . 364
Anethum graveolens
Tomato yellow leaf curl virus Dill . . . . . . . . . . . . . . . . . . . . . . . 385
Tomato yellow leaf curl . . . . . . . . 366
Anthriscus cerefolium
Abiotic disorders Chervil . . . . . . . . . . . . . . . . . . . . . 385
Blossom end rot. . . . . . . . . . . . . . . . . 367 Beta vulgaris subsp. cicla
Swiss chard. . . . . . . . . . . . . . . . . . 386
SPINACIA OLERACEA Brassica rapa subsp. rapa
(spinach) Broccoli raab . . . . . . . . . . . . . . . . 389
Bacterial diseases Brassica spp.
Mustards . . . . . . . . . . . . . . . . . . . 390
Pseudomonas syringae pv. spinacia
Bacterial leaf spot . . . . . . . . . . . . . 368 Cichorium endivia, C. intybus
Endive/escarole, radicchio . . . . . . 391
Fungal diseases
Coriandrum sativum
Albugo occidentalis
Cilantro . . . . . . . . . . . . . . . . . . . . 396
White rust . . . . . . . . . . . . . . . . . . 369
Cymbopogon citratus
Aphanomyces cochlioides,
Lemongrass . . . . . . . . . . . . . . . . . 397
Fusarium oxysporum,
Pythium aphanidermatum, Cynara scolymus
P. irregulare, Rhizoctonia solani Artichoke . . . . . . . . . . . . . . . . . . . 398
Damping-off, root rots. . . . . . . . . 370 Eruca sativa
Cladosporium variabile Arugula . . . . . . . . . . . . . . . . . . . . 404
Cladosporium leaf spot . . . . . . . . 371 Foeniculum vulgare dulce
Colletotrichum dematium Fennel. . . . . . . . . . . . . . . . . . . . . . 406
f. sp. spinaciae Helianthus tuberosus
Anthracnose . . . . . . . . . . . . . . . . 373 Jerusalem artichoke . . . . . . . . . . . 407
Fusarium oxysporum f. sp. spinaciae Mentha spp.
Fusarium wilt . . . . . . . . . . . . . . . . 374 Mint . . . . . . . . . . . . . . . . . . . . . . . 409
Peronospora farinosa f. sp. spinaciae Nepeta cataria
Downy mildew, blue mold . . . . . . 375 Catnip . . . . . . . . . . . . . . . . . . . . . 410
Stemphylium botryosum Ocimum basilicum
Stemphylium leaf spot . . . . . . . . . 376 Basil . . . . . . . . . . . . . . . . . . . . . . . 411
Verticillium dahliae Origanum majorana, O. vulgare
Verticillium wilt . . . . . . . . . . . . . . 378 Marjoram, oregano . . . . . . . . . . . 413
Viral diseases Physalis ixocarpa
Tomatillo . . . . . . . . . . . . . . . . . . . 413
Beet curly top . . . . . . . . . . . . . . . . 379 Rheum rhubarbarum
Rhubarb. . . . . . . . . . . . . . . . . . . . 414
Beet western yellows virus
Beet western yellows . . . . . . . . . . 380 Rorippa nasturtium-aquaticum
Watercress . . . . . . . . . . . . . . . . . . 416
Cucumber mosaic . . . . . . . . . . . . 381 Salvia officinalis
Sage . . . . . . . . . . . . . . . . . . . . . . . 418
Tragopogon porrifolius,
Scorzonera hispanica
Salsify, scorzonera . . . . . . . . . . . . 419
Valerianella locusta,V. olitoria
Corn salad . . . . . . . . . . . . . . . . . . 420
Zea mays var. saccharata
Sweetcorn. . . . . . . . . . . . . . . . . . . 421
Glossary . . . . . . . . . . . . . . . . . . . . . 422
Index . . . . . . . . . . . . . . . . . . . . . . . . 437
8
Preface
FROM THE LAND that is clean and good, by the will of its Cherisher, springs up produce,
(rich) after its kind: but from the land that is bad, springs up nothing but that which is niggardly:
thus do we explain the signs by various (symbols) to those who are grateful.
7 (Al-Araf): Verse 58 , The Quran
MAY THE WINDS blow sweetly,

May the rivers flow sweetly,
May plants and herbs be sweet to us,
May days and nights be sweet to us. . . .
X. 48–50, Yajur Veda. Taitt. Aranyaka
. . . IF THERE IS FAMINE in the land, if there is pestilence,

if there is blight or mildew, locust or grasshopper. . . .
I Kings 8:37, The Bible
IF THERE IS BLIGHT OR MILDEW on one’s crops, what is diseases that affect vegetables compromise such quality
one to do? The topic of diseases that damage and kill and therefore are of great importance to grower,
plants is hardly a new subject. For as long as humans shipper, marketer, and consumer. Vegetable production
have foraged for, grown, traded, or eaten edible plants, and marketing in the 21st Century has been fashioned
disease-causing organisms have been present and by technology and developments that are unique to our
exacted their toll on quality, yields, and consumer satis- times, including molecular biology, globalization of
faction of these commodities. Impacts of plant diseases international trade, awareness of the benefits and
on the lives of people range from the nuisance of losing dangers of synthetic pesticides, and insights into specific
a few plants in one’s garden, to significant economic health benefits of vegetable foods.
losses to a farmer, and finally to widespread famine due This book is written to address the broad topic of
to extensive crop losses in a region. Throughout human diseases that affect vegetables. Part 1 offers a brief
history, devastating crop losses have sometimes resulted introduction to vegetable crops, descriptions of the
in subsequent loss of human life and disruptive migra- disease-causing agents, suggested strategies for identi-
tions of the inhabitants. Humanity’s dependence on fying and diagnosing vegetable diseases, and general
healthy crops and reliable sources of food, therefore, principles in controlling them. In this book we describe
transcends all barriers of culture, nation, and time. We diseases that are primarily caused by pathogens (biotic
all need to eat and to feed our children. diseases). Problems caused by nutritional and physio-
Vegetables are an essential and increasingly popular logical disorders and environmental and cultural
component of human diets today. Collectively, vegeta- factors (abiotic problems) are mostly not covered.
ble crops are a major part of agricultural commerce. The rest of the book (Part 2) is divided into chapters
The vegetable industry produces large volumes of high on the principal crop groups (and further subdivided if
quality commodities that are intensely marketed and different plants within the group suffer from distinct
can be delivered locally and regionally or shipped sets of diseases) and describes the major diseases that
internationally. Consumer standards and market affect those vegetables. The diseases are, for the most
requirements mandate excellent quality produce. The part, organized first by pathogen type and then by
P REFACE 9
pathogen name. (We should point out that each crop In an effort to keep this book timely and reduce the
chapter does not include all possible diseases and that amount of information that rapidly becomes outdated,
the disease list is therefore not exhaustive.) Of special we have not included specific information on vegetable
note are chapters devoted to spinach – an increasingly crop cultivars, pesticide product recommendations, and
popular vegetable – and to specialty crops and herbs. seed treatments. Such information can change from
Each disease entry includes a brief introduction to the year to year and also varies greatly between regions,
disease, detailed description of symptoms, information countries, and continents. Seed treatments, in particu-
on the pathogen and disease development, and sugges- lar, can be implemented in many ways depending upon
tions on how to manage the problem. For pathogens the practitioner, the nature and location of the seed
that affect several crops, full details are presented in treatment facility, and so on. For up-to-date and area-
only one chapter in order to reduce unnecessary repeti- appropriate recommendations on vegetable cultivars
tion; for other crops that are subject to the same disease, and disease control chemicals and treatments, consult
reference will be made to the more complete chapter. local extension agents, agricultural consultants, or other
Selected references are included that will allow interest- professionals who are familiar with the location.
ed readers to further research the subject. We have written this book with a very broad and
Our collective experience in applied research, diverse audience in mind. We hope this effort will help
extension education, and working closely with farmers and be of interest to the following persons: research and
and industry members has shaped our approach. Our extension plant pathologists; diagnosticians and plant
aim is to increase recognition and diagnosis of vegetable lab personnel; teachers of agriculture and related
diseases and to provide information on biology and subjects; university students in agriculture and related
control of the problems. A particular feature of this fields; commercial farmers, vegetable producers, and
book are the many high-quality color photographs that farm managers; agriculturalists in the fields of seed
illustrate most of these vegetable diseases and which production, vegetable breeding, agrichemicals, pest
will assist the reader in identifying and understanding control, marketing, and other subjects; government and
them.The glossary at the end lists much of the termi- regulatory persons dealing with agriculture; home
nology used in plant pathology and related fields. gardeners and hobbyists.
ACKNOWLEDGEMENTS
We have many collaborators with the University of We greatly thank the following persons for
California, ADAS, and other agencies who have contributing photographs to this book:
assisted us with research and extension projects on Mike Asher, Lindsey du Toit, John T Fletcher,
vegetable diseases. We acknowledge the following Philip Hamm, Mary Hausbeck, Nikol Havranek,
persons for such contributions: DM Ann, Gerald Holmes, David R Jones, AP Keinath,
NJ Bradshaw, CT Bull, EE Butler, WS Clark, Frank Laemmlen, David Langston, Robert McMillan,
DA Cooksey, JML Davies, RM Davis, Gene Miyao, Krishna Mohan, Tim O’Neill,
Dorothy M Derbyshire, BW Falk, RL Gilbertson, Ken Pernezny, Melodie Putnam, Richard Smith,
TR Gordon, AS Greathead, Kim Green, GW Griffin, Mike Stanghellini, Tom Turini, William Wintermantel.
MJ Griffin, S Hammond, P Headley, D Henderson, We thank Manson Publishing for providing us the
DR Jones, OW Jones, K Kammeijer, BC Knight, opportunity to present this work. We especially thank
FN Martin, GM McPherson, the late SC Melville, Jill Northcott for assistance, guidance, and encourage-
R Michelmore, the late JM Ogawa, TM O'Neill, ment with this project, and Ayala Kingsley and Derek
GS Saenz, RF Smith,KV Subbarao, HJ Wilcox, Hall for their careful work on our manuscript.
DJ Yarham. Steven Koike thanks the many farmers, pest control
We thank David Yarham, John Fletcher, and our advisors, and agriculturalists in California who taught
two reviewers for their efforts in evaluating the book him so much about vegetable crops.
and suggesting improvements.
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11
PART 1
Introduction to
Vegetable Crops
and Diseases
• VEGETABLE PRODUCTION • DIAGNOSING DISEASE
The increasing importance of The importance of accurate, timely
vegetables; vegetable commodities; diagnosis; overall strategy; asking the right
technological advances; challenges in questions; conducting the examination;
vegetable production; the challenge of incorporating laboratory tests;
plant diseases diagnosing virus diseases; digitally assisted
diagnosis; compiling information and
• CAUSES OF DISEASE
Diseases caused by biotic agents (bacteria, drawing a conclusion
viruses, fungi, fungus-like pathogens); • CONTROLLING DISEASE
disorders caused by abiotic factors and Criteria for commercial control of
physiological conditions vegetable diseases; disease control options;
other aspects of disease management
12 I NTRODUCTION TO V EGETABLE C ROPS AND D ISEASES
Vegetable production
Vegetables are a critically important part of the human diet. Along with grains and fruits,
vegetables are one of the three major food groups of plant origin. The highly perishable nature of
most vegetable commodities, along with the market demand for a steady supply of high-quality,
disease-free produce, makes vegetable production a challenge for the farmers of the world.
The increasing importance of vegetables diverse vegetable and salad components that are
The role of vegetables in the human diet has increased washed, chopped into consumable portions, mixed
for several reasons. Nutritional and medical research together, and sealed into plastic bags that allow for
elucidates the value and role of these foods in keeping many days of shelf-life.
us healthy. Vegetables provide essential carbohydrates, Finally, the modern world market situation is
proteins, fibers, vitamins, and minerals. Researchers are responsible for allowing significant increases in
indicating that components found in vegetables provide vegetable production to take place. The current global
additional health benefits such as the following: economy and intense export/import businesses make it
reduced cancer risk associated with lycopene in tomato possible for vegetables produced in one part of the
and watermelon fruit, beta-carotene from carrots and world to be quickly shipped and made available to
squash, lutein from broccoli and peas, and glucosino- markets and consumers anywhere else in the world.
lates from crucifers; lowered blood pressure and other Transportation systems and postharvest handling have
benefits for the circulatory system associated with improved over the years, resulting in high-quality
anthocyanins in beets, red cabbage, and kidney beans; produce with excellent shelf-life being available year-
assistance with depression associated with B vitamin round to the consumer.
folate in legumes and spinach; prevention of age-related The emergence of large corporate, national, and
macular degeneration of the eye attained from the international marketing chains and companies has also
antioxidant lutein in spinach leaves; reduced heart affected the way vegetables are produced. Such huge
disease and cancer risk associated with allicin in onion conglomerates in large measure are able to exert
and garlic. These and other examples highlight specific control over commodities such as vegetables. Vegetable
roles that vegetables have in possibly addressing human growers and suppliers must agree to provide steady
diseases. supplies of high-quality produce at fixed prices in order
In addition to nutritional and health issues, vegeta- to sell to such chains. These business agreements place
bles bring a welcome aesthetic value to the table. pressure on growers who cannot allow disease and
Because there are so many different kinds and varieties other production problems to interfere with harvest
of vegetables, these commodities are an important schedules and projections.
source of diversity, color, taste, and texture in cooking. Total world vegetable production has increased
Specialty vegetables, baby leaf and baby vegetable almost three-fold over the last 30 years according to
products, and organically produced commodities FAO reports (Table 1). This phenomenal growth
provide additional choices to the people preparing and applies to many of the major vegetable crops, including
eating vegetables. New vegetable types, vegetable tomato, onion, eggplant, pepper, carrot, cucurbits,
products, and the changing tastes and demands of the spinach, and lettuce. Increases in corn, pea, and bean
consumer have further encouraged growth in the production have doubled. In comparison to the growth
vegetable producing industry. For example, ready-to- of vegetable production, over the same 30-year period
eat bagged vegetable products have greatly increased in the human population has increased approximately 1.6
popularity and availability. These products consist of times, from 3.84 to 6.22 billion people.
V EGETABLE P RODUCTION 13
TABLE 1 Thirty-year trends for world production of major vegetable crops
Vegetable crop 1972 1982 1992 2002

Artichoke 1.40 1.18 1.24 1.26
Asparagus 1.16 1.42 2.24 5.08
Bean 2.68 3.18 3.66 5.65
Bean, string 1.02 1.12 1.32 1.72
Broad bean 0.66 0.87 1.00 1.02
Cabbage 27.39 39.39 39.78 62.47
Carrot 7.96 11.24 13.99 21.02
Cauliflower 4.48 6.57 10.24 15.05
Corn 4.84 5.77 7.26 8.40
Cucumber, gherkin 10.63 14.72 18.61 36.40
Eggplant (aubergine) 6.59 9.14 11.47 29.93
Garlic 2.98 4.76 7.34 12.11
Leek and other alliums 0.79 0.80 1.41 1.52
Lettuce 6.89 9.00 12.42 18.75
Mushroom 0.79 1.14 1.94 3.07
Okra 1.82 2.61 3.61 4.90
Onion and shallot, fresh 1.60 2.53 3.25 4.36
Onion, dry 16.94 24.57 32.35 51.91
Pea 4.86 5.98 6.75 9.06
Pepper 6.19 8.23 11.33 22.17
Pumpkin, squash, gourd 6.23 8.60 10.84 16.91
Spinach 2.34 3.40 4.42 10.31
Tomato 38.49 57.67 74.76 108.50
Total fresh vegetables 158.73 223.89 281.23 429.40
Units = million metric tonnes [ million MT]

Listed vegetables are for fresh market and do not include crops grown for dried or processed products. Source: FAO
(http://apps.fao.org)
Vegetable commodities
What exactly is a vegetable? Like many words, the term horticultural understanding of ‘vegetable’ which usually
itself has different meanings and degrees of ambiguity excludes traditional fruit commodities such as peach,
depending upon the context of its use. A formal dic- pear, apple, cherry, grape, blackberry, strawberry, and
tionary definition is the following: vegetable = usually many others. Botanically, a vegetable is usually defined
an herbaceous plant grown for the edible part that is as those parts of a plant derived from a vegetative organ
eaten as part of a meal; also, such an edible part (root, bulb, crown, stem, rhizome, petiole, leaf) and so
(Merriam-Webster’s Collegiate Dictionary). This defi- would not include reproductive structures like tomato
nition, however, is broader than the agricultural/ and pepper fruit, cauliflower and artichoke flower
buds, and bean and pea pods and seeds. The conven- TABLE 2 Plant families and selected commercial
vegetable crops
tional usage of ‘vegetable’ is a combination of all these
meanings. Vegetables traditionally cover all crops Plant family Examples of vegetable crops
derived from vegetative plant parts, and also include
Alliaceae Onion, garlic, leek, chives, shallot
selected flower, fruit, and seed commodities that over
Amaranthaceae Beet, Swiss chard, spinach
time were considered vegetables through common use
Apiaceae Carrot, celery, celeriac, parsley,
and inclusion in non-dessert foods. parsnip, cilantro, fennel, dill,
In the USA, the issue of ‘what is a vegetable’ needed chervil
to be addressed by the country’s highest court. In 1893, Asparagaceae Asparagus
the US Supreme Court ruled on whether tomato was a Asteraceae Lettuce, endive, radicchio,
vegetable or fruit. This authoritative legal body decided artichoke, Jerusalem artichoke,
salsify
that for Americans the tomato would be considered a
vegetable. This ruling was necessary because business- Brassicaceae Broccoli, Brussels sprout, cabbage,
cauliflower, mustard, arugula,
es and regulatory agencies did not know whether radish, broccoli raab, watercress
tomatoes were subject to commerce laws for fruits or Cucurbitaceae Cucumber, squash, melon,
vegetables. Interestingly, ketchup derived from pumpkin, watermelon
processed tomatoes was quite popular many years Fabaceae Bean, broad/faba bean, pea
before this legal discussion; ketchup was declared Lamiaceae Mint, basil, oregano, marjoram,
America’s National Condiment in 1830. sage, catnip
Like all other plants, each vegetable crop plant is Poaceae Corn, lemongrass
given scientific genus and species names. Each vegetable Polygonaceae Rhubarb
is then grouped taxonomically into plant families Solanaceae Pepper, tomato, eggplant, potato,
(Table 2). Knowledge of these plant families and the tomatillo
relatedness between certain vegetable commodities is Valerianaceae Corn salad
often useful in understanding plant pathogen dynamics
and devising disease management strategies. While
some pathogens are able to infect hundreds of plants in
many different plant families, most of these organisms
have much smaller host ranges. In many cases, the
pathogens will tend to infect only crops within these
plant families. Rust (Puccinia allii) of garlic infects
onion and chives, but not non-alliums. The black rot
pathogen of crucifers (Xanthomonas campestris pv.
campestris) attacks many plants in the Brassicaceae, but
not plants in other families. The extensive research
information available for sugar beet diseases can in
large measure be used to help understand diseases of the
closely related table beet and Swiss chard.
Technological advances stock sources, placement of seed increase plantings in

There have been major changes and improvements in arid regions, vigilant monitoring of seed fields, roguing
the production of vegetables. To begin with, there is of fields having symptomatic and off-type plants, devel-
now a great awareness of, and appreciation for, the opment and use of sensitive pathogen detection
importance of seedborne pathogens. The seed pro- methods, and treatment of seed to reduce what
ducing industry now invests a great amount of research pathogens might be present.
and effort into providing high-quality, relatively Advances in seed physiology, such as seed priming
pathogen-free seed to growers. Such seed results from and coating treatments, also contribute to improve-
the following steps: establishment of clean mother seed ments in seed quality, seedling vigor, and reduction in
disease problems. Seed coat treatment is a highly dioxide inside the bags and allow these products to have
developed, sophisticated science. Seeds are coated with significant shelf-life. Properly refrigerated, these cleaned
various substances so that they can be more easily and chopped products may last perhaps as long as 7 to
handled during planting, germination can be modified 10 days after they go on the market. Products are
and controlled, and protection against pests and intended to be ready-to-eat and do not usually need
diseases can be ensured. Seed priming is a relatively further preparation. These ‘value added’ or ‘lightly
recent development. Seed priming treatments are processed’ products have greatly changed the vegetable
applied before seeds leave the packaging facility, and market by providing novel products that are convenient
consist of processes that invigorate seeds and actually for the consumer. Vegetables included in these products
initiate some physiological steps in germination. When include lettuce, carrot, celery, cauliflower, broccoli,
primed seeds are placed in the soil or rooting medium, cabbage, mustards, arugula, endive, radicchio, spinach,
seeds will germinate more rapidly and uniformly than beet leaves, Swiss chard, and others.
non-primed seeds. Research on plant pathogens has also aided the
Vegetable transplants to start new plantings are less vegetable industry. More sensitive, highly accurate
frequently grown in the ground, but instead now are pathogen detection methods are now available for
often produced in sanitized transplant trays, using soil- many seedborne pathogens of vegetables. In-depth
less rooting media, and placed in greenhouses where studies on disease epidemiology help explain the
conditions can be strictly controlled. In the USA, the biology of vegetable pathogens and enable better
great majority of celery, cauliflower, tomato, pepper, disease control strategies to be devised. Extensive
lettuce, and melon transplants are grown under this breeding efforts develop resistant cultivars. Safer fungi-
system. cides that are less disruptive to the environment are
Vegetable crop breeding programs continue to being used on vegetables. Compared to older genera-
produce new, vigorous, productive cultivars. The tion pesticides, such chemicals are applied at very small
creation of improved hybrids brings about increases in rates and enable growers to control diseases while
yield and in some cases resistance to diseases and pests. adding less fungicide to the environment.
While not universally accepted at the consumer level,
the fields of molecular biology and genetic engineering Challenges in vegetable production
potentially can further advance vegetable plant Despite advances in vegetable production and disease
breeding. management, many challenges face growers of vegeta-
Postharvest handling methods have improved bles. Because of the nature of today’s worldwide
greatly. Postharvest research has informed the industry market, there are extremely high expectations for
about the optimum ways of harvesting, transporting, growers to provide ample supplies of high-quality,
and storing vegetable commodities. Improvements have disease-free produce that has extended shelf-life.
therefore been made in the ways these vegetables are Markets are looking to suppliers to provide such
handled once they leave the field. These improvements produce over many months each year. Competition to
have increased the overall quality of marketed vegeta- maintain a market share in this global vegetable market
bles, improved their shelf-life, and made possible the is intense.
long-range transport and sale of vegetables to distant In addition to requiring high quality, the world
overseas destinations. market is demanding food that is safe to consume.
A revolutionary postharvest advancement for veg- Vegetables for both local and regional markets and for
etables was the rapid development and marketing of use overseas must be free of human, foodborne
bagged, ready-to-eat vegetable products. Developed on pathogens and contaminants such as Escherichia coli,
a large scale within the past 10 years, a wide variety of Salmonella, other enteric bacteria, and various other
vegetable commodities are harvested and taken to pro- microorganisms. Mistakes in the handling chain from
cessing facilities where they are washed, cut and field to table can result in consumer exposure to such
prepared, and placed in bags made of specialized, semi- pathogens. This requirement for cleanliness and careful
permeable materials. These specially designed plastics handling adds another pressure in the vegetable
control the concentrations of oxygen and carbon producing business.
Another challenge is the need to produce high- human health reasons, some pesticides are no longer
quality vegetables while reducing the use of synthetic available for use on vegetables and others will either be
pesticides. Consumers worldwide want fewer chemicals eliminated in the future or their use will be severely
on their food products, but still demand high quality restricted. Therefore, a disease control program that
and long shelf-life. Vegetable growers must grapple relies on fungicides requires revision and development
with both demands. As time passes, there are fewer of new and integrated strategies. Because of the chal-
fungicides remaining to control diseases, fewer insecti- lenges posed by plant pathogens, it will be imperative
cides to control insect vectors of pathogens, and fewer for growers and field personnel to be familiar with the
herbicides to control weeds that harbor both insect vegetable diseases they may face.
vectors and pathogens. Reduction in pesticide use is a
food safety and health issue as well as an environmen-
tal one. Individuals and groups are seeking to better
preserve the wildlife and environment around us, and
hence seek reduced pesticide use. The example of the
soil fumigant methyl bromide and the international
movement to ban the agricultural use of this chemical is
a prominent case study that illustrates these trends and
issues.
The challenge of plant diseases

For as long as humans have foraged for, grown, traded,
sold and bought, or eaten vegetables and other edible
plants, disease-causing organisms have reduced quality,
yields, shelf-life, and consumer satisfaction of these
commodities (see the references cited in this chapter that
give examples of plant disease concerns throughout
history). Therefore, managing these diseases is an
essential task of all producers. If a particular grower
cannot provide vegetables having these high standards,
then other farmers in the region or the world will take
over that market share. Therefore, disease control has
become an extremely critical aspect in the drive to
produce excellent quality vegetables. Ironically, the
same extensive international system that makes possible
the selling, buying, and transporting of harvested veg-
etables across the globe also can create new disease
problems for growers. Pathogens that occur in one part
of the world can be moved on contaminated or diseased
seed and plant material to other parts of the world
where that pathogen never before had occurred.
The cost of producing vegetables continues to climb,
placing ever-increasing economic pressure on growers.
Rising land use, water, seed, equipment, fuel, fertilizer,
pesticide, and labor expenses force growers to
maximize yields and seek economical ways to control
diseases. A final contemporary challenge is the
worldwide trend of reducing the use of certain pesti-
cides on food commodities. For environmental and
References on vegetables and general production Ryder, E. J. 1999. Lettuce, Endive, and Chicory. Crop
Production Science in Horticulture Series, No.9. CABI
Anonymous. 2003. Basic Horticultural Statistics for the United Publishing.
Kingdom Calendar and Crop Years 1992/93–2002/3. Defra Savona, N. 2003. The Kitchen Shrink. Duncan Baird Publishers,
Publications, London.
London, 144 pp.
Anonymous. 1992. Basic Horticultural Statistics for the United
Schneider, E. 2001. The Essential Reference: Vegetables From
Kingdom Calendar and Crop Years 1981–1990. Ministry of
Amaranth to Zucchini. William Morrow.
Agriculture, Fisheries and Food Publications, London.
University of California. 1998. Specialty and Minor Crops
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Causes of disease
A MULTITUDE of microscopic and sub-microscopic pathogens threaten vegetable crops
and can cause significant damage: principal among them are bacteria, fungi, and viruses.
Knowledge of the names, characteristics, and biology of these pathogens is critical
in the effort to identify and control them.
Diseases caused by biotic agents BACTERIA

Some understanding of the taxonomy of plant patho- Bacteria are microorganisms placed in the kingdom
genic organisms is required to identify them accurately, Prokaryota and are typically single-celled organisms,
understand their biology, and ultimately to best control lack a membrane-bound nucleus, and usually have an
them. Taxonomy is the science that classifies, catego- enclosing cell wall. Most plant pathogenic bacteria are
rizes, and names organisms. The taxonomy of plant rod-shaped, Gram-negative species in the genera
pathogens, like that of all organisms, continues to Acidovorax, Agrobacterium, Erwinia, Pseudomonas,
change and develop. Ongoing research, discovery of Ralstonia, Serratia, and Xanthomonas. Rhizomononas
additional species, and modern molecular and bio- bacteria are thus far only pathogenic on lettuce, are
chemical methods allow researchers to more precisely Gram-negative, and live in the soil as soil inhabitants.
define these classifications, resulting in occasional but Pathogenic Clavibacter bacteria, previously in the genus
significant changes in previous taxonomic schemes. Corynebacterium, are rod-shaped Gram-positive
The major groups of plant pathogens are the fungi species. Streptomyces species are Gram-positive actin-
and fungus-like organisms, bacteria and other prokary- omycete bacteria that are found in soils, produce an
otes, and viruses and viroids. These major groups cover aerial mycelium and chains of spores, and form fila-
the vast majority of the pathogens that affect plants, mentous, branching colonies. Xylem-inhabiting, path-
though a few other miscellaneous pathogens exist. A ogenic bacteria in the Xylella group are not pathogenic
few plant pathogens are higher vascular plants such as on vegetables but cause diseases of woody plants and
dodder (Cuscuta species), broomrape (Orobanche trees.
species), witchweed (Striga species), and mistletoes There are many vegetable crop pathogens in the
(species of Arceuthobium, Phoradendron, and Erwinia, Pseudomonas, and Xanthomonas genera. In
Viscum). In very humid or tropical areas there are a few most cases these pathogens are readily isolated onto
other pathogens that are classified in other microor- standard microbiological agar media. Presumptive
ganism groups. The alga Cephaleuros virescens is path- identification to genus, and sometimes species, level
ogenic on citrus and other plants in warmer regions of requires matching strain features with known charac-
the world. Flagellate protozoa, or flagellates, are path- teristics such as colony morphology and color on
ogenic on plants in tropical areas. Examples of flagel- certain agar media, reactions to a number of biochemi-
lates are Phytomonas species on coffee, cassava, and cal tests, serological reactions, chemical composition,
coconut palm. Microscopic unsegmented worms, or fatty acid and other physiological profiles, and
nematodes, are important parasites on plants but are molecular profiles.
usually considered parasitic pests and not pathogens. Species in the Pseudomonas and Xanthomonas
Tables 3, 4 (page 21), and 5 (page 23) list the primary genera are often further divided into sub-species cate-
bacterial, fungal, and viral pathogens that affect gories based on host ranges. For example, the P.
vegetable crops. Table 7 (page 26) lists the vegetable syringae pathogen that infects tomato is primarily
diseases that are discussed and illustrated in this book. restricted to tomato. Therefore, pathologists go further
C AUSES OF D ISEASE 19
in their classification scheme for P. syringae and passes through fields can all become contaminated,
designate the tomato pathogen as a specific pathovar harbor bacteria, and spread these pathogens to clean
(pv.). This organism is therefore named Pseudomonas plants. A few bacterial pathogens are vectored by
syringae pv. tomato. In official taxonomic systems, the insects that become contaminated by feeding, then
pathovar designation is not a taxonomic term, but is a move and spread the pathogen to other plants. A
useful means for pathologists and agriculturalists to significant number of bacteria are seedborne in vege-
identify host–pathogen relationships and distinguish tables because they are inside the seed or present on the
between closely related but distinct bacterial pathogens. seed as external contaminants. Germination of the
Mollicutes are prokaryotes that differ from other infested seed can result in a plant that has the bacterial
bacteria in important ways. Mollicutes notably lack cell disease. Plant pathogenic bacteria rarely survive free in
walls, have very small genomes, and previously were the soil, but can persist on crop residues that are not
called mycoplasma-like organisms (MLOs). There are completely decomposed. There are a few exceptions, as
two groups of mollicutes that are pathogenic on plants. Agrobacterium tumefaciens, Ralstonia solanacearum,
Spiroplasmas are mollicutes that are single-celled and Rhizomonas suberifaciens, and Streptomyces scabies
form helical structures. Phytoplasmas are the more are true soilborne organisms.
commonly encountered mollicute on plants and take on
various shapes (called pleomorphism). Plant pathogen-
ic phytoplasmas are usually transmitted by insects such
as leafhoppers for the aster yellows phytoplasma, and
plant hoppers for clover phyllody phytoplasma.
Diseases caused by phytoplasmas often cause virus-
like symptoms to develop on plants; therefore, for many
years researchers attributed these problems to viruses.
In 1967, MLOs were found in plants for the first time,
thereby documenting that such diseases were caused by
these bacteria and not by viruses. MLOs that are found
in plants are now called phytoplasmas or spiroplasmas.
Phytoplasmas thus far have not been cultured in vitro.
For the most part, confirmation of phytoplasmas
requires molecular or serological tests and examination
of plant tissues using electron microscopy.
Bacteria find their way to plant hosts in a number of
ways. Most of these organisms survive on plant surfaces
as epiphytes until sufficient population numbers are TABLE 3 Common prokaryotes that cause
achieved. Bacteria reproduce by cell division, or fusion. diseases of vegetables
With the exception of Streptomyces, these plant patho-
genic bacteria do not make spores or other differentiated Bacteria Acidovorax
reproductive cells or structures. When high epiphytic Clavibacter
populations are attained, the bacteria are able to enter Erwinia
the plant via natural openings (stomata, hydathodes) or Pseudomonas
wounds, reproduce inside plant tissues, and cause Ralstonia
disease. Bacteria present on diseased plants are Rhizomonas
dispersed to other plants by splashing rain or irrigation Serratia
Streptomyces
water. Winds generally do not spread bacteria, so this
Xanthomonas
pathogen does not travel far like fungal spores. Bacteria
are readily spread by contact. Transplant trays, green- Phytoplasma Aster yellows phytoplasma
house benches, shears used to prune plants, workers
who handle diseased plants, and even equipment that
VIRUSES now grouped into families of closely related virus

Viruses are sub-cellular entities and are made up of pathogens.
some form of nucleic acid that is usually encased in a In general, viruses do not exist and survive in nature
coat of protein or other biochemical substance. Virus without another organism. The plant host is the
genomes can be single- or double-stranded DNA or primary refuge of these pathogens. Viruses typically
RNA, and can consist of single (monopartite) or infect plants in a systemic way, and thereby make their
multiple (multipartite) components. Viroids are similar way into plant leaves, stems, seeds, and even flowers,
to viruses except that they consist of only an RNA pollen, and roots. Cuttings, crown divisions, and other
genome; viroids do not have any protective outer coat. vegetative means of dividing plants will therefore result
The outer virus coats take on diverse shapes such as in progeny that are already infected with the virus
flexuous threads, spherical polyhedrals, cylindrical agent. Only certain viruses have the capability of
rods, and others. Some viruses consist of multiple, entering plant seeds and becoming seedborne patho-
attached particles, with each sub-unit containing part gens. A limited number of plant viruses are carried in
of the genome. pollen.
Being sub-microscopic entities, virus particles cannot With the exception of pollen-borne viruses, in the
be observed with the light microscope. Therefore, to field viruses mostly move between plant hosts via a
confirm the presence and identification of a particular mobile organism, called a vector, that carries the virus.
virus, plant tissue must be observed with an electron Vectors usually feed on the infected plant, become con-
microscope and tested using serological and molecular taminated or infested with the virus, then move to
techniques. Extensive development of virus-specific healthy plants and infect them by feeding. Arthropods
antisera and the enzyme-linked immunosorbent assay are the most common plant virus vectors and include
(ELISA) detection methods have facilitated confirma- aphids, leafhoppers, whiteflies, thrips, beetles, and
tion of virus agents. The now commonly used spider mites. Soilborne nematodes in the Longidoridae
molecular method called the polymerase chain reaction family (genera are Trichodorus, Paratrichodorus,
(PCR) is a powerful tool used for identifying viruses and Longidorus, Paralongidorus, Xiphinema) and
other organisms. PCR matches pieces of known genetic protozoan soil microorganisms such as Olpidium and
sequences (primers) with the unknown virus sample. If Polymyxa species are also virus vectors. Two viruses in
the match is positive, then the identity of the virus agent the tombusvirus group, Tomato bushy stunt virus and
can be confirmed. Labeling viruses with fluorescing Lettuce necrotic stunt virus, present an interesting
substances has proven useful in fluorescent antibody exception to the dependence on vectors. These two
microscopy. In addition, some plant viruses induce the pathogens have no known vector, but apparently exist
host to form various crystals and other structures freely in soil and water. The viruses are distributed when
within the cell; these objects are called virus inclusions infested soil is moved and infested water floods fields or
and can aid in the identification of the virus. The use of is used in irrigation. Some viruses are readily spread
indicator plants, in which a test plant such as tobacco is mechanically in plant sap and fluid. The rubbing and
rubbed with a plant extract that may contain viruses, abrasion that takes place between plants in the field can
may show that the plant sap was infected with a virus- therefore theoretically spread virus agents; however, this
like agent. However, the resulting symptoms on these means of virus spread is not significant in the field.
indicator plants are generally not specific enough to More significant is the spread of virus that takes place
pinpoint precisely which virus was present in the sap. when people handle infected plants, become contami-
Plant virus taxonomy divides viruses into different nated with plant sap having viruses, and then touch
groups depending on the natures of the genome and uninfected plants.
external coat. Therefore there are DNA and RNA Viruses do not reproduce independently. Once a
viruses. Within each of these two groups there are virus has been introduced into a host cell, the viral
single- or double-stranded nucleic acid viruses. Further genome is released into that cell and induces the cell to
dividing criteria are the shape of the virus external coat manufacture the nucleic acid and protein components
and whether there are one or more strands of nucleic needed to assemble more virus particles. Newly
acid per virus. Using these and other criteria, viruses are assembled viruses then spread from cell-to-cell via
TABLE 4 Common viruses that cause diseases of vegetables

Virus family Virus
Virus family Virus
Potyvirus Asparagus virus 1
Alfamovirus Alfalfa mosaic virus
Bean common mosaic virus
Begomovirus Sinaloa tomato leaf curl virus Bean yellow mosaic virus
Beet mosaic virus
Carlavirus Pea streak virus
Celery mosaic virus
Shallot latent virus
Garlic yellow streak virus
Caulimovirus Cauliflower mosaic virus Garlic yellow stripe virus
Leek yellow stripe virus
Closterovirus Beet pseudo-yellows virus
Lettuce mosaic virus
Beet yellows virus
Onion yellow dwarf virus
Cilantro yellow blotch virus
Papaya ringspot virus type W
Comovirus Broad bean stain virus Pea seedborne mosaic virus
Broad bean true mosaic virus Potato virus Y
Squash mosaic virus Tobacco etch virus
Cucumovirus Cucumber mosaic virus Turnip mosaic virus
Watermelon mosaic virus
Enamovirus Pea enation mosaic virus Zucchini yellow mosaic virus
Furovirus Beet necrotic yellow vein virus Rhabdovirus Beet leaf curl virus
Geminivirus Beet curly top virus Rymovirus Onion mite-borne latent virus
Squash leaf curl virus
Tomato yellow leaf curl virus Sequivirus Parsnip yellow fleck virus
Ilavirus Asparagus virus 2 Tobamovirus Pepper mild mottle virus

Tobacco streak virus Tobacco mosaic virus
Tomato mosaic virus
Luteovirus Bean leaf roll virus
Tobravirus Pea early browning virus
Nepovirus Artichoke Italian latent virus
Artichoke yellow ringspot virus Tombusvirus Lettuce necrotic stunt virus
Tobacco ringspot virus Watercress yellow spot virus
Ophiovirus Mirafiori lettuce virus Tospovirus Tomato spotted wilt virus
Polerovirus Beet chlorosis virus Umbravirus Carrot mottle virus

Beet mild yellowing virus
Beet western yellows virus Viroid
Carrot red leaf virus
Watercress chlorotic leaf spot viroid
Potexvirus Artichoke curly dwarf virus
Asparagus virus 3
cytoplasmic connections between adjacent cells (plas- tative plant propagation units (transplants, cuttings,
modesmata). When viruses reach phloem vascular crown divisions), vectors that have obtained the virus,
tissue, the viruses are rapidly dispersed to other parts of pollen, virus-infected seed, and in some cases, infested
the plant, in particular the actively growing shoots and soil and water. Disease development and rate of spread
new leaves. will depend on the biology, distribution, and movement
Pathogen life cycle and disease development can be of the vector. Virus diseases initiated by seedborne
complex and must take into account multiple factors. viruses will depend on the number of infested seeds in
The primary source of the virus can be any number of any one seed lot. Transmission of the virus depends
plants in the field (crops, weeds, volunteer hosts), vege- either on how the vector feeds on plants and how the
virus is able to survive on or in the vector, or on the gametes or two compatible mycelia, which is followed
degree that infested plant sap is infectious. Therefore, a by meiosis. Meiotic division results in sexually
clear understanding of virus disease epidemiology produced spores, with the fungi in Zygomycota having
requires extensive research and information. zygospores, Ascomycota producing ascospores, and
Basidiomycota forming basidiospores.
FUNGI Many of the fungi in these three phyla also produce
This group of microorganisms encompasses the great a different, asexual spore type. These spores are not the
majority of plant pathogens. Fungi are predominantly result of sexual recombination. For fungal pathogens of
multicellular organisms, lack chlorophyll, have cell vegetables, the asexual spore is often the most
walls, and have DNA in a membrane-bound nucleus. prominent inoculum type and is classified as either a
These organisms usually produce a filamentous, sporangiospore or conidium. Sporangiospores are
branching structure (hyphae) that collectively is called formed within enclosed structures (sporangia) and do
the mycelium. A great variety of reproductive structures not share a common cell wall with the sporangia. In
are found in this kingdom of organisms. The taxonomy some cases the mature sporangiospore has flagella and
of fungi is primarily based on the shape and nature of can swim in water; these spores are called zoospores.
sexual spores, asexual conidia and sporangia, fruiting Conidia are asexual spores that form as a result of cell
structures, structure of the hyphae, and other physical division on the tips of conidiophores. For this spore type
features (morphology). Molecular and biochemical the conidium and conidiophore at some point shared a
profiles are now being incorporated into taxonomic common cell wall. Conidiophores can be formed singly,
schemes as well. in clusters (fascicles), or on a variety of fungal struc-
Kingdom Fungi contains the phyla Chytridio- tures, including cushion-shaped pads of mycelium
mycota, Zygomycota, Ascomycota, and Basidio- (sporodochia), open cup-shaped structures (acervuli),
mycota. Fungi are placed in these phyla based on or enclosed spherical bodies (pycnidia). Another
morphological structures and genetic characteristics. asexual structure, the chlamydospore, is a vegetative
Chytrids produce zoospores and gametes that have cell that has enlarged, formed thick walls, and functions
flagella and can therefore swim in water, fungal struc- as a survival structure for the fungus.
tures without cell cross walls (coenocytic), and are often Ascomycete and Basidiomycete taxonomy is com-
single-celled. Few chytrids cause plant diseases, and no plicated by the fact that many species produce both
chytrid directly causes important vegetable diseases. sexual and asexual phases. The sexual form of a species
However, the chytrid Olpidium vectors a virus patho- is called the teleomorph (or perfect stage), and includes
gen of lettuce. Zygomycetes have asexual sporangia the ascospore or basidiospore stage. The teleomorph
that form on sporangiophores and dark, thick-walled name of a fungus generally has priority and is the
zygospores. A few zygomycetes are plant pathogens: primary name used in taxonomy. The same fungus,
Choanephora, Mucor, Rhizopus. Ascomycetes form however, can produce an asexual phase called the
sexual spores in a sac-like structure called the ascus; asci anamorph (or imperfect stage). The anamorph includes
are usually borne within a distinct fungal structure such those forms of fungi that make conidia. All asexual
as a perithecium, apothecium, or cleistothecium. forms are placed in the Fungi Imperfecti, or Deutero-
Basidiomycetes form the sexual basidiospores on a mycete, category. Further, not all Fungi Imperfecti
microscopic, club-shaped structure called the basidium. species produce a known teleomorph stage, making
A great many of the vegetable diseases are caused by fungal taxonomy even more complex. When referring
Ascomycte and Basidiomycete fungi. to a fungus in scientific publications, the current con-
Plant pathogenic fungi either penetrate host tissues vention is to use the teleomorph name. However, in the
directly or enter via wounds or plant openings like field, the teleomorph form may have a limited or
stomata. The pathogens then colonize host tissues and unknown role in disease development. Therefore, in
usually produce reproductive structures and infective many cases it is practical to refer to the anamorph name
propagules that can disperse and infect other plants. because this is the fungal form that will be more readily
Propagules generally fall into one of two categories. present on the crop and play the more significant role in
Sexual propagules result from the fusion of two disease development.
TABLE 5 Common fungi and fungus-like organisms that cause diseases of vegetables*
FUNGI
Group Genus Fungi imperfecti (cont.) Macrophomina
Microdochium
Zygomycota Choanephora
Mycocentrospora
Mucor
Oidiopsis
Rhizopus
Oidium
Ascomycota Didymella Penicillium
Erysiphe Phloeospora
Golovinomyces Phoma
Leptosphaeria Pseudocercosporella
Monosporascus Pyrenochaeta
Mycosphaerella Ramularia
Pleospora Rhizoctonia
Podosphaera Sclerotium
Sclerotinia Septoria
Sphaerotheca Stemphylium
Zopfia Thielaviopsis
Basidiomycota Helicobasidium Verticillium
Itersonilia
Puccinia FUNGUS-LIKE ORGANISMS
Urocystis Group Genus
Uromyces
Oomycetes Albugo
Ustilago
Aphanomyces
Fungi imperfecti Acremonium Bremia
Alternaria Peronospora
Ascochyta Phytophthora
Aspergillus Plasmopara
Botrytis Pseudoperonospora
Cercospora Pythium
Cercosporidium
Plasmodiophoromycetes Plasmodiophora
Chalaropsis
Spongospora
Cladosporium
Colletotrichum
* For fungi having both teleomorph and anamorph stages, if one of
Cylindrosporium the stages is not commonly found on vegetables or is not involved in
Fusarium pathogenesis, that name is not included in this table.
Plant pathogenic fungi occupy diverse and interest- fungi, like Sclerotinia, retain the ability to infect many
ing ecological niches. Some fungi, like the powdery different types of plants. Fungi are dispersed in a variety
mildews, are obligate pathogens and can only survive of ways. Most species produce spores that are spread in
and remain active on a living plant host. Other fungi are the air and via winds. Airborne and other spore types
pathogens on plant foliage and flowers, and can also can also be splash-dispersed by rain and sprinkler irri-
live as saprobes on dead and decaying organic matter. gation. Soilborne fungi are spread by spores and
Soilborne plant pathogenic fungi survive as pathogens mycelia that are carried in water or moved in soil and
in host roots and other tissues, soil inhabitants that mud. Some species form specialized, hardened mycelial
persist on soil organic matter, or free living in the soil. aggregates called sclerotia that are readily spread in soil
Some fungi, such as rusts, have evolved in specialized and infested plant material. A number of important
ways and can only infect one or a few plant hosts. Other fungal pathogens are seedborne in vegetables.
FUNGUS-LIKE PATHOGENS TABLE 6 Selected physiological and abiotic

problems of vegetable crops
Two groups of plant pathogenic microorganisms were
traditionally classified as fungi but are now considered
Crop Disorder Cause
to be taxonomically distinct based on morphological,
Celery Black heart Calcium deficiency
biochemical, and molecular criteria. The first group is
Lettuce Ammonium toxicity Ammonium buildup
the phylum Plasmodiophoromycota, which includes
the clubroot pathogen of crucifers (Plasmodiophora Lettuce Tipburn Calcium deficiency
brassicae) and crook root pathogen of watercress Tomato Blossom end rot Calcium deficiency
(Spongospora). These organisms are now placed in Artichoke Tipburn Calcium deficiency
kingdom Protozoa. Plasmodiophoromycetes are soil-
borne organisms, obligate pathogens, and produce
swimming zoospores.
The second group, phylum Oomycota, contains Disorders caused by abiotic factors and
extremely important vegetable pathogens such as the physiological conditions
downy mildews (Bremia, Peronospora, Plasmopara, Apart from the living organisms that cause plant
Pseudoperonospora), water molds (Pythium, Phytoph- diseases, there are a number of non-living factors that
thora, Aphanomyces), and the white rust organism contribute to problems and disorders of vegetable
(Albugo). These organisms are mostly soilborne, with crops. Such abiotic factors include environmental
the exception of most downy mildews and some species extremes, nutrient deficiencies and toxicities, damage
of Phytophthora. Swimming zoospores are produced from crop production steps, soil and water conditions,
by most species, vegetative hyphae are nonseptate and others. In addition, problems with the plant’s
(coenocytic), and sexual oospores are produced by the physiology and genetics can result in disorders and
fusion of male (antheridia) and female (oogonia) mutations. This book covers only a few of the abiotic
gametangia. and physiological problems that can affect vegetable
Recent phylogenetic investigations indicate that crops; a summary can be found in Table 6.
reclassification of oomycetes was appropriate because
these organisms lack chitin in their cell walls, usually
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http://www.umu.se/myconet/curr/outline.03.html
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TABLE 7 Vegetable diseases discussed and illustrated in this book
CROP BACTERIAL DISEASES FUNGAL DISEASES VIRAL DISEASES
Alliums Bacterial blight Black mold Garlic mosaic

Botrytis leaf blight Onion yellow dwarf
Cladosporium leaf blotch Shallot latent
Downy mildew
Fusarium basal plate rot
Neck rot
Penicillium blue mold
Pink root
Purple blotch
Rust
Smut
White rot
White tip
Artichoke Bacterial crown rot Ascochyta rot Artichoke curly dwarf

Gray mold Artichoke Italian latent
Powdery mildew Artichoke yellow ringspot
Pythium root rot
Ramularia leafspot
Verticillium wilt
Arugula Bacterial blight Downy mildew

White rust
Asparagus Cercospora blight Asparagus virus 1

Fusarium crown, root rot Asparagus virus 2
Phytophthora spear rot Asparagus virus 3
Purple spot Tobacco streak
Root rots
Rust
Basil Bacterial leaf spot Fusarium wilt Tomato spotted wilt

Gray mold
White mold
Bean Common bacterial blight Anthracnose Bean common mosaic

Halo blight Fusarium wilt Bean yellow mosaic
Gray mold
Powdery mildew
Root and foot rot diseases
Rust
White mold
Beet Bacterial leaf spot Black leg Beet chlorosis

Cercospora leaf spot Beet curly top
Damping-off Beet leaf curl
Downy mildew Beet mild yellowing
Powdery mildew Beet mosaic
Ramularia leaf spot Beet necrotic yellow vein
Rust Beet pseudo-yellows
Scab Beet western yellows
Beet yellows
Cucumber mosaic
TABLE 7 Vegetable diseases discussed and illustrated in this book (continued)
Brassicas Bacterial blight Alternaria head rot Beet western yellows

Bacterial head rot Alternaria leaf spot Cauliflower mosaic
Bacterial leaf spot Black leg Turnip mosaic
Black rot Clubroot
Downy mildew
Fusarium yellows
Gray mold
Light leaf spot
Phytophthora root rot
Phytophthora storage rot
Powdery mildew
Rhizoctonia diseases
Ring spot
Verticillium wilt
White leaf spot
White mold
White rust
Broad bean Chocolate spot Bean leaf roll

Downy mildew Bean yellow mosaic
Fusarium root rot Broad bean stain
Leaf and pod spot Broad bean true mosaic
Rust
White mold
Broccoli raab Bacterial blight Alternaria leaf spot

Powdery mildew
White rust
Carrot Bacterial leaf blight Alternaria leaf blight Carrot motley dwarf
Black mold Parsnip yellow fleck
Black rot
Cavity spot
Cercospora leaf blight
Crater rot
Crown rot
Licorice rot
Powdery mildew
Rust
Scab
Southern blight
Violet root rot
White mold
Catnip Bacterial leaf spot
Celery Aster yellows Crater spot Celery mosaic

Bacterial leaf spot Damping-off Cucumber mosaic
Early blight
Fusarium yellows
Late blight
Phoma crown, root rot
Pink rot
Celery continued... Powdery mildew

Pythium root rot
Chervil Powdery mildew

White mold
Cilantro Bacterial leaf spot Fusarium wilt Cilantro yellow blotch
Corn salad Powdery mildew

White mold
Cucurbit Angular leaf spot Anthracnose Cucumber mosaic

Bacterial fruit blotch Charcoal rot Papaya ringspot
Bacterial wilt Damping-off Squash leaf curl
Cucurbit yellow vine disease Downy mildew Squash mosaic
Fusarium crown, foot rot Tobacco ringspot
Fusarium wilt Watermelon mosaic
Gummy stem blight, black rot Zucchini yellow mosaic
Monosporascus root rot
Phytophthora crown & root rot
Powdery mildew
Scab
Verticillium wilt
Dill Itersonilia canker

Powdery mildew
Endive/escarole Bacterial soft rot Alternaria leaf spot Beet western yellows
Powdery mildew
Rhizoctonia blight
Rust
White mold
Fennel Bacterial leaf spot Cercosporidium blight

White mold
Horseradish Black rot Cercospora leaf spot Turnip mosaic

Downy mildew
Ramularia leaf spot
Verticillium wilt
White rust
Jerusalem artichoke Powdery mildew

Sclerotinia rot
Southern blight
Lemongrass Rust
Lettuce Aster yellows Anthracnose Beet western yellows

Bacterial leaf spot Bottom rot Lettuce mosaic
Corky root Downy mildew Lettuce dieback
Varnish spot Fusarium wilt Lettuce big vein
Gray mold Tomato spotted wilt
Lettuce drop Turnip mosaic
Phoma basal rot
Powdery mildew
Verticillium wilt
Marjoram Rust
Mint Powdery mildew

Rust
Verticillium wilt
Mustards Alternaria leaf spot

White leaf spot
White rust
Oregano Rust
Parsley Powdery mildew

Root rot
Septoria blight
White mold
Parsnip Downy mildew Celery mosaic

Itersonilia canker Parsnip yellow fleck
Phloeospora leaf spot
Phoma canker
Powdery mildew
Ramularia leaf spot
Pea Bacterial blight Aphanomyces root rot Bean leaf roll

Ascochyta blight Pea early browning
Downy mildew Pea enation mosaic
Foot rot complex Pea seedborne mosaic
Fusarium wilt Pea streak
Gray mold
Leaf and pod spot
Powdery mildew
Pythium root rot, damping-off
White mold
Pepper Bacterial spot Anthracnose Beet curly top

Damping-off Cucumber mosaic
Gray leaf spot Pepper mild mottle
Gray mold Potato virus Y
Phytophthora blight, root rot Sinaloa tomato leaf curl
Powdery mildew Tobacco etch
Southern blight Tobacco mosaic
Verticillium wilt Tomato mosaic
White mold Tomato spotted wilt
Radicchio Bacterial leaf spot Alternaria leaf spot Tomato spotted wilt
Powdery mildew
White mold
Radish Alternaria leaf spot

Downy mildew
Fusarium wilt
White rust
Rhubarb Bacterial soft rot Anthracnose Turnip mosaic

Crown rot Ascochyta leaf spot
Downy mildew
Gray mold
Ramularia rot
Root rots
Rust
Sage Phytophthora root rot

Powdery mildew
Salsify Rust
White rust
Spinach Bacterial leaf spot Anthracnose Beet curly top

Cladosporium leaf spot Beet western yellows
Downy mildew Cucumber mosaic
Fusarium wilt
Root rot complex
Stemphylium leaf spot
Verticillium wilt
White rust
Sweetcorn Maize smut

Stalk rot
Swiss chard bacterial leaf spot Cercospora leaf spot Beet curly top
Damping-off
Downy mildew
Powdery mildew
Rust
Tomatillo Fusarium wilt Turnip mosaic
Tomato Bacterial canker Alternaria stem canker Alfalfa mosaic

Bacterial speck Anthracnose Beet curly top
Bacterial spot Black mold Cucumber mosaic
Tomato pith necrosis Corky root rot Potato virus Y
Damping-off Tobacco mosaic
Early blight Tomato mosaic
Fusarium crown and root rot Tomato spotted wilt
Fusarium wilt Tomato yellow leaf curl
Gray mold
Late blight
Phytophthora root rot
Powdery mildew
Southern blight
Verticillium wilt
White mold
Watercress Crook root Turnip mosaic

Downy mildew Watercress chlorotic leaf spot
Septoria leaf spot Watercress yellow spot
31
Diagnosis of disease
THE FIRST STEP in managing vegetable diseases is to identify them correctly.
Plant disease diagnosis is the science and art of identifying the causal agents behind these
problems. Prompt and accurate diagnosis is of the utmost importance in
vegetable production systems.
The importance of timely, accurate diagnoses It is essential to conduct the diagnostic process in a sys-
Diseases, disorders, and other problems of vegetable tematic, organized way. Such a system includes the
crops are critical concerns for agricultural and horticul- following elements:
tural production worldwide. The perishable nature of • Ask and answer the appropriate questions so as to
vegetable commodities and the market demand for high define the problem and obtain information that is
quality, virtually defect-free produce places great relevant to the case under investigation.
pressure on growers, field managers, pest control • Conduct a detailed, thorough examination of the
advisors, and other personnel to minimize damage plants and production areas.
caused by these problems. Growers and other field • Use appropriate laboratory tests to obtain clinical
personnel who have the ability to accurately and rapidly information on possible causal agents and factors.
diagnose vegetable disease problems will have a com- • Compile all the collected information and consult
petitive advantage over those who have not developed additional resources and references. Keep an open
such skills. mind as the information is analyzed and do not
There are two general categories of plant problems. make unwarranted assumptions; in particular, do
Biotic problems are caused by living organisms such as not assume that only one causal factor is involved.
pathogens, nematodes, and insects and other pests. • Finally, make an informed diagnosis.
Abiotic problems are caused by nonliving factors such
as temperature and moisture extremes, mechanical Asking the right questions
damage, chemicals, nutrient deficiencies or excesses, As a problem-solving process, the diagnostic strategy
salt damage, and other environmental factors. Disease requires that information be obtained in three major
control is most efficient if the causes of biotic and areas of investigation:
abiotic problems are both identified in a timely and • Comparison of the plant in its healthy state with its
accurate way. diseased condition.
• The presence or nature of the possible agents
Overall strategy responsible for the problem.
Diagnosis is the science and art of identifying the agent • The surrounding environment, growing conditions,
or cause of the problem under investigation. When one and production practices that form the context of
renders a diagnosis, one has collected all available infor- the case. Such information is best obtained by
mation, clues, and observations and then arrives at an asking and then answering, as completely as
informed conclusion as to the causal factor(s). Hence, possible, a series of questions. Examples of such
plant problem diagnosis is an investigative, problem- questions follow.
solving process. This process relies on current observa-
tions as well as historical records. Growers and field
personnel should therefore maintain records of what
problems occurred, when problems developed, and any
other information pertinent to the case.
Questions about the healthy plant GROWTH STAGE

• What are the genus, species, and cultivar names of • What is the growth stage of the affected plant
the plant in question? (seedling, new transplant, mature plant,
• Is this particular plant suited to the production flowering/fruiting plant, senescent plant)?
area? Is the cultivar resistant or especially suscepti- • Is a particular growth stage associated with the
ble to diseases and other problems? problem?
• Is the plant sensitive to certain environmental • What was the condition of the plant when first
factors (salinity, excess or deficient soil moisture, placed in the production area?
etc.)? • How does the growth rate of the affected plant
• What are the characteristics, appearance, and compare with that of a healthy plant?
growth habits of a healthy plant?
• How does the plant normally appear when grown SYMPTOMS ON OTHER PLANTS
under various conditions (greenhouse vs. outdoors, • Are symptoms restricted to one species or one
coastal vs. inland production locations, winter vs. cultivar of a vegetable plant or are multiple cultivars
summer) or at different stages of growth and devel- and different species involved?
opment (seedling vs. transplant vs. mature plant)? • Do the same symptoms occur in only one field or
• What is the normal growth rate? one greenhouse, while adjacent or nearby plantings
of the same crop remain symptomless, or are many
Questions about the unhealthy plant plantings of that particular vegetable affected?
SYMPTOMS • Do adjacent plantings, weeds, or nearby crops
• What are the symptoms of the affected plant? exhibit similar symptoms?
• Which plant parts are affected? • If other plants are affected, do they belong to a
• Are symptoms restricted to external plant surfaces common group or family of plants?
(spots and lesions) or are there also internal • Are symptomatic plants associated with a particu-
symptoms (vascular streaking, discolored pith or lar set of transplants or lot of seed?
crown tissue)?
• Are symptoms present only on exposed plant PATTERNS
surfaces or also on protected, covered tissues such • How are the symptoms distributed within the
as unexpanded inner leaves or unopened flowers? specific production area of concern?
• What is the distribution of the symptoms on any • Are there patterns (repeating numbers of plants or
one particular plant (do symptoms occur on one plant rows) to the symptoms or are they completely
side of the plant, only on older or newer leaves, on random throughout the planting?
secondary roots but not on primary roots, etc.)? • Are symptomatic plants found in clustered groups?
• What were the initial symptoms? • Do the symptomatic plants occur in lines, streaks,
• How do early symptoms differ from more circles, or other discernable pattern?
advanced symptoms? • Are symptomatic plants found mostly along the
• How rapidly do early symptoms change into edges of the planting?
advanced ones? • Are affected plants next to buildings, roads, ditches,
• How long have the symptoms been present? weedy areas, other crops, or other production
areas?
• Are symptoms associated with sub-sets of plants
within the planting, indicating an association with
plants from certain transplant trays, different
sources of plant material, or other production
factors?
D IAGNOSIS OF D ISEASE 33
• Are symptoms associated with physical features in ABIOTIC AND PHYSIOLOGICAL

the field such as low or high spots of the field, places • Compile a list of physiological and abiotic factors
where water does not drain well, presence or known to cause problems for the plant in question
absence of underlying gravel or clay, changes in soil (examples: tipburn in lettuce, blossom end rot of
types? tomato).
• Do such areas become flooded after rains or receive
irrigation runoff? Take note of the irrigation system SIGNS
and possible patterns associated with each type. For • A ‘sign’ is the visible presence of a biotic causal
example, in the field a plant growth pattern can agent. Are such signs present? Examples of signs are
occur in which linear stretches of plants grow fungal growth and spores, bacterial ooze, and insect
poorly depending upon how the sprinkler lines bodies or frass (insect droppings).
were arranged. • Are there multiple signs that indicate more than one
factor may be involved?
TIMING • What is the distribution of signs on the affected
• What is the timing of symptom occurrence in plant (present on all or only on certain plant parts)?
relation to other factors? • Are signs present on all symptomatic plants?
• When did the symptoms first occur? • Are signs present on adjacent plantings or non-
• Are there various stages of symptoms indicating symptomatic plants?
new infections vs. older ones? • Are there signs on surrounding soil, irrigation pipe,
• Have symptom features or severity changed over or other inanimate objects in the area?
time?
• Do symptoms appear to have developed gradually Questions about the surrounding environment,
over a period of time or rapidly and all at once? growing conditions, production practices
• Have the same or similar symptoms occurred TIMING
before? • What time of year did the problem occur?
• From year to year, does the problem recur during
BIOTIC OR ABIOTIC the same month or time of year?
• Do symptoms resemble those caused by biotic
agents such as pathogens, nematodes, arthropods, ENVIRONMENTAL CONDITIONS AND CONTEXT
or vertebrate pests, or are symptoms more sugges- • What are the current and past weather conditions?
tive of physiological or abiotic factors such as nutri- • Have there been any unusual weather patterns,
tional problems, physiological disorders, genetic changes, or developments recently or in the past few
mutations (chimeras), chemical damage, or envi- weeks or months?
ronmental extremes? • Have there been any conditions that would hinder
• Do the symptoms provide evidence that more than plant growth or favor pathogen and pest develop-
one factor or pathogen is involved? ment?
• Is there evidence of abiotic stress factors (tempera-
Questions about possible agents and factors ture extremes, water stress or excess, salt buildup,
BIOTIC mineral deficiencies and toxicities, pollution, wind
• Which pathogens, nematodes, and arthropod pests or other mechanical damage, etc.)?
are known to occur on the host? • What is the general location of the field or green-
• Which biotic agents occur in the geographic area of house (coastal vs. inland, next to other crops or
concern? Compile a list of common biotic agents production areas, next to roads, etc.)?
that occur in the area.
ROOTING MATERIALS AND FIELD SOILS GENERAL PRODUCTION PRACTICES

• For greenhouse-produced transplants, what type of • What are the normal, typical production practices
rooting medium is used? for the crop (propagation steps, planting arrange-
• What is the condition of the mix (pH, porosity, ment, irrigating, fertilizing, pruning, pest manage-
salinity, nutrient level, etc.)? ment)?
• Has the rooting medium been subject to any envi- • What is the condition of the facility, including struc-
ronmental extremes (excess water or salts, water tures, fertilizer injection systems, irrigation systems,
deficit conditions, high temperatures in the spray equipment, etc.?
container, etc.)? • What experience do you have with this crop or par-
• What supplements have been added to or omitted ticular cultivar?
from the rooting medium? • What production steps were completed or omitted?
• Has the rooting medium been used previously, • What was previously planted or placed in the area
recycled, or exposed to contaminating factors? of concern?
• What is the condition and cleanliness of the pots, • What equipment, particularly spray equipment,
trays, or other containers used to hold the rooting was recently used in the area?
medium? • Were any new production practices recently imple-
• For field or greenhouse crops grown in the ground, mented?
what is the soil type (heavy clay, porous sand) and • Did the onset of symptoms correspond with any
soil condition (compacted layers, change in soil type cultural practice?
from affected to unaffected areas, pH, salinity • Compile a complete record of production practices
levels, alkalinity, etc.)? used on and around the symptomatic plants.
• Is there a history of this transplant crop grown at • Which fertilizers, pesticides, or other chemicals
this site? were applied to the plants, adjacent crops, green-
house benches for transplants, and non-production
WATER areas in the vicinity? Compile information on all
• What is the water source and quality? materials, formulations, rates, additives, and spray
• How does the water drain off the site? volumes used on symptomatic, non-symptomatic,
• Are there low spots where water collects or drains and surrounding plants. Special attention should be
poorly? placed on herbicide (selective, non-selective, pre-
• What type of irrigation system is used? emergent, post-emergent) and pesticide tank mix
• Does the system deliver water uniformly? applications.
• What is the frequency and duration of irrigations? • What weather patterns occurred before, during,
• How does the irrigation schedule correspond to and after the spray applications?
other production practices such as pesticide sprays, • What chemicals and additives were used previously
fertilizer applications, transplanting, and other pro- in the spray equipment and how was the equipment
cedures? cleaned afterwards? Chemical damage may be the
subject of future litigation and careful records and
photographs should be taken when such damage is
suspected. Careful analysis will be required to
determine if there is evidence that damage is associ-
ated with spray patterns or if untreated plants lack
such symptoms.
HISTORY Collect and label representative plant samples for

• What is the sequence of crops that was planted at possible laboratory analysis. Samples should include
this site in the past few years? various stages of affected plants (initial and more
• Has the same crop been placed here frequently in advanced symptoms) taken from multiple sites. In
the past few seasons? many cases and if feasible, the entire plant should be
• Have cover crops, composts, or other amendments collected and not just a few leaves and stems; foliar
and inputs been used here? symptoms may be caused by root and crown problems,
• What is the history of plant diseases that occur at so laboratory personnel need to see the entire specimen.
this site? Include a healthy plant for comparison. Keep samples
• Are there field notes, laboratory reports, or other cool and deliver them in a timely manner to the lab. If
information that document the presence and the plant being examined is a sample brought in from
problems due to soilborne or foliar diseases? the field or greenhouse, what is the condition of the
sample? Samples that are in poor condition, incom-
Conducting the examination plete, or of limited size and number may not yield useful
Gather appropriate equipment for use in examining the information. Is the sample representative of the
production site. Equipment includes the following: problem? Have unaffected plants also been included in
notebook, hand lens, knife, pruning shears, shovel, the sample for comparison? If warranted, collect appro-
plastic bags for plant and soil samples, bottles for water priate soil and water samples for various analyses.
samples, labels and marking pens, soil sampling tube,
flags for tagging plants for future observations, camera, Incorporating laboratory tests
ice chest/cooler, disinfectant for tools. Because diagnosis based solely on symptoms is risky
Examine all relevant propagation and production and may lead to inaccurate conclusions, laboratory
areas in an attempt to answer the pertinent informa- analysis is usually highly recommended. If pathogens
tion-gathering questions. Tour off-site areas such as are possibly involved, send good quality, representative
adjoining roads, fields, and landscaped areas. samples to a plant pathology laboratory. Pathology labs
Thoroughly examine symptomatic plants. Carefully use various tests and techniques to identify biotic causes
examine all roots, above-ground parts of the plants, and of plant problems. Direct examination of plant tissues
internal tissues of stems. Examine and dissect multiple is used to search for signs such as fungal structures and
examples of affected plants. Conduct a similar exami- bacterial ooze. Culturing techniques using microbio-
nation of healthy or asymptomatic plants to make a logical media are designed to isolate and recover fungal
comparison. or bacterial pathogens from symptomatic tissues.
Record all observations. Draw maps to indicate Various extraction methods can recover nematodes
patterns of symptoms and locations of plantings having from plant tissues and soils. Serological methods, such
the problem. Take photographs to document symptoms as the enzyme-linked immunosorbent assay (ELISA),
and distribution of patterns. Photograph asymptomatic employ antisera that will identify specific pathogens
plants for comparison. from either plant tissues or from cultures. Molecular
identification techniques for plant pathogens are con-
stantly being developed and improved. In some cases
these molecular tests can be used directly on sympto-
matic plant tissues to confirm the presence of the target
pathogen. Note, however, that the detection or recovery
of a pathogen does not necessarily mean that this agent
caused the symptoms of the disease. Interpretation of
lab results using any method often requires the expertise
of diagnosticians and plant pathologists.
For many fungi, fungal-like organisms such as Diagnosing virus diseases

oomycetes, and bacteria, isolating suspect pathogens For any pathogen group (fungi, bacteria, viruses), the
from symptomatic plant tissue is a critical step in the symptoms may vary due to any number of factors.
diagnosing of plant pathogens. Different strategies are However, for viruses, the incidence and expression of
adopted for this purpose. The plant sample is first disease symptoms can fluctuate and vary a great deal
usually washed to remove debris and soil. Typically the depending on the strain and virulence of the agent, the
sample is then surface sterilized to reduce interference particular crop and cultivar host, age of host when
from secondary decay organisms and non-pathogenic infected, mode of infection (mechanical abrasion,
microflora that are present on the plant surfaces. Small seedborne inoculum, or arthropod vector), factors
pieces of diseased tissue, taken from the edges of the involving the biology of the vector (type, strain, and
infection, are placed in or on solid agar media. For population), and environmental conditions. With some
isolating fungi and oomycetes, general purpose micro- exceptions, symptoms caused by different viruses often
biological media are usually recommended: potato resemble each other, thereby making field diagnosis
dextrose agar, corn meal agar, water agar. These media difficult and ill advised. Virus disease diagnosis is
can be acidified if secondary decay bacteria are prob- further complicated when more than one viral agent
lematic and might interfere with recovery of the infects the host plant. Clinical tests are required to pos-
pathogen. In some cases the use of semi-selective media itively identify viral agents in plants.
can help recover suspect pathogens. Semi-selective
media are used to inhibit the growth of non-target Digitally assisted diagnosis
organisms while facilitating growth of the target Mention should be made of new technology involving
pathogen. Examples of semi-selective media are PARP digitally assisted diagnosis (DAD). DAD is the process
for Phytophthora, Sorensen’s NP-10 for Verticillium, of acquiring digital images of plant problems and
and Komada’s medium for Fusarium. sending these images to researchers, diagnosticians, and
Isolating plant pathogenic bacteria follows a similar other experts for viewing and diagnosing. This diag-
strategy. Samples are prepared in similar ways as for nostic approach therefore relies almost exclusively on
fungal diseases. Small pieces of symptomatic tissue are digital photographs. In some cases, such images may be
taken from the edges of the infection and are macerated very helpful in reducing the time required to identify the
in a drop of water. A few microliters of this water are cause of the problem. Digital images can also be appro-
streaked onto general purpose media such as nutrient priate when distinctive symptoms and signs character-
agar, yeast extract dextrose calcium carbonate agar, or ize the problem (such as powdery mildews, downy
sucrose peptone agar. At times a semi-selective medium mildews, clubroot of crucifers, and others). However,
is useful if a particular pathogen is suspected. Examples care should be taken not to rely on such images alone.
of semi-selective media for bacteria are SX agar for DAD can be a useful supplement to the diagnostic
Xanthomonas campestris pv. campestris and KBC process, but will not be able to completely replace field
medium for several Pseudomonas syringae pathovars. visits and hands-on examination of plant samples.
Many book and journal references provide specific
details on the appropriate media to consider for Compiling information and drawing a conclusion
isolating and growing plant pathogenic fungi and Compile all notes, observations, maps, laboratory
bacteria. Several books are particularly useful in this results, photographs, and other information. Consult
regard and are listed in the references below. with and record information from printed references
and books, on-line website resources, and university
and other experienced professionals. This compilation
will be the information base for the present diagnosis
and can also be a useful resource for future diagnostic
cases. After considering all the information, render an
informed diagnosis.
References on disease diagnosis References on culture media

Barnes, L. W. 1994. The role of plant clinics in disease diagnosis Atlas, R. M. 1997. Handbook of Microbiological Media. Second
and education: A North American perspective. Annual edition. CRC Press.
Review of Phytopathology 32:601–609. Dhingra, O. D. and Sinclair, J. B. 1995. Basic Plant Pathology
Fox, R. T. V. 1993. Principles of Diagnostic Techniques in Plant Methods. Second edition. CRC Press.
Pathology. CAB International. Kirsop, B. E. and Doyle, A. 1991. Maintenance of
Green, J. L., Maloy, O., and Capizzi, J. 1990. A systematic Microorganisms and Cultured Cells: A Manual of Laboratory
approach to diagnosing plant damage. Plant Diagnostics Methods. 2nd Edition. Academic Press.
Quarterly 11(3):139–165. Lelliott, R. A. and Stead, D. E. 1987. Methods for the Diagnosis
Grogan, R. G. 1981. The science and art of plant disease of Bacterial Diseases of Plants. Volume 2. Blackwell Scientific
diagnosis. Annual Review of Phytopathology 19:333–351. Publications.
Hansen, M. A. and Wick, R. L. 1993. Plant disease diagnosis: Schaad, N. W., Jones, J. B., and Chun, W. 2001. Laboratory
present status and future prospects. Advances in Plant Guide for Identification of Plant Pathogenic Bacteria. Third
Pathology 10:65–126. edition. American Phytopathological Society Press.
Henson, J. M. and French, R. 1993. The polymerase chain Shurtleff, M. C. and Averre, C. W. 1997. The Plant Disease
reaction and plant disease diagnosis. Annual Review of Clinic and Field Diagnosis of Abiotic Diseases. American
Phytopathology 31:31–109. Phytopathological Society Press.
Holmes, G. J., Brown, E. A., and Ruhl, G. 2000. What’s a picture Singleton, L. L., Mihail, J. D., and Rush, C. M. 1992. Methods
worth? The use of modern telecommunications in diagnosing for Research on Soilborne Phytopathogenic Fungi. American
plant diseases. Plant Disease 84:1256–1265. Phytopathological Society Press.
Horne, C. W. 1989. Groundwork for decision: Developing
recommendations for plant disease control. Plant Disease
73:943–948.
Kabashima, J. N., MacDonald, J. D., Dreistadt, S. H., and
Ullman, D. E. 1997. Easy on-site tests for fungi and viruses in
nurseries and greenhouses. UC DANR Publication no. 8002.
Kim, S. H. 1988. Technological advances in plant disease
diagnosis. Plant Disease 72:802.
Marshall, G. 1996. Diagnostics in Crop Protection. Symposium
Proceedings No. 65. British Crop Protection Council. Major
Print Ltd.
Newenhouse, A. C. 1991. How to recognize wind damage on
leaves of fruit crops. HortTechnology 1:88–90.
Putnam, M. L. 1995. Evaluation of selected methods of plant
disease diagnosis. Crop Protection 14:517–525.
Schubert, T. S. and Breman, L. L. 1988. Basic concepts of plant
disease and how to collect a sample for disease diagnosis.
Plant Pathology Circular No. 307. Florida Dept. Agric. &
Consumer Services.
Shurtleff, M. C. and Averre, C. W. 1997. The Plant Disease
Clinic and Field Diagnosis of Abiotic Diseases. American
Phytopathological Society Press.
Stowell, L. 1999. Digital disaster and the ethics of virtual plant
pathology. Phytopathology News 33:62.
Thomas, M. B., Crane, J. H., Ferguson, J. J., Beck, H. W., and
Noling, J. W. 1997. Two computer-based diagnostic systems
for diseases, insect pests, and physiological disorders of citrus
and selected tropical fruit crops. HortTechnology 7:293–298.
Walker, S. E. and Schubert, T. S. 1997. Assessing plant problems
in cropping systems: A systematic approach. Plant Pathology
Circular No. 381. Florida Dept. Agric. & Consumer Services.
Wallace, H. R. 1978. Diagnosis of plant diseases of complex
etiology. Annual Review of Phytopathology 16:379–402.
Waller, J.M., Lenné, J.M., and Waller, S.J. 2001. Plant
Pathologist’s Pocketbook. Third edition. CABI Publishing,
Wallingford, UK.
Waller, J.M., Ritchie, B.J., and Holderness, M. 1998. Plant Clinic
Handbook. (IMI Technical Handbooks No.3). CABI
Publishing, Wallingford, UK.
Controlling disease
AS WITH DIAGNOSIS, management of diseases depends on a thorough knowledge of the three
major components of a disease: susceptible host plant, virulent pathogen, and favorable
environment. For disease to develop, all three factors must be present. Therefore, understanding
these host-pathogen-environment dynamics is essential in devising disease management
strategies. Such strategies target these three areas and manipulate them so that disease is not
possible or is hampered in its development.
Criteria for commercial control resistance, cultural practices, application of disease

of vegetable diseases control materials, and other steps is the modern
For commercial agriculture, the practical disease man- approach to disease control in vegetables.
agement options that ultimately are deployed must
meet four main criteria. Management steps must first of Disease control options
all be effective at achieving commercially acceptable SITE SELECTION
levels of control. Some disease control options may Select sites that do not have a history of problematic
reduce disease severity and incidence, or result in the diseases. Pick fields that contain features that discour-
death of pathogens. However, if such effects do not age pathogen survival and disease development.
result in vegetable crops that have commercially accept- Considerable time and planning are required for
able levels of yield and quality, that disease control strategic selection of such locations. Growers and field
measure will not be practical for the farmer. advisors must monitor and record the distribution and
Secondly, the disease control option must be eco- occurrence of persistent, soilborne plant pathogens
nomical to use. The cost of disease control must be sig- such as Fusarium, Plasmodiophora, Sclerotium,
nificantly lower than the final value of the marketed Verticillium, and others. Susceptible crops should not
crop. For example, the practice of using effective but be placed in locations having known, high populations
expensive soil fumigation with tarps can significantly of these pathogens. For some soilborne fungi such as
reduce soilborne diseases of most vegetables. However, Phytophthora, Pythium, and Rhizoctonia, distribution
such treatments are usually prohibitively expensive in is often so widespread that site selection and avoidance
relation to the values and profit margins of many of is usually not possible. In some cases, soil tests can give
these crops. Therefore, such fumigation is usually not estimated population levels for some soilborne
used on a regular basis for most vegetables. pathogens. These tests can be used to give some indica-
Thirdly, a disease control option must be available tions of possible disease risk, though precise pathogen
for use at a commercial level. A number of research populations cannot be known for certain.
efforts have identified possible biocontrol agents in Other site-specific situations create risks that should
which a microorganism can be used to kill or manage be avoided. Pastures, foothills, riverbanks, and grass-
plant pathogens. However, most of these agents have lands support weeds and natural vegetation that can be
not been formulated or commercialized into viable reservoirs for viruses and other pathogens. The aster
products. Hence, such agents are of limited use to com- yellows phytoplasma and its leafhopper vector can be
mercial agriculture. Finally, disease control measures found in weedy grasslands in coastal California. Once
must be amenable to being set within the context of an this vegetation dries up in the summer, the leafhoppers
integrated disease management system. Few diseases migrate from the grasslands and move into nearby
are controlled by only one measure. Integrating host lettuce or celery fields, resulting in aster yellows disease
C ONTROLLING D ISEASE 39
in these fields. Lettuce fields should not be placed conditions with no rain during the crop cycle); careful,
adjacent to plantings of perennial hosts, such as regular monitoring of seed fields for disease symptoms;
Gazania species, of Lettuce mosaic virus. Crucifer veg- roguing (removing) symptomatic and off-type seed
etables may experience increased pressure from several plants; applying preventative spray treatments; employ-
diseases if planted near oilseed rape fields. ing appropriate harvest and processing methods so as
Consider other pertinent environmental factors that to avoid contaminating seed; using seed health testing
are related to sites. Crops planted close to an ocean may to evaluate seed for pathogens and viability. These
be more at risk from downy mildew diseases due to the advances in seed pathology are important to the
consistently high humidity and cool temperatures. vegetable industry because a number of damaging
However, moving a few miles inland from the ocean diseases are seedborne in these crops (see Table 8, page
can change these conditions and reduce downy mildew 40).
severity. Choosing a site that has lighter textured soils Seed treatments are an important means of excluding
that drain well reduces the risk of damping-off and root pathogens from the seed used to initiate transplants and
rot for sensitive crops such as spinach. crops. Effective seed treatments that do not significant-
ly reduce germination of the seed depend on the
EXCLUSION following factors: the species of vegetable seed being
Exclusion is preventing any contaminated, infested, or treated; the target pathogen(s); the treatment itself (hot
infected materials from entering the propagation, pro- water, steam, chlorine, other chemicals); dose of the
duction, and harvest systems. Because seedborne treatment substance; length of treatment time; volume
pathogens are a primary means of pathogen introduc- of seed being treated at any one time; post treatment
tion for a number of vegetable diseases, do not allow handling of the seed (cooling, rinsing, drying, coating,
infested or infected seed to be used in the propagation storing, etc.). Examples of seed treatments commonly
system or production field. Growers should purchase used to deal with seedborne pathogens include the
seed that has been tested and certified to be below a following: hot water soaks (carrot: 50° C for 30
certain infestation threshold level, or seed that has been minutes; celery 48° C for 30 minutes; crucifers: 50° C
treated to reduce pathogen infestation levels. Some for 20–30 minutes); sodium hypochlorite (tomato:
seedborne diseases have well defined seed infestation 1.05% for 40 minutes; pea: 10% for 1–5 minutes);
levels, such as black rot of crucifers (caused by Xantho- antibiotics such as agrimycin; fermentation and acid
monas campestris pv. campestris) and Lettuce mosaic treatments (various cucurbits); other chemical treat-
virus of lettuce. For many others, however, seedborne ments such as trisodium phosphate (tomato: 10% for
thresholds have not been established. Note that the des- 15 minutes for treating for Tomato mosaic virus); dry
ignations ‘pathogen-free seed’ and ‘disease-free seed’ are heat treatments (tomato: 70° C for 2–4 days for treating
convenient marketing terms only, as it is not possible to for Tomato mosaic virus).
scientifically prove that a seed lot is actually void of all Other seed treatments are intended to deposit pro-
pathogens; pathogen-free seed usually means that the tecting fungicides onto the seed coat. Such deposits will
pathogen incidence in a seed lot is below that which can protect the seed during the first few days after planting
be detected with standard methods. and will protect seed and newly emerged seedling from
The field of seed pathology and seed treatments is soilborne damping-off pathogens. These seed treat-
a highly developed one. The nature of seedborne ments usually consist of fungicides applied to seeds such
pathogens and how to manage them has been exten- as beans, sweetcorn, and cole crops.
sively researched and studied. Many refinements have Because of the intense international marketing and
been made in producing seed so that pathogens on seed transporting of vegetable seed, the importance of seed
plants are minimized, pathogen detection is improved, health needs to be continually examined. International
and seed treatments are more effective. Some key steps standards for seedborne pathogen detection, testing
in growing seed having minimal pathogen populations methodology, seed treatment, seed viability levels, and
are the following: selecting and placing seed production other pertinent parameters will require continual
sites in areas where the pathogen is not present and con- research and subsequent discussion and acceptance by
ditions do not favor disease development (dry, arid nations producing and selling vegetable seed.
TABLE 8 Important seedborne pathogens of vegetables*
CROP PATHOGEN CROP PATHOGEN
Alliums Aspergillus niger Cucurbit Pseudomonas lachrymans

Botrytis allii continued... Squash mosaic virus
Pseudomonas syringae pv. porri Tobacco ringspot virus
Zucchini yellow mosaic virus
Asparagus Asparagus virus 2
Fusarium oxysporum f. sp. asparagi Lettuce Lettuce mosaic virus
Septoria lactucae
Basil Fusarium oxysporum f. sp. basilicum
Bean Bean common mosaic virus Xanthomonas campestris pv. vitians
Colletotrichum lindemuthianum
Parsley Septoria petroselini
Pseudomonas syringae pv. phaseolicola
Xanthomonas campestris pv. phaseoli Parsnip Phoma complanata
Beet Beet mild yellowing virus Pea Ascochyta pinodes

Beet western yellows virus Ascochyta pisi
Cercospora beticola Fusarium oxysporum f. sp. pisi
Peronospora farinosa f. sp. betae Pea early browning virus
Phoma betae Pea seedborne mosaic virus
Pseudomonas syringae pv. pisi
Brassicas Alternaria brassicae
Alternaria brassicicola Pepper Colletotrichum species
Phoma lingam Cucumber mosaic virus
Mycosphaerella brassicicola Xanthomonas campestris pv. vesicatoria
Pseudomonas syringae pv. alisalensis Pepper mild mottle virus
Pseudomonas syringae pv. maculicola Tobacco mosaic virus
Xanthomonas campestris pv. campestris Tomato mosaic virus
Broad bean Ascochyta fabae Spinach Cladosporum variabile

Broad bean stain virus Cucumber mosaic virus
Broad bean true mosaic virus Stemphylium botryosum
Broccoli raab Alternaria brassicae
Pseudomonas syringae pv. alisalensis Sweetcorn Ustilago maydis
Carrot Alternaria dauci Swiss chard Cercospora beticola

Alternaria radicina
Tomato Alfalfa mosaic virus
Cercospora carotae
Alternaria solani
Xanthomonas campestris pv. carotae
Clavibacter michiganensis
Celery Cercospora apii subsp. michiganensis
Phoma apiicola Colletotrichum coccodes
Pseudomonas syringae pv. apii Cucumber mosaic virus
Septoria apiicola Fusarium oxysporum f. sp. lycopersici
Pseudomonas syringae pv. tomato
Cilantro Cilantro yellow blotch virus
Tomato mosaic virus
Pseudomonas syringae pv. coriandricola
Xanthomonas campestris pv. vesicatoria
Cucurbit Acidovorax avenae subsp. citrulli
Watercress Septoria sisymbrii
Cladosporium cucumerinum
Colletotrichum orbiculare
Didymella bryoniae
Fusarium oxysporum * This table lists those pathogens that have been documented to be
seedborne, and in which the seedborne aspect plays a role in vegetable
Fusarium solani f. sp. cucurbitae disease epidemiology .
Diseased or contaminated transplants likewise example) or through multiple genes that result in a
should not be purchased or used to plant production broad resistance to many pathogens. Single gene resist-
fields. The growing of high-quality, healthy transplants ance is called vertical resistance, and it limits the initial
entails the use of many disease management steps, level of infection and subsequent production of
many of which are discussed in the sanitation section of inoculum. However, single gene resistance can be
this chapter. For a few vegetable crops such as overcome by new strains of the pathogen. The
asparagus and artichoke, vegetative crown tissue is breakdown of resistance due to such changes in the
divided and used as propagation material to start new pathogen poses a constant concern for growers. For
fields. The disease control principle of exclusion example, during the past 50 years in California, a new
demands that only healthy, uninfected crown divisions race of spinach downy mildew (caused by Peronospora
be used to propagate such crops. farinosa f. sp. spinaciae) would periodically occur and
Exclusion also means preventing contaminated cause significant damage to the previously resistant
equipment, water, soil, and other objects from entering cultivars. Plant breeders would counter with new
the vegetable production area. While not always cultivars having resistance genes to the new race.
practical or easy to achieve, tractors and vehicles should Growers would then enjoy several years of mildew-free
be washed or cleaned of contaminated soil prior to spinach until the development of yet another race. This
entering a clean field. For at least two diseases, varnish back-and-forth dynamic has taken place for each of the
spot (caused by Pseudomonas cichorii) and lettuce races that so far has been found in California. Similar
dieback (Lettuce necrotic stunt virus) of lettuce, the dynamics exist for lettuce downy mildew (caused by
pathogen is found in infested water; such water should Bremia lactucae) in both Europe and the USA. In
be excluded and not be used to irrigate the crop. If contrast, multiple gene resistance is called horizontal
livestock are fed crucifer residues containing the resistance, and it limits the rate of disease development,
clubroot organism (Plasmodiophora brassicae), the meaning that some disease may develop but at a low,
pathogen’s resting spores survive passage through generally tolerable level.
animal digestive systems and can infest manure. Such Perhaps the greatest limitation of resistant plants as
manure should be excluded from the field. Aspects of a disease control option is that resistance is not available
contaminated objects are also discussed under sanita- for all crops. For several of the most damaging plant
tion and cultural practices. diseases, such as late blight of tomato (caused by
Phytophthora infestans) and white rot of onion and
RESISTANT PLANTS AND CULTIVARS garlic (caused by Sclerotium cepivorum), growers do
Resistant plants are an obvious and effective control not yet have cultivars with high degrees of acceptable
measure and are one the most important components resistance. There are no known disease resistant
in an integrated disease control program. Cultivars cultivars for most of the smaller acreage, specialty veg-
should be selected that are resistant to the main etables such as the following: arugula, broccoli raab,
pathogens of concern. The most valuable cultivars will cilantro, fennel, jicama (Pachyrhizus erosus), leafy
also have resistance to other pathogens, desirable mustards, radicchio, Swiss chard, tomatillo, and many
horticultural characteristics, and be suitable for the par- Asian vegetables and herbs. Another major limitation is
ticular region and climate where it is placed. Likewise, that resistance may be present in cultivars that lack
growers can select cultivars that can tolerate the adequate horticultural characteristics. There are celery
pathogen even if such plants are not technically cultivars with acceptable resistance to the Fusarium
resistant. For Verticillium wilt of cauliflower in Cali- yellows pathogen (Fusarium oxysporum f. sp. apii);
fornia, some vigorous hybrids showed excellent however, some of these selections lack the color, yield,
tolerance to the pathogen in the field and produced high and appearance qualities that the celery market
yields, even though under experimental conditions the currently requires. Finding a cultivar with multiple
cultivar was susceptible to the pathogen (V. dahliae). resistances can also be difficult for growers. Lettuce that
Resistance in a plant can be expressed through the is resistant to Lettuce mosaic virus may be quite sus-
action of a single gene that confers immunity (resistance ceptible to corky root disease (caused by Rhizomonas
to certain races of the Fusarium wilt pathogen, for
suberifaciens); a lettuce selection that resists corky root readily if the crop rotation strategy includes a period of
may be very susceptible to downy mildew. time in which no fields of the host plant are present in
Modern molecular technology and the production of the region. For example, in coastal California’s Salinas
genetically modified plants will provide novel sources Valley, government regulations enforce a host-free
of disease resistance and other benefits. One example is period in which no celery can be planted in the field for
the development of transgenic summer squash the month of January and no lettuce can be present in
(Cucurbita pepo) cultivars that are resistant to several fields from December 6 to 20. These mandatory host-
important virus pathogens. This resistance is an free periods greatly assist in the management of Celery
example of pathogen-derived resistance in which genes mosaic virus and Lettuce mosaic virus, respectively,
from the virus pathogen itself (in this case genes that because of the elimination of the primary virus hosts
code for the virus coat protein) are introduced and inte- during a time in the winter when the aphid vectors are
grated into the genome of the squash host. In 1994 a inactive and reduced in populations. This step prevents
yellow crookneck summer squash was the first virus- the virus pathogens from bridging from the fall pro-
resistant transgenic plant to be marketed in the USA. duction season into the following spring plantings. In
However, this technology has not yet gained general another example, researchers found that overwintered
public support, so most vegetable breeding efforts carrot fields in the Salinas Valley were the primary
apparently will rely, in the short term, on conventional source of the virus complex that causes carrot motley
breeding methods. dwarf of carrot. When carrot growers stopped the
practice of keeping carrot fields through the winter, the
CULTURAL PRACTICES virus disease almost disappeared from the region.
The disease control category of cultural practices is a Research indicates that certain plants, in addition to
broad and diverse collection of production practices being revenue-generating crops, also have partial sup-
and choices used to reduce the effects of diseases. Such pressive effects on various pathogens. For example,
practices are designed to help plants avoid contact with after broccoli crops are harvested and the plant residue
pathogens, reduce inoculum in the environment of the is plowed into the soil, the decomposition of the
host plant, and create environmental conditions unfa- broccoli stems and leaves releases chemicals that either
vorable for disease development. directly inhibit soilborne pathogens or perhaps alter soil
microflora populations that subsequently compete with
Crop rotations pathogens. Broccoli as a rotation crop and even as a
A significant factor in disease problems is the growing cover crop is now being used by California growers to
of the same crop or closely related crops in consecutive take advantage of this suppressive effect. Cabbage crop
plantings, or growing the same crop too frequently over residues and mustard cover crops show similar effects
a period of a few seasons. Growers need to rotate crops on soilborne pathogens.
so that the pathogens of one crop do not continue to When devising crop rotation strategies, growers
increase and survive on that particular crop. must consider which crops and cover crops might
Implementing crop rotations that have diverse species increase disease problems. Vetch cover crops, if planted
will also encourage diversity in the soil microbe popu- in fields having populations of Sclerotinia minor, can
lation. Crop rotations are useful, advisable strategies for greatly increase the number of infective sclerotia of this
all crops and for all diseases; however, rotating crops is pathogen. Oilseed radish cover crops can be used as
particularly important for combating soilborne trap crops to reduce cyst nematode (Heterodera species)
pathogens. Crop rotations should also include, when populations in the soil; however, oilseed radish could
possible, the use of cover crops that encourage soil cause increases in clubroot disease.
microbe diversity and add organic matter to soil.
Accurate records must be maintained so that crop Fertilizers, soil amendments, and composts
rotation schemes are documented for future planning. Adding amendments and composts to the soil is benefi-
The subject of crop rotations also encompasses the cial for a number of fertility and soil conditioning
strategy of host-free periods. Researchers have found reasons. However, with few exceptions, there is a lack
that some virus diseases are controlled much more of empirical data that clearly document a commercial
level disease control benefit from such additions to soil. reduce the severity of many diseases. Drip irrigation
One exception is the application of lime that success- usually allows for a more precise delivery of water,
fully reduces clubroot disease of crucifers. Amendments resulting in better water management, reduced soil sat-
and composts should continue to be used, however, for uration, and a lowered risk of soilborne diseases such as
plant nutrition and growth considerations. Implement root rots. Where overhead irrigation is required, appli-
balanced, appropriate fertilizer programs to encourage cation should be made early in the day so that foliage
vigorous growth. Do not over apply fertilizers such as can dry during the remainder of the day. For all irriga-
nitrogen, as too much nitrogen can result in excessive, tion schedules, carefully monitor irrigations so that
succulent foliage that can be more susceptible to foliar excess water is not applied to the crop. For a few
pathogens. diseases, the pathogen can be present in irrigation water.
Examples of such pathogens are Pseudomonas cichorii
Planting and Lettuce necrotic stunt virus in lettuce and Phyto-
Time of planting can offer an opportunity for minimiz- phthora capsici in several vegetable crops. In such cases,
ing diseases. In California, susceptible cauliflower that exercise caution when using such infested water.
is planted in Verticillium-infested fields in the spring or
summer will likely experience significant disease; SANITATION
however, cauliflower planted in the same fields in the Sanitation is the general practice of cleaning up or
late fall or winter will exhibit no Verticillium wilt removing diseased or contaminated materials. During
symptoms. This difference in disease severity is attrib- the process of producing vegetable transplants, for
uted to soil temperatures; winter soil temperatures are example, sanitation involves the use of clean or
too cool for the fungus to develop and cause significant sanitized transplant trays, bench tops, and mowing
problems. In the UK, delayed planting can reduce the equipment (used to mow the tops of transplants and
impact of Aphanomyces on beet because warmer soils encourage thicker stem development). Workers should
encourage rapid germination of seedlings. Early wash or sanitize their hands or gloves before moving to
planting can reduce rhizomania on beet and clubroot and working with different transplant lots.
on crucifers because of reduced pathogen activity in Sanitation can include removal of diseased material
cold soils. Therefore, choose planting dates that might from fields. Roguing, or the removal of diseased plants
reduce disease pressure for the particular crop under from a crop, is not often done in production fields but
consideration. can help prevent spread of diseases and inoculum
Proper soil preparation prior to planting can reduce increase. Roguing is a common practice used in
seed decay and seedling damping-off diseases by tilling vegetable seed crops. For asparagus diseases, the
to reduce plant residues left from previous crops and by removal of diseased asparagus fern foliage can signifi-
making raised beds with good soil tilth and drainage. cantly reduce inoculum of foliar pathogens. Once
Proper bed preparation will also assist in the establish- vegetable crops are harvested, the plowing under and
ment of transplants. At planting, place seed and trans- destroying of the remaining plants and crop residues
plants at proper depths. Placing plants too deeply can aids in the destruction of inoculum. Destroying old
delay plant emergence or establishment, and thus plants also helps reduce virus reservoirs if such plants
increase disease problems. were infected with viruses or infested with virus vectors.
Plowing and disking the soil assists in the breakdown of
Irrigation old crop residues, which will help reduce some seed and
For most foliar diseases, overhead sprinkler irrigation seedling diseases for the next crop and will decrease
enhances pathogen survival and dispersal, and subse- inoculum levels for foliar diseases.
quent disease development. Bacterial diseases are espe- As mentioned under exclusion, as much as possible
cially dependent on rain and sprinkler irrigation. prevent the movement of contaminated field equipment
Therefore, eliminate or reduce the use of sprinkler irri- from infested to clean fields. While not always practical,
gation if possible. The use of surface or buried drip tape attempt to wash or otherwise sanitize tractors and farm
for vegetable production has increased greatly in implements after using these in fields having important
California and other areas in recent years and helps soilborne pathogens.
A form of sanitation is used for combating lettuce possible by applying appropriate insecticides, planting
drop caused by Sclerotinia minor. This disease occurs crops on reflective mulches to repel vectors, and
when sclerotia from infected lettuce residues remain in planting crops under netting, fabric, or plastic tunnels
the top few inches of soil and are positioned for the next to exclude vectors.
lettuce planting. A sanitation step is deep plowing in
which a mold-board plow inverts the soil and buries the USING FUNGICIDES, BACTERICIDES,
sclerotia. Note that this procedure is effective only if AND OTHER DISEASE CONTROL CHEMICALS
sclerotia are low to moderate in number. Applying fungicides, bactericides, and other disease
control materials is an important option that must be
ENVIRONMENTAL MANIPULATION used judiciously and integrated into other disease
Growers should create conditions that are unfavorable control choices. There is a current worldwide trend to
for disease development. Some cultural methods that reduce the use of synthetic chemicals on food com-
achieve this include using optimum plant spacing to modities for both human health and environmental
reduce relative humidity around plants, providing good concerns. Therefore, use such chemicals only when
soil drainage through proper soil preparation and irri- needed. New products often are safer, reduced risk
gation practices, and using mulches to physically isolate materials that are effective at much lower volumes than
above-ground plant parts from contact with the soil. older fungicides.
Solarization can be included here. This practice works Pre-plant fumigants are often highly successful in
best in regions having high summer temperatures and reducing soilborne inoculum, though their use is
solar radiation. Fallow fields are covered with plastic expensive and strictly regulated. The following fumi-
tarps, and the resulting heat generated below the tarp gants are most commonly used to control soilborne
reduces soilborne pathogen populations. pathogens: methyl bromide alone, methyl bromide plus
Environmental manipulation is much more attain- chloropicrin combinations, chloropicrin alone, chloro-
able in greenhouse settings. For greenhouse-grown picrin plus telone, metham sodium. The application of
transplants, the use of heaters and coolers allows fumigants is often combined with the placing of plastic
growers to control temperatures. Venting the green- tarps over the treated soil. These tarps help prolong
house reduces humidity and helps manage gray mold exposure periods at effective fumigant concentrations.
(caused by Botrytis). While most transplants are still Fumigants, however, do not eradicate soilborne patho-
watered with overhead sprinklers, other systems can be gens because of limitations inherent in the chemical,
used. For example, absorbent irrigation mats are placed failure to penetrate all parts of the soil profile, survival
on benches; transplants are placed on top of the mats of pathogen propagules that are protected by plant
and water moves up into the tray cells by capillary residues, and other factors. In addition, even if the
action. Greenhouses also employ fans to increase air fumigant treatment is successful, soilborne pathogens
movement and enhance drying of foliage. can recolonize treated soils. For example, researchers
found that the Fusarium wilt pathogen of melon, F.
CONTROLLING OTHER BIOTIC FACTORS oxysporum f. sp. melonis, readily recolonized soils that
Weeds, volunteer plants, and other hosts can harbor had been treated with various fumigants.
pathogens that spread to the vegetable production field. Fungicide-treated seed is an important tool in
Therefore, these inoculum sources should be eliminated. combating certain seed and seedling diseases. In some
Another biotic factor is the vector of pathogens. situations fungicides applied immediately post-planting
Vectors, primarily insects (aphids, whiteflies, leafhop- can be effective for managing diseases. For example, the
pers, thrips) and nematodes that transmit viruses, application of fungicides at planting to spinach seed
should be monitored and managed. However, lines can effectively prevent damping-off caused by
managing these organisms will not prevent virus trans- Pythium. A way of controlling lettuce drop caused by
mission because in many cases only a brief feeding time Sclerotinia minor is to apply fungicides to plants at the
is needed for insects to inject the virus pathogen into thinning stage. However, for the majority of soilborne
plants. Despite this difficulty in preventing virus trans- pathogens, field-applied fungicides are usually not very
mission, control insect and other vectors as much as effective.
TABLE 9 Historical list of some disease control materials used on vegetables*
Chemical group Name Date** Chemical group Name Date**
1, 2 Thiadazole Etridiazole 1969 Dinitrophenyl crotonate Dinocap 1946
2, 6 Dinitroaniline Fluazinam 1987 Dithiocarbamate Ferbam 1931

Flutolanil 1981
Acetamide Cymoxanil 1977
Mancozeb 1961
Anilinopyrimidine Cyprodinil 1994 Maneb 1950
Pyrimethanil 1990 Metiram 1958
Thiram 1931
Antibiotic Kasugamycin 1965
Zineb 1943
Mildiomycin 1979
Ziram 1930
Oxytetracycline 1974
Polyoxin 1965 Guanidine Dodine 1954
Streptomycin 1944 Guazatine 1968
Validamycin 1970
Hydroxy (2-amino)
Aromatic hydrocarbon Dicloran 1959 pyrimidine Bupirimate 1975
Pentachloronitrobenzene 1930 Dimethirimol 1968
Tolclofos methyl 1973 Ethirimiol 1968
Benzamide Zoxamide 1994 Hydroxyanilide Fenhexamid 1989
Benzene-sulfonamide Flusulfamide 1986 Inorganic Calcium polysulfides 1852
Copper sulfate 1880s
Benzimidazole Benomyl 1968
Potassium bicarbonate 1990s
Carbendazim 1972
Sulfur 1800s
Thiabendazole 1962
Zinc 1932
Benzothiadiazole Acibenzolar-S-methyl 1995
Morpholine Fenpropimorph 1979
C-14 DMI: Imidazole Imazalil 1973 Tridemorph 1968
Prochloraz 1974
Organo tin Triphenyl tin hydroxide 1954
C-14 DMI: Piperazine Triforine 1967
Phenylamide Mefenoxam 1996
C-14 DMI: Pyrimidine Fenarimol 1975 Metalaxyl 1977
C-14 DMI: Triazole Cyproconazole 1986 Oxadixyl 1983
Difenoconazole 1988 Phenylpyrrole Fludioxonil 1990
Fenbuconazole 1988
Phosphonate Fosetyl aluminium 1977
Myclobutanil 1984
Phosphorous acid 1980s
Propiconazole 1979
Tebuconazole 1986 Phthalimide Captafol 1961
Triadimefon 1975 Captan 1949
Triadimenol 1977
QoI (Quinone-outside
Carbamate Propamocarb 1978 inhibitor) Azoxystrobin 1990
Kresoxim-methyl 1990
Carboxamide Boscalid 2003
Pyraclostrobin 2002
Carboxin 1966
Trioxystrobin 1997
Oxycarboxin 1966
Quinoline Quinoxyfen 1992
Chloronitrile Chlorothalonil 1964
Thiophanate Thiophanate methyl 1969
Cinnamic acid Dimethomorph 1988
Dicarboxamide Iprodione 1970 * This is not a complete list of materials used to control diseases of
Procymidone 1976 vegetables. Many of these products are no longer approved for use.
Vinclozolin 1975 ** Approximate discovery or release date
The effectiveness of fungicides applied to foliage and fungicides are usually non-systemic and remain only on
above ground parts of plants depends on several the plant surfaces that received the spray. Protectants
factors. Timing is the first consideration. Most available usually prevent pathogen infection before it takes place,
fungicides must be applied to the plant surface prior to and provide little benefit if the pathogen already entered
infection and are classified as protectants. If applied the host. Therefore, protectants must be applied
after infection has already occurred, such materials will multiple times to protect new growth. Eradicant fungi-
be less effective. Timing also deals with the interval cides are usually systemic materials capable of localized
between multiple sprays. Most materials need to be (e.g. translaminar) or more general movement within
used several times on the vegetable plant. Environ- the plant. Eradicants stop or reduce fungal growth after
mental conditions, susceptibility of the plant, plant host penetration has occurred. Only eradicant fungi-
growth rate, inoculum level and pressure, and nature of cides can control some latent infections; infections are
the fungicide product will dictate how many days can latent if the pathogen has succeeded in penetrating and
elapse between applications. Because of the importance initially colonizing the host, but is not actively growing
of timing, it is essential to have thorough and regular and progressing in the host. See Table 9 (previous
monitoring of fields for early symptoms and signs of page)for a list of some fungicides and other materials
disease. used to control diseases of vegetables and other plants.
Product rates are important factors as well and are The chemical mode of action of fungicides targets
set by the manufacturer. Maximum label rates are metabolic sites in the pathogen. Some chemicals act on
established by the fungicide producer and cannot be a single site while others act on multiple sites.
exceeded. However, in some cases lower rates are Researchers still have not identified all the mechanisms
allowable. Such reduced rates should be used based on involved. Fungicides may affect processes such as
manufacturer recommendations, disease pressure and energy production, major biosynthetic pathways, or
situation, and prior experience with the product. The membrane function. The triazoles or demethylation
final factor for successful deployment of fungicides is inhibitors (DMIs) interfere with sterol biosynthesis and
the selection of the product and formulation. Choose impair membrane synthesis and function. Strobilurins
products based on label information on how the are QoI inhibitors that inhibit mitochondrial respiration
product controls a particular pathogen, recommenda- by binding to the Qo site of cytochrome b. Phenyl-
tions by university, extension, and other professionals, amides affect RNA polymerase, and the aminopyrim-
prior experience of industry members and other idines inhibit the enzyme adenosine deaminase.
growers, and published information and research. It is Protectant, broad-spectrum fungicides such as the
important to use multiple products, if available, to delay dithiocarbamates, copper, and tin have multi-site
or prevent the development of fungicide resistance. activity and interfere with energy production.
Most vegetable crops are considered minor crops Mutations in the organism that result in changes at
when compared with the extensive plantings of field the site of action can render the once effective pesticide
crops, grains, soybean, and cotton. Therefore, the ineffective, and pathogens carrying such mutations are
choices of registered fungicides are often limited for considered resistant or insensitive to that material.
vegetable crops. For specialty crops and herbs, few Pesticide resistant individuals exist naturally within
fungicides will be labeled for use. Before purchasing or pathogen populations. When a fungicide or bactericide
using any fungicide product, check the label for use is applied to plants, individuals that are resistant to that
restrictions and safety guidelines. Consult with local chemical survive and increase in number. With repeated
extension, regulatory, and manufacturer agents for use, these resistant individuals increase in proportion
information and regulations on product application. within the population and become sufficiently
There are several categories of fungicides. Systemic numerous so as to cause damaging levels of disease.
fungicides move within the plant after application, The development of resistance is most rapid against
usually in the vascular xylem tissue. Benzimidazoles pesticides having only a single site of action. A single
were the first widely used systemic products, and mutation enables the fungus or bacterium to block or
phenylamide fungicides are probably the most overcome the toxic effects of the material. Resistance in
important systemic group in current use. Protectant fungal pathogens occurred rapidly, within a few years
of product introduction, with benzimidazoles, pyrim- stimulated to do so by sulfur compounds released by

idines, and phenylamides. Pathogens with short, roots. Diallyl disulfide, derived from allium plants, can
repeating life cycles and abundant spore production be applied to fallow soils to stimulate sclerotia germi-
develop fungicide resistance problems faster than nation. Germinated sclerotia will die because no allium
slower cycling pathogens. Powdery mildews and crop is present. Oils, plant extracts, microorganism by-
Botrytis cinerea are examples of pathogens prone to products and metabolites, and other natural plant
developing resistance to new fungicides. Fungicides products are being investigated for use for disease
with multiple sites of action generally develop resistance control.
less frequently or remain effective for longer periods.
For example, pathogens have not developed resistance BIOLOGICAL CONTROL
to the dithiocarbamates probably because these Classical biological controls, in which a product con-
products are multi-site inhibitors. A number of bacterial taining a viable antagonistic organism is applied to
pathogens readily develop resistance to copper and combat the target pathogen, are still being developed
antibiotic materials used for disease control. but are not yet available or effective for most diseases of
To combat and delay onset of pathogen resistance vegetables. A Coniothyrium minitans product has
(or insensitivity), several strategies must be employed. shown some field efficacy for controlling Sclerotinia
Only apply fungicides when needed; the overuse of sclerotiorum. Other products containing Trichoderma,
chemicals contributes greatly to the development of Gliocladium, Streptomyces, Bacillus, and other
resistance. In general, fungicides should be applied microorganisms have not demonstrated consistent,
before pathogens become established on the host plant. commercially acceptable levels of control.
Different fungicide products having different modes of
action should be applied either in tank mix combina- DISEASE FORECASTING
tions in one spray or in alternating schedules. Careful A number of forecasting systems have been developed
monitoring of unusually severe disease problems that for diseases in vegetable crops. These weather data and
occur despite fungicide applications and close collabo- computer supported programs attempt to predict either
ration with extension researchers and other profession- when pathogens will threaten crops or the degree of
als can help the industry detect outbreaks of resistant disease severity that might be expected given current
pathogens. conditions and inoculum load. Research on forecasting
In addition to fungicides and bactericides, other systems has been on-going for many years. Successful
types of chemical treatment may be used to control systems depend on a satisfactory understanding of the
diseases. The majority of these alternative substances, biology of the pathogen, development of the plant host,
however, are not yet commercially effective or viable and environmental parameters that favor pathogen and
products that consistently provide adequate control. disease development. Some proposed forecasting
Plant stimulants or conditioners such as plant or systems may function in a research context, but not
seaweed extracts and compost teas may show disease provide sufficient information that results in commer-
suppressive effects under certain experimental or small cially acceptable levels of disease control. The biologi-
scale conditions. Some chemicals are elicitors, which cal systems involving plant host, pathogen organism,
induce resistance to pathogens in the host plant. This and surrounding environment are extremely complex;
resistance is distinct from that resulting from gene-for- predictive models generated by researchers often fail to
gene interactions and is termed systemic acquired resist- capture this complexity. Validation is therefore required
ance (SAR). Salicyclic acid, jasmonates, some fatty to test forecasting systems over several seasons, and
acids, and yeast cell wall components can induce such reliance on new systems should be carefully considered.
resistance. At least one synthetic plant activator, aciben-
zolar-S-methyl, is used commercially. Some chemicals
stimulate fungal propagules to germinate and die in the
absence of the host plant. Sclerotia of the allium white
rot pathogen, Sclerotium cepivorum, normally only
germinate in the presence of allium crops and are
TABLE 10 Checklist of vegetable disease management options following the general production sequence
Options before planting Options at planting

Examine the history and records of the proposed site. If Ensure that the bed tops are suitably prepared for good
possible, choose a different site if significant problems seed germination and transplant establishment.
occurred on previous plantings of the same or related
vegetable. Ensure that clean seed and disease-free, high-quality
transplants are brought on site. Exclude unacceptable
Avoid this site if it has features that will be problematic plant materials.
for some diseases, such as heavy, poorly draining soils
that will enhance damping-off problems or consistently Place seed and transplants at appropriate depths. Plant
high humidity that favors foliar diseases. materials that are placed too deeply are subject to addi-
tional disease problems.
If available, collect soil samples and have them tested for
important soilborne pathogens and problem factors In some cases, apply post-plant fungicides to the seed
such as high salt content. lines or transplants after they are placed in the ground.
The vegetable being considered might be a high risk crop Schedule appropriate irrigations so that plant material is
due to factors such as the following: the previous crop not over or under watered.
was the same or related vegetable and subject to the
same pathogens; poor crop rotation has been practiced Options after planting
in the past; this vegetable has been frequently cropped
at this location. If these factors apply, consider another After plants are established, attempt to eliminate the use
site or plant a different, unrelated crop. of overhead sprinkler irrigation systems.
Consider if the target planting date might cause disease Practice good growing methods to enhance plant
severity to be worse. If this might be the case, alter the development and reduce stress. Especially monitor
planting date. irrigations so that excess water is not applied.
Though usually prohibitively expensive for vegetable Regularly and thoroughly monitor the field for signs of
crops, treat the soil with fumigants to reduce inoculum disease and for the presence of insects and weeds.
of soilborne pathogens. Manage insect and weed pests in and around the field.
Select a resistant cultivar. Select cultivars suitable to the If contagious diseases occur in other fields, avoid
region and to the production system being used. If bringing possibly contaminated equipment into a
resistant cultivars are not used, seek tolerant cultivars. healthy field.
For seedborne pathogens, seek to use seed that does not Apply fungicides as available, needed, and appropriate.
have significant levels of the pathogen. If appropriate, As disease prediction systems become available, use
treat seed with hot water, effective fungicides, or other these to time the applications. Use diverse fungicide
treatments. Have seeds treated with fungicides if directly products so as to reduce the onset of resistance.
seeded in the field.
If transplants are to be used, arrange for vigorous, Options at and after harvest
healthy, symptom-free transplants.
Harvest crops when commodities are still healthy, in
Remove weeds, volunteer plants, and any other possible good condition, and not over mature. If diseases begin
host plants from the field and surrounding areas. to occur in a field, harvest dates should be moved up and
Work the soil and time the planting so that previous crop plants removed early.
residues are absent or minimized. Harvested commodities should be kept clean, free of soil,
Add appropriate materials (lime, gypsum, fertilizers) that and undamaged. Commodities should be properly
will enhance plant growth or create conditions unfavor- packed and rapidly placed in cold storage or another
able to the pathogen. appropriate storage environment.
Ensure that tractors and equipment used for soil prepa- Plow under and otherwise destroy unharvested plants
ration are not contaminated with infested soil from other and weeds in and around the field.
fields. Schedule disking and other soil preparation steps so that
Properly prepare the soil so that it drains well, does not crop residues break down in a timely manner. Allow suffi-
have low spots, and is in suitable condition to encourage cient time for residues to dissipate prior to the next crop.
rapid seed germination, transplant establishment, and Consider planting a cover crop or broccoli that can
subsequent growth of the crop. reduce soilborne pathogen populations.
Devise and install an appropriate irrigation system. Consider adding compost and other beneficial amend-
ments to the soil prior to planting the next crop.
In warmer regions, try soil solarization treatments for
reducing inoculum from soilborne pathogens.
Other aspects of disease management general production practices is another aspect consis-
POSTHARVEST HANDLING tent with this approach.
When vegetable commodities reach harvestable stage, For organic growers, the application of disease
the crop can be healthy but exposed to pathogen control materials is limited. Mineral-based control
inoculum, infected by pathogens but not yet showing materials, primarily copper and sulfur fungicides, are
symptoms, or diseased and showing symptoms in generally inexpensive and widely available. However,
various stages. In all cases, these commodities may be disease control efficacy varies. Copper fungicides have
harvested, packed, and placed in storage. Depending on some activity against a wide range of fungal and
length of storage, temperature, humidity, and other bacterial pathogens but generally are not extremely
environmental factors, the stored commodities can effective. Sulfurs also exhibit some activity against
develop postharvest diseases that originated from field many pathogens, but usually only provide excellent
pathogens. To minimize postharvest disease develop- control against certain pathogens such as powdery
ment, harvest crops when commodities are undamaged, mildew fungi. Bicarbonate based fungicides have
still healthy, in good condition, and not over mature. If recently become available for control of plant diseases
diseases begin to occur in a field, harvest dates should and have shown activity primarily against powdery
be moved up and plants collected early. Harvested com- mildews. Of note is recent research indicating that
modities should be kept clean, free of soil, and copper and sulfur materials, previously thought to have
undamaged. Commodities should be properly packed minimal impact on the environment, may actually have
and rapidly placed in cold storage or other appropriate deleterious effects on the ecosystem.
storage environment. Time in storage is a critical factor,
and the longer commodities are stored, the greater is the INTEGRATED DISEASE MANAGEMENT
chance that postharvest diseases can occur. The optimum way to control diseases of vegetables is to
use all available disease management tools in an inte-
CONTROLLING DISEASES IN ORGANIC SYSTEMS grated, strategic system. Reliance on only chemicals or
The challenge of disease control is accentuated for some other one-dimensional approach will not provide
organic vegetable growers because they do not use the best means of controlling damaging problems. To
synthetic fungicides and fumigants. These growers have be most successful, growers must integrate and coordi-
fewer insecticides to use against pathogen vectors and nate all of the aspects discussed in this chapter: site
fewer herbicides to manage weeds. Yet the world selection, exclusion, resistant and tolerant cultivars, a
market will continue to be extremely competitive and wide range of cultural practices, sanitation, manipula-
require organic growers to supply high-quality, disease- tion of the environment, control of reservoir hosts and
free produce having acceptable shelf-life. This makes vectors, fungicides and other disease control materials,
disease control a challenging task for organic vegetable disease forecasting systems, and proper postharvest
growers. In principle and with the exception of handling. See Table 10 for a chronological checklist of
synthetic chemicals, the integrated disease management these options that is arranged in a sequence that fits
strategy for organic vegetable producers should be general vegetable production.
similar to that for conventional growers. All options A good case study that illustrates an integrated
that do not involve synthetic chemicals are applicable disease management system is the control strategy for
and appropriate for this segment of the industry. Lettuce mosaic virus (LMV) on lettuce grown in
In addition, organic growers generally try to California’s Salinas Valley. A productive partnership
emphasize strategies that have an ecological basis. For between University of California campus-based
example, the organic system encourages as much as researchers, Cooperative Extension researchers, lettuce
possible the growth and diversity of soil-inhabiting and growers, and regulatory agencies resulted in a manage-
leaf-epiphytic microorganisms that might have benefi- ment program that successfully keeps lettuce mosaic at
cial and pathogen-antagonistic influences. Increasing minimal levels in this valley, which is the world’s largest
the genetic diversity of the crop rotation is another eco- lettuce growing region. County government ordinances
logical management step. Integrating disease manage- enforce the first four aspects of the integrated program
ment decisions with insect and weed control and with outlined overleaf.
• Lettuce seed assays for LMV • Resistant lettuce cultivars

All lettuce seed to be planted in the Salinas Valley is While not used extensively in the Salinas Valley,
tested for seedborne-LMV. Researchers found that cultivars resistant to LMV are available and con-
a zero in 30,000 seed infection threshold is the key tribute to this integrated program.
for LMV control here; if no infected seed are found • Aphid control
in a 30,000 lettuce seed sample serologically tested Spraying for the aphids that vector LMV does not
by the enzyme-linked immunosorbent assay prevent the transmission of virus because aphids
(ELISA), the seed lot is approved for planting. can transfer this pathogen to lettuce before the
• Weed control insecticides act to kill the insects. However, aphid
Because weeds can be a significant reservoir of the control clearly helps to slow LMV spread and
virus and the source from which aphids obtain the therefore should be included.
virus, weeds must be regularly controlled and • Research on LMV
removed in the lettuce production areas. University and extension researchers continue to
• Plow-down of old lettuce plantings examine the LMV system, attempting to increase
Old, infected lettuce plants, like weeds, are a source understanding of disease dynamics, improve upon
of virus and vectors. Aphids can obtain LMV from antiserum used for seed assays, delve into the
these old plants and transport the virus to younger, genetic nature of LMV strains, and watch for
nearby lettuce plantings. Old plantings, once changes in the local and worldwide situation
harvested, must be plowed down in a timely regarding this important virus.
manner.
• Lettuce host-free period
To prevent continuous, year-to-year buildup of
LMV, an annual host-free period is enforced for
two weeks in December. This step is effective
because LMV is an obligate pathogen and cannot
survive in nature without living plant hosts. The
ban on lettuce production in this winter period
helps reduce the amount of virus that might ‘bridge’
over from one season to the next. Vector activity
during this winter period is limited, which also con-
tributes to the effectiveness of the lettuce free
period.
• Site selection
Over time, growers find that certain fields are prone
to developing lettuce mosaic disease due to virus
reservoirs in the area. Such sites are not planted to
lettuce, if possible. In specific examples, lettuce
mosaic tended to occur in fields adjacent to a
business storage area where weeds were not con-
trolled, and in another area where LMV-infected
Gazania species ground covers were a part of the
landscape.
References on disease control Lyr, H., et al. 1999. Modern Fungicides and Antifungal
Compounds II. 12th International Reinhardsbrunn
Agarwal, V.K. and Sinclair, J. B. 1997. Principles of Seed Symposium, Thuringia Germany. Intercept.
Pathology. Second Edition. CRC Press. Maloy, O. C. 1993. Plant Disease Control: Principles and
Brent, K. J. 1995. FRAC Monograph No. 1 Fungicide resistance Practice. John Wiley & Sons.
in crop pathogens: How can it be managed? GIFAP, Brussels, Maude, R. B. 1996. Seedborne diseases and their control:
48pp. Principles and Practice. CAB International, Wallingford, UK,
Brown, R. G. 1999. Plant Diseases and Their Control. Sarup & 280 pp.
Sons. Ristaino, J. R. and Thomas, W. 1997 Agriculture, methyl
Brown, S., Koike, S. T., Ochoa, O. E., Laemmlen, F., and bromide, and the ozone hole: can we fill the gap? Plant
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fosetyl-Aluminium in California isolates of the lettuce downy
Skylakakis, G. 1981. Effects of alternating and mixing pesticides
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88:502–508.
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Clarkson, J.P., Kennedy, R., and Bowtell, J. 1998. A
Smith, I. M., Dunez, J., Lelliot, R. A., Phillips, D. H., and Archer
methodology for evaluation of the efficacy of fungicide
S. A. (eds). 1988. European Handbook of Plant Diseases.
dosage and plant resistance in the control of fungal diseases of
Blackwell Scientific Publications, Oxford, UK, 583 pp.
vegetable crops. Proceedings of the 1998 Brighton
Conference. Pests & Diseases 3: 869–874. Soper, D. 1995. A Guide to Seed Treatments in the UK. British
Crop Protection Council. Major Print Ltd.
Crute, I. R. 1998. British Society for Plant Pathology Presidential
Address 1995 The elucidation and exploitation of gene-for- Staub, T. 1991. Fungicide resistance: practical experience with
gene recognition. Plant Pathology 47: 107–113. anti-resistance strategies and the role of integrated use.
Annual Review of Phytopathology 29:421–442.
Ebbels, D. L. 2003. Principles of Plant Health and Quarantine.
CABI Publishing, Wallingford, UK, 320 pp. Subbarao, K. V., Hubbard, J. C., and Koike, S. T. 1999.
Evaluation of broccoli residue incorporation into field soil for
Fry, W. E. 1982. Principles of Plant Disease Management.
Verticillium wilt control in cauliflower. Plant Disease
Academic Press.
83:124–129.
Fuchs, M., Tricoli, D. M., Carney, K. J., Schesser, M., McFerson,
Tomalin, C. D. S. (ed.). 2000. The Pesticide Manual. 12th
J. R., and Gonsalves, D. 1998. Comparative virus resistance
Edition. British Crop Protection Council, Farnham, UK.
and fruit yield of transgenic squash with single and multiple
coat protein genes. Plant Disease 82:1350–1356. Thompson, D. C., Baron, J. J., and Kunkel, D. L. 2000. The IR-4
Project – a minor-use program for pest management solutions
Gaskell, M., Fouche, B., Koike, S., Lanini, T., Mitchell, J., and in the United States. Proceedings of the BCPC Conference.
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California—science and practice. HortTechnology
10:699–713. Thurston, H. D. 2004. Ten thousand years of experience with
sustainable plant disease control. Plant Disease 88:550–551.
Grogan, R. G. 1980. Control of lettuce mosaic with virus-free
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53
PART 2
Diseases of
Vegetable Crops
• ALLIACEAE (onion family) • FABACEAE (pea family)
Phaseolus species (beans)
• APIACEAE (parsley family)
Apium graveolens (celery) Pisum sativum (pea)
Daucus carota (carrot) Vicia faba (broad bean)
Pastinaca sativa (parsnip) • LACTUCA SATIVA (lettuce)
Petroselinum crispum (parsley)
• SOLANUM LYCOPERSICUM
• ASPARAGUS OFFICINALIS (asparagus) (tomato)
• BETA VULGARIS (beet) • SPINACIA OLERACEA (spinach)
• BRASSICACEAE • SPECIALTY AND HERB CROPS
(cabbage and mustard family) (horseradish, dill, chervil, Swiss chard,
broccoli raab, mustards, endive/escarole,
• CAPSICUM (pepper)
radicchio, coriander, lemongrass, artichoke,
• CUCURBITACEAE (gourd family) arugula, fennel, Jerusalem artichoke, mint,
catnip, basil, marjoram, oregano, tomatillo,
rhubarb, watercress, sage, salsify, scorzonera,
corn salad, sweetcorn)
54 D ISEASES OF V EGETABLE C ROPS
Alliaceae Onion family
ALLIUMS, formerly classified with the Liliaceae (lilies and relatives), now have their own family,
the Alliaceae. The plants in this crop group are widely used for seasoning and cooking. The most
familiar allium crops include bulb onion (Allium cepa), spring or salad onion (A. cepa),
bunching onion (A. fistulosum), garlic (A. sativum), leek (A. porrum = A. ampeloprasum var.
porrum), elephant garlic (A. ampeloprasum), shallot (A. cepa var. ascalonicum), chives
(A. schoenoprasum), Chinese chives (A. tuberosum), and Egyptian tree onion (A. cepa var.
aggregatum). Allium plants are monocots and may have originated in Asia.
Pseudomonas syringae pv. porri pseudomonads. When cultured on Kings medium B,

BACTERIAL BLIGHT this organism produces a diffusible pigment that fluo-
resces blue under ultraviolet light.
Introduction and significance A number of other bacterial pathogens affect
In commercial settings this bacterium affects primarily alliums. Slippery skin disease is caused by Pseudo-
leek and has been reported from the USA, England, monas gladioli pv. alliicola and results in a water-
France, and New Zealand. Onion, chives, and garlic soaked bulb rot that initially only affects a few fleshy
have developed bacterial blight when inoculated with scales. At room temperature, however, these infected
this pathogen in experimental situations. scales rapidly lead to a extensive rot of the bulb. Sour
skin is caused by Pseudomonas cepacia, which
Symptoms and diagnostic features produces a pale yellow or light brown rot of the inner
Young leaves show water-soaked then yellow longi- fleshy scales. Bacterial streak and bulb rot of sweet
tudinal lesions or stripes that later split and rot. The onion occurs in the USA and is incited by Pseudomonas
leaves can become curled and twisted as growth
continues (1, 2). On older leaves, the pathogen causes
yellow spots around wounds. Flowering stalks are very
susceptible and develop deep, water-soaked lesions that
ooze a bacterial exudate. Older stalk lesions are sunken,
1
first yellow, then finally brown in color. Leek trans-
plants can develop the disease while growing in green-
houses. Leaves of transplants develop yellow, then
brown, elongated lesions (3). Lesions usually involve
the tips of the leaves .
Causal agent
Bacterial blight is caused by Pseudomonas syringae pv.
B ACTERIAL D ISEASES
porri. The designation pathovar (pv.) indicates this

pathogen is host specific to the allium group and does
not infect other crops, such as tomato, celery, and bean,
which are susceptible to other P. syringae pathogens.
The pathogen is an aerobic, Gram-negative bacterium
and can be isolated on standard microbiological media. 1 Water-soaked lesion and leaf deformity of early
It produces the cream-colored colonies typical of most symptoms of bacterial blight of leek.
A LLIACEAE 55
viridiflava. Soft rot is caused by Erwinia carotovora References

subsp. carotovora and is associated with very wet con- Alvarez, A. M., Buddenhagen, I. W., Buddenhagen, E. S., and
ditions in the field or poor handling at harvest. The bulb Domen, H. Y. 1978. Bacterial blight of onion, a new disease
caused by Xanthomonas sp. Phytopathology 68:1132–1136.
develops a watery rot with a pungent odor. Another
Gitaitis, R., MacDonald, G., Torrance, R., Hartley, R., Sumner,
bacterial disease is onion bacterial blight caused by a D. R., Gay, J. D., and Johnson, W. C. 1998. Bacterial streak
seedborne Xanthomonas species. This problem occurs and bulb rot of sweet onion: II. Epiphytic survival of
Pseudomonas viridiflava in association with multiple weed
mostly in tropical and subtropical areas and causes hosts. Plant Disease 82:935–938.
elongated yellow lesions that may have water-soaked Koike, S. T., Barak, J. D., Henderson, D. M., and Gilbertson, R.
edges; lesions later turn brown and necrotic. L. 1999. Bacterial blight of leek: a new disease in California
caused by Pseudomonas syringae. Plant Disease 83:165–170.
Nunez, J. J., Gilbertson, R. L., Meng, X., and Davis, R. M. 2002.
Disease cycle First report of Xanthomonas leaf blight of onion in
Pseudomonas syringae pv. porri is seedborne, so disease California. Plant Disease 86:330.
can be initiated in the field with direct seeded leek, or Paulraj, L. and O’Garro, L. W. 1993. Leaf blight of onions in
begin at the transplant stage in greenhouses. Spread of Barbados caused by Xanthomonas campestris. Plant Disease
77:198–201.
the pathogen at the seedling, transplant, or field stage is Roberts, P. 1973. A soft rot of imported onions caused by
dependent on splashing water from rain or overhead Pseudomonas alliicola (Burkh.) Starr and Burkh. Plant
sprinkler irrigation. The bacterium can survive in leek Pathology 22:98.
crop residues but will not persist in soil once residues Roumagnac, P., Gagnevin, L., and Pruvost, O. 2000. Detection
of Xanthomonas sp., the causal agent of onion bacterial
are completely decomposed. blight, in onion seeds using a newly developed semi-selective
isolation medium. European Journal of Plant Pathology
Control 106:867–877.
Samson, R., Poutier, F., and Rat, B. 1981. Une nouvelle maladie
Use seed that does not have significant levels of the du poireau: la graisse à Pseudomonas syringae. Revue
pathogen. Appropriate seed treatments can also con- Horticole 219:20–23.
tribute to the management of seedborne inoculum. Samson, R., Shafik, H., Benjama, A., and Gardan, L. 1998.
Rotate away from allium crops to reduce inoculum Description of the bacterium causing blight of leek as
Pseudomonas syringae pv. porri. Phytopathology
from crop residues. Irrigate using drip or furrow 88:844–850.
systems. Copper sprays may reduce spread. Avoid over- Teviotdale, B. L., Davis, R. M., Guerard, J, P., and Harper, D. H.
fertilizing with high nitrogen materials. 1989. Effect of irrigation management on sour skin of onion.
Plant Disease 73:819–822.
2 3
2 Deformed leeks severely affected by bacterial blight. 3 Brown lesions of advanced symptoms of bacterial
blight of leek.
Alternaria porri, Stemphylium vesicarium Disease cycle

PURPLE BLOTCH Infection requirements are similar for both pathogens,
and disease severity is worse with warm and humid or
Introduction and significance wet conditions. Spores are airborne and infect the leaves
This disease occurs throughout the world but is most via stomata or directly through the epidermis. Inoculum
damaging in areas with warm, humid climates. It is an comes from infested crop residue in the field.
important concern on onion, garlic, and leek. Purple The optimum temperature for A.porri is 18–25º C
blotch is caused by two fungal pathogens which may for germination and 15–25º C for infection. The
co-infect the plant or act independently in causing pathogen can still be active at lower temperatures
disease. (4–13º C), however, enabling disease to develop in
autumn and winter. Conidia are produced at night and
Symptoms and diagnostic features released early in the day as the humidity decreases.
The first symptoms are small, water-soaked leaf spots, More than 8 hours of leaf wetness at 15–25 ºC are
which gradually enlarge, turn yellow, and develop a required for infection. When dew duration lasts for 16
pale tan center. Older lesions turn brown or purple, are hours or more, A. porri conidia infect leaves and result
oblong in shape, and may be several centimeters long in typical lesions; if there is less than 12 hours of dew,
(4, 5, 6). Under humid conditions dark fungal sporula- infections result only in small leaf flecks. The older
tion occurs in the center of the lesion. Large lesions are leaves are more susceptible to infection than the young
produced on flower stalks and these can be dark purple. leaves, although damage by thrips may increase the sus-
When numerous lesions occur on leaves, dieback of the ceptibility of young leaves. As symptoms appear in 1–4
foliage can take place. Microscopic examination is days and new spores are produced after only 5 days,
required to confirm diagnosis of purple blotch, as epidemics develop quickly under favorable conditions.
symptoms may be confused with those of Clado-
sporium leaf blotch, white tip, and other leaf diseases.
Causal agents
4
Purple blotch is caused by two pathogens in the fungi
imperfecti group. Purple blotch lesions can be caused by
either fungus alone or by both fungi together. Alternaria
porri forms conidia that are brown to gold-brown, with
the main spore body being ellipsoidal with 8–12 trans-
verse septa and usually a few longitudinal septa.
Conidia have a long, tapering beak and are borne
singly. Overall conidial dimensions are 100–300 x
15–20 μm.
The other purple blotch pathogen is Stemphylium
vesicarium. This fungus produces olive-brown to gold-
brown, oblong to oval conidia that have up to four
longitudinal septa and varying numbers of transverse
septa. Conidia measure 25–48 x 12–22 μm and have a
length-to-width ratio of 1.5–3.0. Conidia are borne
singly on conidiophores that have a distinctly swollen
F UNGAL D ISEASES
tip. In some regions the pseudothecia and ascospores of

the sexual stage, Pleospora allii, can be found associated
with crop debris.
4 Leaf spots of purple blotch, caused by Alternaria

porri, on leek.
A LLIACEAE 57
Control
Plant resistant or tolerant varieties. For example, avoid Everts, K. L. and Lacy, M. L. 1996. Factors influencing infection
of onion leaves by Alternaria porri and subsequent lesion
using sweet Spanish onions because these are reportedly expansion. Plant Disease 80:276–280.
very sensitive to A. porri. Plow under crop residues after Gladders, P. 1980. New or unusual records of plant diseases and
harvest to reduce spread and survival of inoculum. pests – Purple blotch of leeks caused by Alternaria porri. Plant
Pathology 30:61.
Rotate crops with non-hosts. Select sites and practice
Gupta, R. B. L. and Pathak, V. 1988. Yield losses in onions due to
irrigation so that foliage drying is enhanced. Apply purple blotch disease caused by Alternaria porri.
fungicides, especially as the crop canopy ages and Phytophylactica 20:21–23.
becomes more dense and if leaf-wetness periods favor Koike, S. T. and Henderson, D. M. 1998. Purple blotch, caused
by Alternaria porri, on leek transplants in California. Plant
infection.
Disease 82:710.
Meredith, D. S. 1966. Spore dispersal in Alternaria porri (Ellis)
References Neerg. on onions in Nebraska. Annals of Applied Biology
Basallotte-Ureba, M. J., Prados-Ligero, A. M., and Melero-Vara, 57:67–73.
J. M. 1999. Aetiology of leaf spot of garlic and onion caused Prados-Ligero, A. M., Melero-Vara, J. M., Corpas-Hervías, C.,
by Stemphylium vesicarium in Spain. Plant Pathology and Basallotte-Ureba, M. J. 2003. Relationships between
48:139–145. weather variables, airborne spore concentrations and severity
Bisht, I. and Agrawal, R. C. 1993. Susceptibility to purple leaf of leaf blight of garlic caused by Stemphylium vesicarium in
blotch (Alternaria porri) in garlic (Allium sativum). Annals of Spain. European Journal of Plant Pathology 109:301–310.
Applied Biology 122:31–38. Suheri, H. and Price, T. V. 2000. Infection of onion leaves by
Boiteux, L. S., Lima, M. F., de Menezes Sobrinho, J. A., and Alternaria porri and Stemphylium vesicarium and disease
Lopes, C. A. 1994. A garlic (Allium sativum) leaf blight development in controlled environments. Plant Pathology
caused by Stemphylium vesicarium in Brazil. Plant Pathology 49:375–382.
43:412–414. Suheri, H. and Price, T. V. 2001. The epidemiology of purple leaf
Everts, K. L. and Lacy, M. L. 1990. The influence of dew blotch on leeks in Victoria, Australia. European Journal of
duration, relative humidity, and leaf senescence on conidial Plant Pathology 107:503–510.
formation and infection of onion by Alternaria porri.
Phytopathology 80:1203–1207.
5 6
F UNGAL D ISEASES
5 Leaf spots of purple blotch, caused by Stemphylium 6 Close-up of leaf spots of purple blotch, caused by
vesicarium, on leek. Stemphylium vesicarium, on leek.
Aspergillus niger Disease cycle

BLACK MOLD The pathogen is seedborne in onion. In addition, the
fungus occurs widely in field soils and is a saprophyte
Introduction and significance that colonizes dead plant foliage. Aspergillus niger first
This disease is most prevalent in subtropical and grows on senescing onion leaves, then progresses to the
tropical production areas where high temperatures neck of the bulb and finally into the bulb itself. Bulb
favor its development. While black mold can cause infection in the field is usually associated with damage
some problems in the field, most losses occur in storage. to the fleshy scales, such as when growth splits occur.
Black mold concerns in temperate areas, such as the UK During harvesting operations, spores on infected foliage
in the 1980s, have been associated with poor storage are dispersed and provide another source of the
conditions and elevated storage temperatures. pathogen within the crop and to nearby fields.
Optimum temperatures for growth are 28–34º C and
Symptoms and diagnostic features minimum temperatures for spore germination are
This disease causes unsightly, black, dusty fungal 17º C. Humidity greater than 80% is required for spore
growth on and between the bulb scales (7, 8). The entire germination. The presence of free water for 6–12 hours
surface of the bulb may be turned black in severe cases, on the onion surface is required for infection.
and a bulb rot may follow. Secondary bacterial
organisms usually contribute to the soft rot symptoms. Control
Use seed that does not have significant levels of the
Causal agent pathogen. If clean seed is not available, broad-spectrum
Black mold is caused by the fungus Aspergillus niger. treatments such as thiram have shown good efficacy as
The pathogen is dark brown to black in culture. The seed treatments. Foliar fungicides can reduce black
fungus produces a readily recognized conidiophore that mold when applied towards the end of the crop.
consists of an erect unbranched stalk, a single swollen Harvest the crop under dry conditions and minimize
spherical vesicle, prophialides and phialides that line the damage to the neck tissue of the bulbs. Maintain tem-
surface of the vesicle, and densely packed chains of perature and relative humidity at appropriate levels
spherical black, spiny conidia (2–5 μm in diameter). during storage. Monitor storage conditions when using
Conidia are dry and readily dispersed in the air. high temperatures to dry out the onions after harvest;
7 8
F UNGAL D ISEASES
7 Sporulation of Aspergillus niger on garlic bulb. 8 Severe symptoms caused by Aspergillus niger on a
bulb onion.
A LLIACEAE 59
temperatures should not exceed 30–32º C and the Botryotinia squamosa

relative humidity should be kept below 80% as long as (anamorph = Botrytis squamosa)
possible. Long-term storage at low temperatures stops BOTRYTIS LEAF BLIGHT,
growth of A. niger, but the fungus becomes active at BOTRYTIS BLAST
temperatures above 15º C.
Introduction and significance
References This common foliar disease is an important cause of
Hayden, N. J. and Maude, R. B. 1992. The role of seed-borne quality loss in green onion, where the condition of the
Aspergillus niger in transmission of black mould of onion. foliage is important for market. It can cause serious loss
Plant Pathology 41:573–581.
of foliage in bulb onion, which can impact on yields.
Hayden, N. J., Maude, R. B., and Proctor, F. J. 1994. Studies on
the biology of black mould (Aspergillus niger) on temperate
and tropical onions. 1. A comparison of sources of the disease Symptoms and diagnostic features
in temperate and tropical field crops. Plant Pathology
43:562–569.
The first symptoms are leaf spots that are small, white,
Hayden, N. J., Maude, R. B., El Hassan, H. S., and Al Magid, A. and have pale green halos. Spots are usually elliptical in
A. 1994. Studies on the biology of black mould (Aspergillus shape and can increase to 5–10 mm in diameter (9, 10).
niger) on temperate and tropical onions. 2. The effect of Multiple spots coalesce and result in bleached foliage
treatments on the control of seedborne A. niger. Plant
Pathology 43:570–578. and general collapse and death of leaves (11).
10
10 White spots with halos on salad onions, caused by

caused by Botrytis squamosa.
9 11
F UNGIAL D ISEASES
9 Leaf symptoms
of Botrytis leaf
blight on bulb 11 Severe leaf dieback of onion caused by Botrytis
onions. squamosa.
12
conidia (14–24 x 9–18 μm) than the other common
Botrytis pathogens on onion; B. cinerea (12) has
conidia measuring mostly 9–14 x 7–10 μm, and B. allii
conidia are 7–11 x 5–6 μm. Botyrtis squamosa is
difficult to isolate from young lesions, so examine
senescent leaves and older lesions for B. squamosa
spores. This pathogen produces black sclerotia,
measuring 3–10 mm, on leaf and bulb tissues. Botrytis
squamosa appears to be host specific to Allium species.
In some cases the fungus produces a perfect stage,
Botryotinia squamosa. It is not clear what role this
teleomorph has in disease development.
Disease cycle
Initial inocula are airborne spores that originate from
nearby crops, debris of previously infected crops, and
sclerotia in the soil. Inoculum production within the
crop usually increases after the oldest leaves have
declined. At least 6 hours of leaf wetness is required for
infection by conidia, and the number of lesions that
develop increases as leaf wetness duration is prolonged.
Optimum conditions for development are temperatures
of 12–24º C. Disease development is favored by high
crop density; hence spring onion plantings are more
prone to problems than the wider spaced bulb onion.
Control
Do not plant successive crops, especially of spring
onion, where Botrytis leaf blight occurs regularly. Early
12 Onion seed stalk infected with gray mold season onion crops should not be placed close to over-
(B. cinerea). wintered onion. Use cultivars that are less susceptible.
Because this pathogen is most severe on A. cepa
varieties, if possible plant other types of allium crops.
For example, chives are reported to be immune.
Increase row spacing to improve airflow through the
crop. Avoid excessive nitrogen fertilizations, as this
causes thick leaf canopies and increased susceptibility.
Leaf dieback can be found 5 to 12 days after the first Irrigate early in the day so that leaves dry quickly. If
spotting symptoms. Older leaves are more susceptible available, use forecasting systems to identify periods of
than younger foliage. The white spot symptoms may be disease risk and hence guide timing of fungicides.
confused with hail damage or physical abrasion from BOTCAST, the first prediction system for Botrytis leaf
wind-blown soil. However, these abiotic problems are blight, was developed in North America and has been
F UNGAL D ISEASES
usually confined to the exposed side of the leaf, are modified to suit conditions in various other countries.
more irregular in shape, and lack the diagnostic halo. Multiple fungicide applications may be required for
spring onion, while bulb onion may not need any
Causal agent treatment because of low susceptibility. Incorporate
Botrytis leaf blight or Botrytis blast disease is caused by crop residues after harvest so that inoculum levels are
Botrytis squamosa. Botrytis squamosa has larger reduced.
A LLIACEAE 61
References Botrytis allii (= B. aclada)

Clarkson, J. P., Kennedy, R., and Phelps, K. 2000. The effect of NECK ROT
temperature and water potential on the production of conidia
by sclerotia of Botrytis squamosa. Plant Pathology
49:119–128. Introduction and significance
De Visser, C. L. M. 1996. Field evaluation of a supervised control Neck rot is mainly a storage disease of allium crops.
system for Botrytis leaf blight in spring sown onions in the The disease caused significant losses for the UK bulb
Netherlands. European Journal of Plant Pathology
102:795–805.
onion industry for many years until improvements in
Ellerbrock, L. A. and Lorbeer, J. W. 1977. Survival of sclerotia harvesting and storage techniques were developed.
and conidia of Botrytis squamosa. Phytopathology Producers who lack modern drying facilities still incur
67:219–225. significant losses. Neck rot affects garlic, shallot, multi-
Ellerbrock, L. A. and Lorbeer, J. W. 1977. Sources of primary
inoculum of Botrytis squamosa. Phytopathology
plier onion, and leek, but it is most important on bulb
67:363–372. onion where losses can sometimes be greater than 50%.
Lorbeer, J. W. and Vincelli, P. C. 1990. Efficacy of dicarboximide
fungicides and fungicide combinations for control of Botrytis Symptoms and diagnostic features
leaf blight of onion in New York. Plant Disease 74:235–237.
Sutton, J. C., James, T. D. W., and Rowell, P. M. 1986.
Typical symptoms are a water-soaked or light brown
BOTCAST: a forecasting system to time the initial fungicide decay at the neck of stored bulb onion. Dense gray
spray for managing Botrytis leaf blight of onions. Agriculture mycelium is produced around the neck and between the
Ecosystems and Environment 18:123–143.
bulb scales. Numerous black sclerotia, measuring
Walters, T. W., Ellerbrock, L. A., van der Heide, J. J., Lorbeer, J.
J., and LoParco, D. P. 1996. Field and greenhouse procedures approximately 5 mm in diameter, also develop on the
to evaluate onions for Botrytis leaf blight resistance. shoulders of the bulb (13, 14). This fungal growth only
HortScience 31:436–438. becomes apparent after several weeks in storage. The
pathogen continues to spread from the neck into the
bulb and eventually most of the bulb becomes soft and
rotted. A brown rot may occur on the fleshy scales of
maturing bulb onion in the field, and this is usually
associated with splitting or damage of the bulb. The
pathogen can affect any part of the bulb and is not
limited to the bulb necks. It is possible to find B. allii
sporulating on senescent foliage prior to crop harvest.
13 14
F UNGAL D ISEASES
13 Neck rot on bulb onion showing black sclerotia and 14 Onion bulb with neck rot showing sclerotia and gray
dense gray sporulation. sporulation.
Causal agent Control

Neck rot is caused by Botrytis allii, which is synony- Use seed that does not have significant levels of the
mous with Botrytis aclada. This fungus produces pathogen. Use disease-free sets that are grown from
conidia that measure 7–11 x 5–6 μm; these spores are such seed. A 1% seed infection is regarded as an
smaller than those produced by most other Botrytis economic threshold. Treatment for seedborne B. allii
species found on alliums. The conidia of B. allii are has been very effective. Use heat treatments to control
readily produced in culture. In contrast, the Botrytis leaf the pathogen in sets. Plant resistant types or cultivars of
blight pathogen B. squamosa does not readily sporulate alliums. When topping onions at harvest, leave a rela-
in culture and has significantly larger conidia (14–24 x tively long neck (10 cm) that can be thoroughly dried
9–18 μm). Another Botrytis pathogen, B. porri, is before the fungus spreads down the neck and into the
important on garlic and leek. Botrytis byssoidea is bulb. Bulb necks can be dried by using forced air drying
another species that causes a neck rot disease on onion. or by harvesting and field drying the onions under
This pathogen is distinct from B. allii, and causes a warm, dry conditions. After drying, maintain stored
disease known as gray mold neck rot. commodities below 75% relative humidity and at 0–1º
C. Fungicides applied during the growing season may
Disease cycle provide some suppression of neck rot. Rotate with non-
The pathogen is transmitted on seed and sets of onion hosts so that soilborne sclerotia of B. allii are reduced in
and shallot. If seed is stored at sufficiently low temper- number.
atures, the fungus may survive on seed for more than
three years. The pathogen spreads from the seed coat to References
seedling leaves while the seed coat remains attached to Bertolini, P. and Tian, S. P. 1997. Effect of temperature of
the cotyledon. B. allii infects these leaves and then production of Botrytis allii conidia on their pathogenicity to
harvested white onion bulbs. Plant Pathology 46:432–438.
sporulates when tissue senesces. During the growing
Gladders, P., Carter, M. A., and Owen, W. F. 1994. Resistance to
season, symptoms may be limited on foliage. However, benomyl in Botrytis allii from shallots. Plant Pathology
just prior to harvest the bulb onion foliage is topped or 43:410–411.
bent, creating wounds that are open to inoculum. While Maude, R. B. 1983. The correlation between seed-borne
infection by Botrytis allii and neck rot development in store.
the neck tissue retains moisture, the pathogen grows Seed Science and Technology 11:829–834.
down to the bulb where it causes scale rot. Soilborne Maude, R. B. and Presly, A. H. 1977. Neck rot (Botrytis allii) of
sclerotia are another source of inoculum as these bulb onions. I. Seed-borne infection and its relationship to the
disease in the onion crop. Annals of Applied Biology
germinate to produce conidia. Sclerotia can survive for 86:163–180.
two years in buried debris. Maude, R. B. and Presly, A. H. 1977. Neck rot (Botrytis allii) of
bulb onions. II. Seed-borne infection and its relationship to
the disease in store and the effect of seed treatment. Annals of
Applied Biology 86:181–188.
Maude, R. B., Shipway, M. R., Presly, A. H., and O’Connor, D.
1984. The effects of direct harvesting and drying systems on
the incidence and control of neck rot (Botrytis allii) in onions.
Netzer, D. and Dishon, I. 1967. Selective media to distinguish
between two Botrytis species on onion. Phytopathology
57:795–796.
Nielsen, K., Justensen, A. F., Jensen, D. F., and Yohalem, D. S.
2001. Universally primed polymerase chain reaction alleles
and internal transcribed spacer restriction fragment length
polymorphisms distinguish two serotypes in Botrytis aclada
F UNGAL D ISEASES
distinct from Botrytis byssoidea. Phytopathology

91:527–533.
Yohalem, D. S., Nielsen, K., and Nicolaisen, M. 2003.
Taxonomic and nomenclatural clarification on the onion
neck rotting Botrytis species. Mycotaxon 85:175–182.
A LLIACEAE 63
Fusarium culmorum, F. oxysporum f. sp. cepae, notched. Conidiophores are monophialides. Micro-
F. proliferatum conidia are absent and chlamydospores are present in
FUSARIUM BASAL PLATE ROT culture. Colonies on potato dextrose agar produce
abundant, dense, white aerial mycelia, and the under-
Introduction and significance surfaces of these cultures are distinctly carmine red.
This disease is important worldwide in bulb onion, Fusarium proliferatum produces mostly micro-
chives, garlic, and shallot. It is becoming increasingly conidia in culture. These are one- or two-celled, borne
important in the UK and on leek in the USA. in long chains from polyphialides, and have slightly
flattened bases because of their formation in the chains.
Symptoms and diagnostic features Chlamydospores are not formed. Semi-selective media
Foliar symptoms develop at any stage during the like Komada’s medium can help isolate all Fusarium
growing season and include a general yellowing, pathogens if secondary rot organisms are present.
necrosis of the leaves from the leaf tip downward, and
wilting. There may be a tan to pink root rot on onion
and red purple discoloration of the stems and bulbs of
garlic. For all affected Allium species there is a rot of the 15
basal plate tissue where roots are attached to the crown
(15). Such a rot is initially water-soaked, light tan to
darker brown, with tissues remaining firm. With
further development, the basal infection turns into a
soft rot, extends up into the fleshy scales, and causes the
plant to collapse. Under humid conditions, a fluffy,
white mycelium is produced on the affected tissues.
Bulbs showing no obvious symptoms may still rot in
storage. On leek, affected roots are initially gray and
water-soaked in appearance and later become pink,
soft, and rotted. In addition to the basal plate discol-
oration, leek can develop a tan to pink lesion on outer
leaf sheaths in contact with soil (16). 15 Discolored basal plate of leek infected with Fusarium
culmorum.
Causal agents
Fusarium basal plate rot is caused by several species of 16 Stem lesion of
16
the fungus Fusarium. Fusarium oxysporum f.sp. cepae leek infected with
causes basal plate rot on onion and F. culmorum is the Fusarium
causal agent of the same disease on garlic and leek. culmorum.
Fusarium proliferatum is reported to affect the bulbs of
onion and garlic. Fusarium oxysporum f. sp. cepae has
morphology and colony characteristics that are similar
to other F. oxysporum fungi. The fungus forms one- or
two-celled, oval to kidney shaped microconidia on
monophialides, and four- to six-celled, fusiform, curved
macroconidia. Macroconidia are usually produced
F UNGAL D ISEASES
in cushion-shaped structures called sporodochia.

Chlamydospores are formed in culture. This pathogen
is apparently host specific to Allium species.
Fusarium culmorum produces abundant macro-
conidia that are stout, thick walled, and have prominent
septa. Macroconidia foot cells are indistinctly to slightly
Disease cycle Mycosphaerella allii (anamorph = Cladosporium allii),

M. allii-cepae (anamorph = C. allii-cepae)
Fusarium basal plate rot is a soilborne disease; the
pathogens persist in soil by means of chlamydospores. CLADOSPORIUM LEAF BLOTCH
Pathogens may be carried on onion sets and garlic
cloves. Seedborne inoculum may also exist: in Cali- Introduction and significance
fornia, leek transplants in a soilless medium in trays can Cladosporium leaf blotch is a common, but generally
develop extensive basal plate rot – circumstantial minor, foliar disease of onion and leek. This disease
evidence of seedborne pathogen introduction. The emerged as a serious problem of onion in Ireland and
optimum temperature for disease development is southern England in the late 1970s and early 1980s
25–28º C and few problems occur when soil tempera- when it caused significant loss of yield, but has been of
tures are less than 15º C. These Fusarium species invade limited importance since then. Onion and leek are
the roots and spread to the basal plate, but can also infected by different Cladosporium species.
infect the bulb directly. Damage from insect feeding can
increase problems. Likewise, Fusarium infection can Symptoms and diagnostic features
attract pests and allow for extensive secondary decay The symptoms on onion foliage are conspicuous, large
from soil microorganisms. Wet weather close to harvest white spots or blotches that measure as large as 1.5 x
favors disease development, particularly in garlic. 0.5 cm. These spots can resemble burn from herbicides
or nitrogen fertilizers. These lesions take on a brown or
Control dark brown color as the fungus sporulates on the
Use resistant cultivars, as this is the most important affected tissue. The foliage collapses as lesions merge
component in the control strategy. Rotate crops to non- (17); foliage collapse is especially rapid when crops start
hosts for at least 4 years to help reduce soilborne to senesce. On leek, leaf lesions are large (up to 2.5 x
inoculum and lessen potential disease pressure. It would 1.5 cm), elliptical white blotches that turn brown as the
be desirable to use seed that is tested and found to not fungus sporulates (18) . For both leek and onion, lesions
have detectable levels of the pathogen; however, seed are difficult to distinguish from white tip and purple
assays for these pathogens are not yet fully developed. blotch, which can all occur on the same plant.
Plant only transplants which appear to be disease free.
The storage of bulbs at temperatures below 4º C will Causal agents
reduce further development in storage. In some regions The cause of Cladosporium leaf blotch of onion is
fungicides have been successfully used on seed or sets Cladosporium allii-cepae. Conidia are echinulate,
and as a dip treatment on seedlings. usually one septate, cylindrical with rounded ends,
slightly constricted in the middle, and measure 65–95 x
13–17 μm. The perfect stage, Mycosphaerella allii-
References cepae, has been produced in culture. This pathogen
Abawi, G. S. and Lorbeer, J. W. 1972. Several aspects of the was formerly known as Heterosporium allii-cepae.
ecology and pathology of Fusarium oxysporum f. sp. cepae. Cladosporium allii-cepae also infects chives, shallot,
garlic, and the weed crow garlic (A. vineale).
Armengol, J., Vicent, A., Sales, R., Garcia-Jimenez, J., and
Rodriguez, J. M. 2001. First report of basal rot of leek caused The cause of Cladosporium leaf blotch of leek is
by Fusarium culmorum in Spain. Plant Disease 85:679. Cladosporium allii. Conidia are echinulate, usually one
Dugan, F. M., Hellier, B. C., and Lupien, S. L. 2003. New Disease to two septate, cylindrical with rounded ends, slightly
report. First report of Fusarium proliferatum causing rot of
garlic bulbs in North America. Plant Pathology 52:426. constricted in the middle, and measure 28–42 x
Everts, K. L., Schwartz, H. F., Epsky, N. D., and Capinera, J. L. 12–16 μm. The perfect stage is Mycosphaerella allii.
F UNGAL D ISEASES
1985. Effects of maggots and wounding on occurrence of Pseudothecia and bicellular ascospores (measuring
Fusarium basal rot of onions in Colorado. Plant Disease
69:878–882.
25–40 x 10–20 μm) are produced on host tissue. This
Koike, S. T., Gordon, T. R., and Aegerter, B. J. 2003. Root and pathogen was formerly known as Heterosporium allii.
basal rot of leek caused by Fusarium culmorum in California. It primarily infects leek.
Plant Disease 87:601.
Tamietti, G. and Garibaldi, A. 1977. Observations on basal rot
of leek caused by Fusarium culmorum. Rivista di Patologia
Vegetale 13:69–75.
A LLIACEAE 65
Disease cycle 18
Inoculum is mostly found on infested crop residues,
though spores can move from overwintered to spring
planted crops when they are in close proximity. For
both species, optimum temperatures for spore germi-
nation and infection are 15–20º C, and germination
requires 18 to 20 hours of 100% relative humidity.
Germination can be slightly inhibited if free water is
present. Leaf symptoms can be detected after two days
under optimum conditions. Infection occurs more
readily on damaged or senescing leaves. Interestingly,
the production of conidia is sensitive to light and even
moonlight can inhibit spore production. A minimum of
8 hours darkness, greater than 95% relative humidity,
and temperatures of 9–12º C must occur for large
numbers of conidia to develop. The conidia are released
in the day, mostly during late morning to early
afternoon. In England, most spore production, and
hence most disease development, happens during
October to April when relative humidity tends to be
high. There are indications that these pathogens may be
seedborne, though this aspect requires further investi-
gation.
Control
Incorporate infected crop residues promptly after
harvest, as survival in buried debris may be as short as
2 months. Rotate crops to non-hosts. Apply fungicides
when necessary. 18 Dieback symptoms caused by Cladosporium allii
on leek.
17
References
Jordan, M. M., Burchill, R. T., and Maude, R. B. 1990.
Epidemiology of Cladosporium allii and Cladosporium allii-
cepae, leaf blotch pathogens of leek and onion. I. Production
and release of conidia. Annals of Applied Biology
117:299–312.
Jordan, M. M., Burchill, R. T., and Maude, R. B. 1990.
Epidemiology of Cladosporium allii and Cladosporium allii-
cepae, leaf blotch pathogens of leek and onion. II. Infection of
host plants. Annals of Applied Biology 117:313–336.
Jordan, M. M., Maude, R. B., and Burchill, R. T. 1990. Sources,
survival and transmission of Cladosporium allii and C. allii-
cepae, leaf blotch pathogens of leek and onion. Plant
F UNGAL D ISEASES
Pathology 39:237–242.
Kirk, P. M. and Crompton, J. G. 1984. Pathology and taxonomy
of Cladosporium leaf blotch of onion (Allium cepa) and leek
(Allium porrum). Plant Pathology 33:317–324.
Ryan, E. W. 1978. Leaf spot of onions caused by Cladosporium
17 General dieback from Cladosporium allii-cepae on allii-cepae. Plant Pathology 27:200.
bulb onions.
Penicillium hirsutum
19
PENICILLIUM MOLD,
BLUE MOLD

This is mainly a storage disease, but field symptoms can
occur on maturing bulbs. Blue mold can be an
important problem on garlic.
Symptoms and diagnostic features

On garlic, Penicillium mold can cause the death of
planted cloves prior to emergence. Infected cloves first
show a water-soaked, irregularly shaped lesion that
later becomes tan to light brown. The fungus can 19 Penicillium blue mold under the outer papery scale
produce a blue-green, clustered mycelial growth in the of bulb onion.
lesions. In advanced stages the cloves are extensively
rotted, and the blue-green sporulation is widespread on
the affected tissues and around the base of young garlic 20
plants. Sporulating Penicillium can be present between

the scales of onion extending from the neck into the
shoulder of the bulb (19, 20, 21) where it can cause a
rot. If the pathogen infects commodities near harvest,
the presence of sporulating blue-green mold is unsightly
and can lead to crop rejection.
Causal agent
Penicillium mold is caused by Penicillium hirsutum, pre-
viously known as P. corymbiferum. Several other
Penicillium species are regularly found on allium bulbs.
On diseased tissue and in culture, P. hirsutum produces 20 Penicillium blue mold on onion plant developing
conidiophores that are shaped like a brush (penicillus) shortly after planting.
and bear long chains of dry, windborne conidia.
Conidiophores are conspicuously roughened, form
from surface hyphae or in fascicles, and have complex 21
branching patterns (terverticillate or quaterverticilliate).
In culture the colonies appear gray-green to dull green.
Disease cycle
For garlic, the fungus is carried on the cloves that are
planted in the field. In addition, inoculum can be
present on crop residue in the field; infection of bulbs
takes place if there has been damage or growth splitting.
F UNGAL D ISEASES
The pathogen is spread during harvesting, particularly

if there is damage to onion bulbs or garlic cloves. High
temperatures and dry soil conditions favor disease
development. The optimum conditions for pathogen
development are temperatures of 21–25º C and high
relative humidity. 21 Penicillium blue mold on onion sets.
A LLIACEAE 67
Control 22
Carefully handle bulbs and cloves during harvest to
minimize damage. Avoid high humidity levels in
storage. During storage or shipment, a combination of
low temperatures (less than 5º C) and low relative
humidity are required to restrict disease development.
References
Brammall, R. A. 1989. Resistance to benomyl in isolates of
Penicillium sp. causing clove decay of garlic. Canadian
Journal of Plant Pathology 11:409–414.
Peronospora destructor 22 Onion leaves

DOWNY MILDEW infected with
downy mildew.
Downy mildew is a destructive disease of onion and 23
reduces yield and quality of foliage and bulbs. Severe
attacks occur sporadically because long periods of cool,
wet weather are required for epidemics to develop.
Problems with downy mildew have increased in recent
years in the UK, notably since the increase in produc-
tion of overwintered bulb onions. It is a difficult disease
to control with fungicides, and improved disease
management strategies are a priority for research.
Symptoms and diagnostic features.

Early symptoms of downy mildew are bleaching of leaf 23 Sporulation of
tips and small, irregularly shaped, chlorotic blotches on downy mildew of
leaves. As disease develops, chlorotic blotches enlarge onion.
and coalesce into extensive lesions that can reach up to
10–15 cm long. These diseased areas then turn brown 24
as they age (22). Characteristic purple, fuzzy sporula-
tion grows on the affected lesions (23) and such growth
often has concentric zones. Lesions can girdle the leaf,
causing them to bend over and collapse (24). Lesions
also occur on the flowering stalks, which likewise can
become girdled and collapse. In major epidemics the
entire crop can be defoliated in only four disease cycles.
If downy mildew is severe during bulb formation, final
bulb yields can be significantly reduced. Lesions can be
F UNGAL D ISEASES
colonized by Stemphylium fungi that produce conspic-

uous dark brown to black sporulation and sometimes
purple pigmentation inside the downy mildew lesion.
Plants may be systemically infected by downy mildew 24 Bulb onions
and affected bulbs become soft and discolored in showing severe
storage; some sprout prematurely. downy mildew.
Causal agent the systemic product mefenoxam is often used in com-

Downy mildew is caused by the oomycete Peronospora bination with the protectants. Disease forecasting or
destructor. This obligate pathogen produces thin walled decision support systems such as DOWNCAST and
sporangia that measure 40–72 x 18–29 μm. Sporangio- ZWIPERO are undergoing field evaluation.
phores emerge through stomata over a temperature
range of 4–25º C. Globose oospores, measuring 30–44
μm in diameter, occur in onion bulbs, crop residues, and References
volunteer plants. Peronospora destructor is restricted to Develash, R. K. and Sughai, S. K. 1997. Management of downy
allium hosts and affects many wild and cultivated mildew (Peronospora destructor) of onion (Allium cepa).
Crop Protection 16:63–67.
alliums, including onion, garlic, leek, chives, and
De Visser, C. L. M. 1998. Development of a downy mildew
shallot. Allium cepa, however, is the most seriously advisory model based on Downcast. European Journal of
affected host. Plant Pathology 104:993–943.
Friedrich, S., Leinhos, G. M. E., and Löpmeier, F.-J. 2003.
Development of ZWIPERO, a model forecasting sporulation
Disease cycle and infection periods of onion downy mildew based on
Infection requires cool temperatures (less than 22º C) meteorological data. European Journal of Plant Pathology
and the presence of free moisture on the leaf for at least 109:35–45.
Gilles, T., Phelps, K., Clarkson, J. P., and Kennedy, R. 2004.
3 hours. The optimum temperature for germination of Development of MILIONCAST, an improved model for
sporangia is 10–12º C. Germ tubes form in 2 to 4 hours, predicting downy mildew sporulation on onions. Plant
produce an appressorium, and penetrate the leaf Disease 88:695–702.
through stomata. Spores are produced at night and Jesperson, G. D. and Sutton, J. C. 1987. Evaluation of a
forecaster for downy mildew of onion (Allium cepa L.). Crop
released by wind currents during the day, surviving on Protection 6:95–103.
leaf surfaces for up to 3 days. Periods of dry weather Wright, P. J., Chynoweth, R. W., Beresford, R. M., and Henshall.
will halt disease development. The pathogen overwin- W. R. 2002. Comparison of strategies for timing protective
and curative fungicides for control of onion downy mildew
ters via oospores and mycelium inside bulbs; oospores (Peronspora destructor) in New Zealand. Proceedings of the
are also able to survive in soil. Colder winters appear to BCPC Conference – Pests & Diseases 2002 1:207–212.
reduce the severity of downy mildew epidemics in the
following season, presumably by reducing survival of
the pathogen. The pathogen can be seedborne, though
this factor is not considered important.
Control
Plant onion sets and transplants that are disease free.
Heat treatment of sets may reduce viability of the
pathogen inside infected sets. Some differences exist in
cultivar susceptibility, so plant cultivars and Allium
species that are less susceptible. Rotating onion crops 3
to 4 years may be helpful in reducing soil inoculum,
though this strategy does not eliminate airborne
sporangia. Incorporate crop residues soon after harvest.
Control volunteer plants. Select fields that receive good
air movement; sheltered locations should be avoided
because these create conditions conducive to downy
F UNGAL D ISEASES
mildew development. Crop rows that are orientated

parallel with the prevailing winds will also enhance
drying of the crop environment. Apply fungicides at an
early stage and prior to significant disease development.
Protectants such as dithiocarbamates and copper have
no curative activity to check established lesions, hence
A LLIACEAE 69
Phoma terrestris
25
PINK ROOT

Pink root is a severe disease in tropical and sub-tropical
regions. This pathogen affects many crops, including
eggplant, pepper, tomato, legumes, spinach, carrot,
crucifers, and cucurbits. Even grain crops, such as
maize, millet, and sorghum, are susceptible.
Symptoms and diagnostic features 25 Diseased onion

Infected roots are pink in color; as disease develops, the roots infected with
pink coloration becomes more intense and can even pink root.
turn dark purple (25). Roots are water-soaked and
rotted. If allowed to dry out, such roots are fragile and Causal agent
papery in texture. New roots are affected as they Pink root is caused by Phoma terrestris. This soilborne
emerge. Plants appear stunted and foliage may show fungus produces globose, dark brown to black pycnidia
symptoms of nutrient deficiencies and stress (26). on infected roots or fleshy tissue. Setae grow on these
Severely affected seedlings may die. The outer bulb pycnidia, especially around the ostiole, and measure
scales may become infected and develop pink or red 8–120 μm long. Conidia are ovoid, single-celled,
blemishes or water-soaked rots within 1 to 3 weeks of hyaline, biguttulate, and measure 3.7–5.8 x 1.8–2.4
planting. Symptoms may resemble those of Fusarium μm. The fungus produces chlamydospores. In older lit-
basal plate rot. erature the pathogen is called Pyrenochaeta terrestris.
26
F UNGAL D ISEASES
26 Onion plants infected with pink root.

Disease cycle Phytophthora porri

Pink root is a soilborne disease that is enhanced by WHITE TIP
warm soil temperatures (24–28º C). There is little
infection when soil temperatures are below 16º C. The Introduction and significance
pathogen survives in crop residues or as chlamydo- White tip is one of the most important foliar diseases on
spores in soil for only a few years. Invasion of the root leek in western Europe. It has become more important
occurs just behind the root tip, then spreads upward in the UK with increasing leek production and loss of
into the main body of the root. effective fungicides. The disease has been mainly
reported from Europe, Canada, and Japan. Phyto-
Control phthora porri affects various alliums, including bulb
Rotate onion with non-host crops to reduce soil popu- and green onion, and garlic. In Japan, losses of 70% or
lations of the pathogen. An optimum crop rotation more can occur in onion crops.
scheme allows at least 3 years between susceptible
crops. Use resistant cultivars if such are available. Symptoms and diagnostic features
Because of cooler soil temperatures present during Early symptoms on leek leaves consist of irregularly
autumn, plant at this time of year to reduce disease shaped, water-soaked lesions. Lesions enlarge to several
severity. Fumigation of soil may be justified on badly
infested fields. Soil solarization can be effective in some
regions, especially if combined with soil fumigation.
Fungicide-treated seed and soil fungicide applications 27
are not effective. There is some evidence that reducing
the interval between irrigation applications has lessened
the impact of pink root on yield.
References
Gorenz, A. M., Walker, J. C., and Larson, R. H. 1948.
Morphology and taxonomy of the onion pink-root fungus.
Levy, D. and Gornik, A. 1981. Tolerance of onions to the pink
root disease caused by Pyrenochaeta terrestris.
Phytoparasitica 9:51–57.
Porter, I. J., Merriman, P. R., and Keane, P. J. 1989. Integrated
control of pink root (Pyrenochaeta terrestris) of onions by
dazomet and soil solarization. Australian Journal of
Agricultural Research 40:861–869.
F UNGAL D ISEASES
27 Severe symptoms of white tip on leeks.

A LLIACEAE 71
centimeters long, appear as elliptical blotches, and are Control

usually most prevalent towards the tip of the leaf (27, Rotate onion and leek crops with at least a 3-year break
28). Older lesions develop a bleached white center with with non-host crops. Use fungicides as appropriate, and
a water-soaked margin when the disease is active (29). apply products having different modes of action to dis-
In dry conditions, the water-soaked margin may not be courage development of resistant strains. Avoid
evident. Lesions are readily colonized by secondary planting into wet or poorly draining sites. Prepare soils
fungi and sooty molds, making diagnosis difficult in the so that crops are planted into well-draining beds.
field because of symptom similarities with other foliar
problems such as Cladosporium leaf blotch, purple References
blotch, or frost damage. Badly affected leaves rot and Griffin, M. J. and Jones, O. W. 1977. Phytophthora porri on
plants may be stunted or even killed. The disease autumn-sown salad onions. Plant Pathology 26:149–150.
Man in t’Veld, W. A., de Cock, A. W. A. M., Ilieva, E., and
spreads rapidly in cool, wet weather. On onion and
Lévesque, C. A. 2002. Gene flow analysis of Phytophthora
garlic, this pathogen causes water-soaked leaf blight porri reveals a new species: Phytophthora brassicae sp. nov.
and root rot symptoms. European Journal of Plant Pathology 108:51–62.
Smilde, W. D., van Nees, M., and Frinking, H. D. 1996. Effects of
temperature on Phytophthora porri in vitro, in planta and in
Causal agent soil. European Journal of Plant Pathology 102:687–695.
The cause of white tip is the oomycete organism
Phytophthora porri. The pathogen produces sporangia
that are usually non-papillate and measure 37–75 x
31–48 μm. Sporangia germinate directly to produce a 28
germ tube or release zoospores that measure 10–12 μm.
This pathogen can be observed in the lab by floating
small pieces of infected leaf tissue, taken from the
leading edge of lesions, in water for a few days.
Microscopic examination of the leaf pieces will reveal
the sporangia. Note that sporangia form sparsely or not
at all when cultured on solid agar media. Oospores are
also produced and measure 19–36 μm.
Earlier reports indicated that P. porri caused white tip
of alliums and was also able to infect brassicas.
However, researchers now know that P. porri is host
specific to allium hosts and does not infect brassicas. P.
porri tends to have paragynous (rather than amphigy-
nous) antheridia, produces oogonia more consistently, 28 Close-up of white tip disease of leek.
and has fluffy aerial mycelium on V8 agar. The brassica
pathogen has been given the name P. brassicae, 29
produces large numbers of sporangia on solid agar
medium, has a non-fluffy (appressed) appearance on
agar media, and infects only brassicas.
Disease cycle
The disease is soilborne and infection can occur from
F UNGAL D ISEASES
sporangia or oospores when infested soil is splashed

onto the leaves, or when leaves are in direct contact
with the soil. In the autumn, severe infection of onion
seedlings has occurred when heavy rains flatten the
seedlings onto the ground. Mycelial growth can occur 29 Leek leaf lesions of white tip disease showing water-
between 0–25 ºC, with an optimum of 15–20 ºC. soaked margins.
Puccinia allii
31
RUST

Rust diseases of allium crops occur wherever these
crops are grown and are important production factors
that cause significant crop damage to onion, leek, garlic,
and chives. However, the rust pathogen is comprised of
genetically distinct sub-groups; therefore, rust in one
part of the world may or may not be the same pathogen
as rust elsewhere. For example, rust is the most
important and widespread disease of leek (30) in
western Europe. Leek crops in California, though, are
free from rust concerns while neighboring garlic
plantings have been devastated by rust. Examination of
the California garlic rust isolates demonstrated that 31 Leaf pustules of rust on onion.
these fungi are different morphologically and genetical-
ly from garlic rust isolates in the Middle East region.
Hence Puccinia allii is a complex pathogen.
yield loss accompany severe rust. In garlic, rust causes
Symptoms and diagnostic features severe stunting of plants and bulbs (34). At harvest the
Initial symptoms consist of small, 1–2 mm in diameter, outer garlic bulb sheaths can be split and weak,
leaf flecks and spots that are irregularly shaped and resulting in shattering of the bulb and overall poor
white or light tan in color. These lesions increase to quality. Late in the infection cycle the teliospore phase
3–5 mm spots that develop the typical, bright orange can also be seen in darker brown pustules on diseased
pustules (31, 32) of rust diseases. Pustules erupt through foliage (35).
the leaf surface between the veins, develop on both
upper and lower leaf surfaces, and release copious Causal agent
amounts of dusty orange spores. There may be Rust is caused by the fungus P. allii, which is an autoe-
chlorotic halos around the pustules. Rust usually first cious macrocyclic (full-cycled) rust. However, isolates
occurs on the older foliage and subsequently spreads to with shortened life cycles, which lack pycnia and aecia
newer leaves. Severely infected leaves can be almost stages, are common and referred to as having hemi-
covered with pustules, turn chlorotic, then finally form cycles. The prominent orange pustules are the
become tan, dry, and dead (33). Reduced plant size and uredinia stage that produces roughened, one-celled ure-
diniospores measuring 23–29 x 20–24 μm. The dark
brown, two-celled teliospore is produced later and
30
measures 28–45 x 20–26 μm. In the UK, teliospores are
uncommon on leek but readily occur on chives. In
California, teliospores are very common on garlic and
onion. Pycnia and aecidia stages occur on some hosts
such as chives and A. fistulosum.
Because of variation in rust isolate host ranges and
F UNGAL D ISEASES
morphologies, over the years the allium rust pathogen

has been classified into various genera and species,
including the following: P. allii, P. porri, P. mixta, P.
blasdalei, Uromyces ambiguous, or U. duris. Currently,
it appears justified to group all garlic, chives, and leek
30 Rust uredinia on leek leaf. isolates under P. allii, and to consider P. allii as a species
A LLIACEAE 73
32 34
32 Leaf pustules of garlic rust. 34 Stunted garlic bulbs from severe rust. Healthy bulbs
are on the right.
35 Close-up of 35
33
garlic leaf with
uredinia and telia
of rust.
33 Field symptoms of rust on garlic.
complex. Within this P. allii complex, physiological spe- also be hosts and provide inoculum for commercial
cialization does occur as leek isolates from Europe do crops. Urediniospores are the primary inoculum and
not infect onion or chives, and the California garlic are spread long distances via winds. Optimum condi-
isolates do not infect leek. tions for infection are 15º C and 100% relative
F UNGAL D ISEASES
humidity for 4 hours. The pathogen is active between

Disease cycle temperatures of 10–24º C. Rust infection is favored by
In Europe, overwintered crops are a significant source high nitrogen applications and low potash levels. The
of rust inoculum for spring planted alliums. In the UK, fungus does not survive in the soil. For the devastating
rust is normally active from July onwards and is only garlic rust outbreaks in California in the late 1990s, a
inhibited by cold periods in winter. Weedy alliums can source of primary inoculum was not identified.
Control Sclerotium cepivorum

Crop rotation to nonhosts may help reduce, but not WHITE ROT
eliminate, rust pressure. Control allium weeds and plow
under infected crop residues to help reduce inoculum. Introduction and significance
Avoid planting consecutive host crops; for example, in This is a major root rot disease of alliums, with onion
some regions in Europe a single leek crop planted in the and garlic being particularly affected. White rot can also
spring can often be grown with no or little rust. Apply be a common problem in garden settings. In some
fungicides, such as morpholine or triazole products, regions white rot is an increasing problem due to
where rust occurs. Frequent applications are required intense crop rotations and shortage of uninfested land.
to maintain good control in long season crops. For leek, In the USA and other regions, another Sclerotium
plant resistant cultivars, which are widely used in species, S. rolfsii, causes southern blight disease on
Europe. alliums (36).
References Symptoms and diagnostic features

Anikster, Y., Szabo, L. J., Eilam, T., Manisterski, J., Koike, S. T., White rot affects roots and crowns, and overall
and Bushnell, W. R. 2004. Morphology, life cycle biology, and symptoms are usually first noticed only after root
DNA sequence analysis of rust fungi on garlic and chives from
California. Phytopathology 94:569–577. infection is well established. Foliage of infected plants
Clarkson, J. and Kennedy, R. 1997. Quantifying the effect of turns yellow, wilts, collapses, and eventually dies and
reduced doses of propiconazole (Tilt) and initial disease becomes brown and dry (36, 37). In badly affected
incidence on leek rust development. Plant Pathology
46:952–963.
areas, foliage growth is poor and patches of plants die
Harrison, J. M. 1987. Observations on the occurrence of telia of rapidly. White, persistent mycelium develops on
Puccinia porri on leeks in the UK. Plant Pathology diseased roots and the base of bulbs in contact with soil.
36:114–115. Numerous tiny, black, spherical sclerotia, measuring
Jennings, D. M., Ford-Lloyd, B. V., and Butler, G.M. 1990. Effect
of leaf age, leaf position and leaf segment on infection of leek
less than 1 mm in diameter, form on mycelium and
by leek rust. Plant Pathology 39:591–597. diseased tissue (38). In advanced stages of disease, the
Jennings, D. M., Ford-Lloyd, B. V., and Butler, G.M. 1990. Rust roots and bulbs become soft and rotted due to activity
infections of some Allium species: an assessment of from secondary decay organisms. Symptoms on leek
germplasm for utilizable rust resistance. Euphytica
49:99–109. are usually less severe than on onion or garlic.
Koike, S. T. and Smith, R. F. 2001. First report of rust caused by
Puccinia allii on wild garlic in California. Plant Disease
85:1290.
Koike, S. T., Smith, R. F., Davis, R. M., Nunez, J. J., and Voss, R.
E. 2001. Characterization and control of garlic rust in
California. Plant Disease 85:585–591.
Niks, R. E. and Butler, G. M. 1993. Evaluation of morphology of
infection structures in distinguishing between different Allium 36
rust fungi. Netherlands Journal of Plant Pathology 99,
Supplement 3:139–149.
Smith, B. M., Crowther, T. C., Clarkson, J. P., and Trueman, L.
2000. Partial resistance to rust (Puccinia allii) in cultivated
leek (Allium ameloprasum ssp. porrum): estimation and
improvement. Annals of Applied Biology 137:43–51.
Uma, N. U. and Taylor, G. S. 1986. Occurrence and morphology
of teliospores of Puccinia allii on leek in England.
Transactions of the British Mycological Society 87:320–323.
F UNGAL D ISEASES
36 Onion infected with southern blight.

A LLIACEAE 75
37 38 Garlic infected 38
with white rot.
37 Onion field affected by white rot.
Causal agent
The cause of white rot is Sclerotium cepivorum, which sulphides. Sclerotia germinate and the resulting
has no known perfect stage. Conidia are likewise not mycelium grows 1–2 cm through soil and invades the
produced, though small spermatia occur on germinat- host root and basal plate. Secondary spread can occur
ing hyphae but appear to have no role in disease devel- by mycelial growth from plant to plant if their roots are
opment. Sclerotium cepivorum reproduces, survives, in close proximity. Temperature is a key factor in
and infects by sclerotia (39) that consist of a smooth disease development as sclerotia show little activity
black rind that is two to five cell layers deep and an below 9º C or above 24º C; the optimum range is
inner medulla of closely packed hyphae. The pathogen 14–18º C. Crops planted in the autumn may therefore
can be readily isolated on solid media such as potato
dextrose agar. The white rot fungus is host specific to
allium crops. The other species, S. rolfsii, causes a
watery rot of alliums and produces brown, spherical 39
sclerotia that are usually significantly larger (1–2 mm in
diameter) than those of S. cepivorum. Sclerotium rolfsii
has a very broad host range.
Disease cycle
White rot is associated with soilborne inoculum, so
affected areas and disease incidence increase as alliums
are cropped in infested fields. Sclerotia can persist in
F UNGAL D ISEASES
soil without a plant host for over 20 years. These

propagules remain dormant until allium root exudates,
such as propyl and alyl cysteine amino acids that are
specific to this group of plants, are present in soil. Soil
microorganisms metabolize the amino acids into the
stimulatory compounds alkyl and alkenyl thiols and 39 Sclerotia and mycelium of white rot on onion.
experience reduced disease severity. Sclerotia germinate References

under moist conditions (not below –100 kPa [ = Brix, H. D. and Zinkernagel, V. 1992. Screening for resistance of
–1bar]), but germination is inhibited in very wet soils. Allium species to Sclerotium cepivorum with special reference
to non-stimulatory responses. Plant Pathology 41:308–316.
Bulb onion crops established from transplants are more
Coley Smith, J .R. 1986. Interactions between Sclerotium
severely affected than direct seeded crops because of cepivorum and cultivars of onion, leek, garlic and Allium
more vigorous root systems that develop earlier in the fistulosum. Plant Pathology 35:362–369.
season and hence encounter more soilborne inoculum. Coley Smith, J. R. 1990. British Society for Plant Pathology
Presidential Address 1989. White rot disease of Allium:
problems of soil-borne disease in microcosm. Plant Pathology
Control 39:214–222
Crop rotation is of limited value because sclerotia Coley Smith, J. R. and Entwistle, A. R. 1988. Susceptibility of
garlic to Sclerotium cepivorum. Plant Pathology 37:261–264.
persist in soil for many years. Rather, select fields and
Couch, B. C. and Kohn, L. M. 2000. Clonal spread of Sclerotium
plant crops where there is no history of the disease. cepivorum in onion production with evidence of past
Implement sanitation measures to prevent introduction recombination events. Phytopathology 90:514–521.
of infested soil and contaminated equipment into clean Crowe, F. J .and Hall, D. H. 1980. Vertical distribution of
sclerotia of Sclerotium cepivorum and host root systems
fields. Use only disease-free transplants. Be aware that relative to white rot of onion and garlic. Phytopathology
sclerotia survive passage through the digestive tracts of 70:70–73.
grazing animals and may therefore be present in Entwistle, A. R. 1986. Controlling allium white rot (Sclerotium
manures. Truly resistant cultivars are not yet available. cepivorum) without chemicals. Phytoparasitica 20:121–125.
Entwistle, A. R. 1992. Loss of control of Allium white rot by
Soil fumigation with dazomet, metam sodium, methyl fungicides and its implications. Aspects of Applied Biology
bromide, and chloropicrin on heavily infested soils can 12:201–209.
be useful treatments, though the fungus is not eradicated. Esler, G. and Coley Smith, J. R. 1983. Flavour and odour
Fungicides used as onion seed or garlic clove treatments characteristics of species of Allium in relation to their capacity
to stimulate germination of sclerotia of Sclerotium
or transplant drenches can be partially effective. cepivorum. Plant Pathology 32 :13–22.
Drenches with dicarboximide fungicides were initially Gladders, P., Wafford, J. D., and Davies, J. M. L. 1987. Control
useful, but enhanced microbial degradation of these of allium white rot in module raised bulb onions. In: T. J.
Martin (ed.). Application to Seeds and Soil. BCPC
compounds in some soils led to a decline in their per- Monograph No. 39:371–378.
formance. Triazole fungicides are now used for white Koike, S. T., Gonzales, T. G., and Oakes, E. D. 1994. Crown and
rot control in some countries. root rot of chives in California caused by Sclerotium rolfsii.
Soil inoculum can be reduced if sclerotia can be stim- Plant Disease 78:208.
Leggett, M. E. and Rahe, J. E. 1985. Factors affecting the survival
ulated to germinate in the absence of host plants. Such of sclerotia of Sclerotium cepivorum in the Fraser Valley of
germination is triggered by diallyl disulphide (DADS), British Columbia. Annals of Applied Biology 106:255–263.
which mimics the stimulatory activity of allium roots Melero-Vara, J. M., Prados-Ligero, A. M., and Basallotte-Ureba,
and is now commercially available in some countries. M. J. 2000. Comparison of physical, chemical and biological
methods of controlling garlic white rot. European Journal of
Effectiveness of this treatment relies on thorough appli- Plant Pathology 106:581–588.
cation to soil and appropriate temperature and Smolinska, U. 2000. Survival of Sclerotium cepivorum sclerotia
moisture conditions. Note that not all sclerotia respond and Fusarium oxysporum chlamydospores in soil amended
with cruciferous residues. Journal of Phytopathology
to this treatment. Composted onion waste is also 148:343–349.
showing promise for white rot control in the UK when Smolinska, U. and Horbowicz, M. 1999. Fungicidal activity of
incorporated back into the field. Composting tempera- volatiles from selected cruciferous plants against resting
propagules of soilborne fungal pathogens. Journal of
tures must reach 50º C to kill any sclerotia present in
onion waste.
Though not completely effective, flooding of infested
F UNGAL D ISEASES
fields is used in some regions to manage white rot. This

is most effective when temperatures are above 20º C.
Solarization reduced sclerotial populations in Australia
and Egypt and might form part of an integrated control
strategy where climatic conditions are suitable.
A LLIACEAE 77
Urocystis cepulae (= U. colchici var. cepulae) 40 Smut infection 40

SMUT on green onion.

Smut occurs in many onion growing areas and is occa-
sionally important. It affects bulb and salad onion, leek,
shallot, and chives. Garlic appears to be immune and
resistance is present in Allium fistulosum.

Symptoms can appear as early as seedling emergence,
when cotyledons show infections. Cotyledons, true
leaves, and leaf sheaths develop oblong to elongated,
dark, raised blisters on outer surfaces (40). These
growths can cause downward curling of the leaves.
Mature blisters break open to expose black, powdery
fungal growth (41). There is progressive spread of the
disease inwards, which can kill seedlings within 3 to 4
weeks. Infected bulb tissue remains firm, though
secondary decay organisms can penetrate damaged 41 Black sporula-
41
areas and cause rot. Another disease, smudge (caused tion of smut on
by Colletotrichum circinans), also produces black green onion.
fungal growth on onion, leek, and shallot, so differenti-
ating smut from smudge in the field may be difficult.
Causal agent
Smut is caused by Urocystis cepulae (synonymous with
Urocystis colchici var. cepulae). It is a basidiomycete
fungus belonging to the Ustilaginales. This pathogen
produces distinctive black spore masses that consist of
chlamydospores. These are spherical, single-celled,
brown to black, 12–15 μm in diameter, with an outer
layer of small sterile cells, 46 μm in diameter.
Disease cycle
The pathogen is soilborne and can survive for up to 20
years in soil. The pathogen may be introduced on sets
or transplants. Seedborne infection is not considered
important. Chlamydospores can be spread by winds
and water, and optimum temperatures for germination
are 13–22º C. Most plant infection occurs at 10–12º C
and disease activity is greatly reduced above 25º C.
F UNGAL D ISEASES
Control
Use fungicide-treated seed and resistant cultivars if References
available. Use healthy transplants because these are able Utkhede, R. S. and Rahe, J. E. 1980. Screening world onion
to resist infection from soilborne inoculum. Plant when germplasm collection and commercial cultivars for resistance
to smut. Canadian Journal of Plant Science 60:157–161.
soil temperatures are higher.
Garlic yellow stripe virus, Garlic yellow streak virus, References

Leek yellow stripe virus
Conci, V. C., Canavelli, A., Lunello, P., Di Rienzo, J., Nome, S. F.,
GARLIC MOSAIC Zumelzu, G., and Italia, R. 2003. Yield losses associated with
virus-infected garlic plants during five successive years. Plant
Disease 87:1411–1415.
Introduction and significance Dovas, C. I., Hatziloukas, E., Salomon, R., Barg, E., Shiboleth,
Garlic mosaic is the common name of a virus disease Y., and Katis, N. I. 2001. Incidence of viruses infecting Allium
spp. in Greece. European Journal of Plant Pathology 107:
that affects garlic. There are several viruses that infect 677–684.
garlic and cause this disease, and many of these Mohamed, N. A. and Young, B. R. 1981. Garlic yellow streak
pathogens are not yet fully identified or characterized. virus, a potyvirus infecting garlic in New Zealand. Annals of
van Dijk, P., Verbeek, M., and Bos, L. 1991. Mite-borne virus
Symptoms and diagnostic features isolates from cultivated Allium species, and their classification
Foliar symptoms can vary greatly, but mostly consist of into two new rymoviruses in the family Potyviridae.
mild to severe mosaics, streaking, striping, and chlorotic Netherlands Journal of Plant Pathology 97:381–399.
mottling. Symptoms are often most evident in the
youngest leaves. The overall effect is generally smaller
bulb size and yield reductions of up to 50%.
Causal agent
Some of the viruses in the garlic mosaic complex are
aphid-borne potyviruses that include Garlic yellow
streak virus, Leek yellow stripe virus, and Garlic yellow
stripe virus. The latter two viruses are both reported
from California. Onion mite-borne latent virus is a
rymovirus transmitted by the mite Aceria tulipae and is
difficult to eliminate from stocks by meristem tip
culture.
Disease cycle
Very little information is available on disease develop-
ment of this problem.
Control
The fact that garlic is propagated by vegetative cloves
makes virus management a challenge, and a high per-
centage of garlic cloves can be infected with one or
more viruses. Control of all garlic viruses relies on pro-
duction of virus-free stocks in areas well away from
commercial production areas. Planting larger cloves
may help maintain yield even when viruses are present
in the cloves.
V IRAL D ISEASES
A LLIACEAE 79
Onion yellow dwarf virus References

ONION YELLOW DWARF Bos, L. 1982. Viruses and virus diseases of Allium species. Acta
Horticulturae 127:11–29.
Bos, L., Huttinga, H., and Maat, D. Z. 1978. Shallot latent virus,
a new carlavirus. Netherlands Journal of Plant Pathology
Onion yellow dwarf virus (OYDV) is thought to be 84:227–237.
present in all production areas. Conci, V. C. and Nome, S. F. 1991. Virus free garlic (Allium
sativum L.) plants obtained by thermotherapy and meristem
tip culture. Journal of Phytopathology 132:186–192.
Lot, H., Chovelon, V., Souche, S., and Delecole, B. 1998. Effects
Initial symptoms are yellow streaks at the base of the of onion yellow dwarf and leek yellow stripe viruses on
youngest leaves. All the new leaves are affected and symptomatology and yield from three French garlic cultivars.
result in a general yellowing. The leaves may be
Shiboleth, Y. M., Gal-On, A., Koch, M., Rabinowitch, H. D.,
crinkled, flattened, and tend to fall over. Bulbs are small and Salomon, R. 2001. Molecular characterization of Onion
but remain firm. Flower stalks are yellow and twisted. yellow dwarf virus (OYDV) infecting garlic (Allium sativum
In garlic, OYDV probably contributes to mosaic L.) in Israel: Thermotherapy inhibits virus elimination by
meristem tip culture. Annals of Applied Biology
symptoms in combination with other viruses. 138:187–195.
Walkey, D. G. A., Webb, M. J. W., Bolland, C. J., and Miller, A.
Causal agent 1987. Production of virus-free garlic (Allium sativum L.) and
shallot (A. ascalonicum L.) by meristem-tip culture. Journal of
OYDV is a potyvirus with filamentous particles that Horticultural Science 62: 211–220.
measure 722–820 x 16 nm. Another allium virus
pathogen is Shallot latent virus, a carlavirus first
reported in the Netherlands in 1978. This virus has long
filamentous particles (650–652 nm) and is transmitted
by the shallot aphid (Myzus ascalonicus). Vegetatively
propagated shallot is frequently affected. Shallot latent
virus also occurs in onion, garlic, and leek.
Disease cycle
OYDV is spread by the green peach aphid (Myzus
persicae) and other aphid vectors in a nonpersistent
manner. The virus has a narrow host range within
Allium species.
Control
Control is achieved by using healthy planting
material. Clean stocks of garlic may be obtained by
meristem tip culture and maintained by virus indexing
of stocks. Healthy onion crops may be raised from
seed because OYDV is not seed transmitted. Rotation
away from allium crops and control of volunteers are
required to break the cycle of virus spread between
crops.
V IRAL D ISEASES
Apiaceae Parsley family
PLANTS IN THE APIACEAE (parsley family), formerly known as the Umbelliferae,

are characterized by distinctive umbrella-shaped flowering structures; they are a major group of
vegetables with many uses. Carrot (Daucus carota) and parsnip (Pastinaca sativa) are primarily
grown for their edible roots. Celery (Apium graveolens var. dulce) and fennel (Foeniculum
vulgare) produce thick edible petioles, while celeriac (Apium graveolens var. rapaceum) is grown
for its large storage root and hypocotyl. The foliage of other species is used as herbs, seasonings,
garnish, and other culinary purposes: parsley (Petroselinum crispum), chervil (Anthriscus
cerefolium), dill (Anethum graveolens), cilantro (also known as coriander or Chinese parsley)
(Coriandrum sativum). The seeds of celery, fennel, coriander, anise (Pimpinella anisum),
caraway (Carum carvi), and cumin (Cuminum cyminum)are also widely used.
The different apiaciae plants suffer from generally distinct sets of diseases, as described
in the sections that follow, though they also have some in common.
APIUM GRAVEOLENS (CELERY)

Aster yellows phytoplasma
42
ASTER YELLOWS

Aster yellows occurs sporadically in Apiaceae crops,
notably on celery and carrot. While symptoms can
be unusual and striking, economic losses are rarely
experienced.

In celery, the foliar symptoms are yellowing, stunting,
and overall poor growth (42). The heart of the plant
sometimes becomes necrotic. The petioles are very
brittle and there is peeling back of the epidermis and
cracking on older plants. A characteristic symptom is
the extreme twisting and curling of celery petioles (43,
44). On carrot, parsnip, and parsley, aster yellows
42 Stunted, chlorotic symptoms of aster yellows of causes leaf chlorosis, proliferation of shoots from the
celery. crown, and abnormal greening (virescence) and devel-
opment of leaf structures (phyllody) in flowers of seed
crops.
A PIACEAE 81
Causal agent 43
Aster yellows disease is caused by the aster yellows phy-
toplasma. Phytoplasmas, like typical bacteria, are
prokaryotes but are placed in a distinct category called
mollicutes. Mollicutes are single-celled organisms that
lack a cell wall, appear in various shapes (called pleo-
morphism), and have very small genomes. Phyto-
plasmas inhabit the phloem tissue of their host plants.
This pathogen affects a very wide host range of culti-
vated and wild plants.
Disease cycle
The aster yellows phytoplasma is vectored primarily by
the aster leafhopper (Macrosteles fascifrons), but many
other species of leafhopper can also be vectors. These
insects acquire the aster yellows phytoplasma by 43 Brittle, cracked petioles of celery infected with aster
feeding on infected crops or weeds such as dandelion, yellows.
plantain, sowthistle, and wild lettuce. After an incuba-
tion period, the insects can transmit the phytoplasma in 44
a persistent manner. The phytoplasma reproduces by
division or budding in the phloem sieve cells of host
plants and within their leafhopper vectors. This
pathogen is not seedborne.
Control
Control strategies are rarely needed. Remove inoculum
sources by controlling weeds. Some areas such as
pastures and river or stream banks naturally harbor the
phytoplasma in resident vegetation; avoid planting
celery and other susceptible crops in these areas. Using
insecticides to control leafhoppers rarely affects aster
yellows incidence.
References
Chiykowski, L. N. 1977. Transmission of a celery-infecting
strain of aster yellows by the leafhopper Aphrodes bicinctus.
Khadhair, A. H. and Evans, I. R. 2000. Molecular and
microscopical detection of aster yellows phytoplasma
associated with infected parsnip. Microbiological Research
155:53–57.
Zhang, J., Hogenhout, S. A., Nault, L. R., Hoy, C. W., and Miller,
S. A. 2004. Molecular and symptom analyses of phytoplasma
strains from lettuce reveal a diverse population. 44 Twisted petioles of aster yellows of celery.
Zhou, X., Hoy, C. W., Miller, S. A., and Nault, L. R. 2002.
Spacially explicit simulation of aster yellows epidemics and
control on lettuce. Ecological Modeling 151:293–307.
Pseudomonas syringae pv. apii

46
BACTERIAL LEAF SPOT

Although bacterial leaf spot has been recognized since
1921 in New York State, it remained a relatively minor
disease until 1989 when it was first observed in
California on greenhouse-grown transplants and field-
planted celery. The disease was found in all celery-
growing regions of California by 1991. Further
research is required to clarify the relationship between
the celery bacterial leaf spot pathogen and the
Pseudomonas pathogens causing leaf spots on fennel
and parsley. A similar disease caused by Pseudomonas
syringae pv. coriandricola occurs on cilantro 46 Close-up of leaf spots of bacterial leaf spot of celery.
(coriander) in California, Florida, and parts of Europe.
Symptoms and diagnostic features Causal agent

Initial symptoms are small (2–5 mm in diameter), Bacterial leaf spot is caused by P. syringae pv. apii,
angular shaped, water-soaked leaf spots that have a which is an aerobic, Gram-negative bacterium. The
greasy appearance and appear on both sides of an pathogen can be isolated on standard microbiological
infected leaf. As spots develop, they enlarge and can media and produces cream-colored colonies typical of
turn darker brown (45, 46). Under dry conditions the most pseudomonads. When cultured on Kings medium
lesions are light brown and papery. As disease pro- B, this organism produces a diffusible pigment that flu-
gresses, lesions increase in number, coalesce, and can oresces blue under ultraviolet light. Strains of this
result in extensive leaf death. Plant vigor can be pathogen are host specific to celery. This pathogen is
reduced, but plants are not killed. Bacterial leaf spot is seedborne, which results in infection of celery trans-
strictly a leaf-spot disease. Symptoms can be confused plants. Distinct races have not been documented.
with those of bacterial blight and brown stem caused by
P. cichorii, but bacterial leaf spot does not cause Disease cycle
symptoms on celery petioles. P. syringae pv. apii can survive on celery seed for at least
2 to 3 years; hence seed is the main source of primary
inoculum. The pathogen survives epiphytically on
45 45 Leaf spots of leaves until environmental conditions allow popula-
bacterial leaf spot tions to increase and infection to occur through stomata
of celery. or wounds. Symptoms are most frequently found in
transplants (47) having soft lush growth due to warm
growing conditions, high humidity, and high nitrogen
fertilization. Mowing of transplants to promote
vigorous and uniform growth and irrigating with high-
pressure systems readily spread the pathogen. Symp-
toms appear 7 to 10 days after long periods of leaf

wetness (greater than 7 hours/day) over a 2- to 3-day
period. In the field, disease activity is limited unless
there is rain or overhead irrigation.
A PIACEAE 83
Cercospora apii
47
EARLY BLIGHT

This disease can cause considerable damage, and
severely affected crops have been abandoned, particu-
larly in the southeastern USA and Mexico. Early blight
also affects celeriac.

Early symptoms are small, yellow flecks that enlarge
into round to oval, gray-brown spots that can measure
from 1–2 cm in diameter (48, 49). Under humid condi-
tions, lesions become light gray and fuzzy when the
47 Celery transplants infected with bacterial leaf spot
of celery.
Control 48 Early blight 48

Use seed that does not have significant levels of the symptoms on
pathogen. Treat infested seed with hot water (50º C for celery leaf.
25 minutes). Practice careful sanitation at transplant
nurseries. Disinfect benches, seed trays, mowers, and
other production equipment. Prevent transfer of the
pathogen on worker hands, clothing, and footwear by
using sanitizing agents. Irrigate so that plants dry
quickly after watering, and avoid using high-pressure
irrigation systems that lead to water-soaking of leaves.
Chemical control in the form of copper sprays is of
limited benefit.
References
Koike, S. T., Gilbertson, R. L., and Little, E. L. 1993. A new
bacterial disease of fennel in California. Plant Disease 77:319.
Lacy, M. L., Berger, R. D., Gilbertson, R. L., and Little, E. L.
1996. Current challenges in controlling diseases of celery. 49
Little, E .L., Koike, S. T., and Gilbertson, R. L. 1997. Bacterial
spot of celery in California: etiology, epidemiology, and role
of contaminated seed. Plant Disease 81:892–896.
Pernezny, K., Datnoff, L., and Sommerfeld, M. L. 1994. Brown
stem of celery caused by Pseudomonas cichorii. Plant Disease
78:917–919.
Thayer, P. L. 1965. Temperature effect on growth and
pathogenicity to celery of Pseudomonas apii and P. cichorii.
Phytopathology 55:1365.
F UNGAL D ISEASES
Thayer, P. L. and Wehlburg, C. 1965. Pseudomonas cichorii, the

cause of bacterial blight of celery in the Everglades.
49 Close-up of early blight of celery.

50
relative humidity decreases and are subsequently
dispersed by wind. Spores can also be spread by
splashing water and via field operations. Spores
germinate and penetrate through stomata after only 5
hours of leaf wetness. The disease cycle takes 5 to 14
days.
Control
pathogen. If transplants are still produced in the
ground, rotate seedbeds to avoid soilborne inoculum.
Irrigate early in the day to allow foliage to dry quickly.
Plant resistant or tolerant cultivars if such are available.
Use wider plant spacing and raised beds to improve air
50 Severe blighting due to early blight of celery. circulation. Apply fungicides if celery is produced in
high-risk areas. A disease forecasting system has been
developed to help schedule fungicide sprays.
pathogen sporulates. The lesions have indistinct
margins and do not contain discrete, dark fruiting References
structures as seen with late blight. Disease usually pro- Berger, R. D. 1969. A celery early blight spray program based on
gresses from the oldest leaves to the newer foliage. disease forecasting. Florida State Horticultural Society
Proceedings 81:107–111.
Celery petioles also become infected and have elongated
Berger, R. D. 1973. Early blight of celery: analysis of disease
lesions. Severe infection results in necrosis and death of spread in Florida. Phytopathology 63:1161–1165.
foliage and typical blight-like symptoms (50). Seedlings Koike, S. T., Tjosvold, S. A., Groenewald, J. Z., and Crous, P. W.
can exhibit symptoms. Field symptoms of early blight 2003. First report of a leaf spot disease of bells-of-Ireland
(Moluccella laevis) caused by Cercospora apii in California.
usually appear earlier in the season than those of late Plant Disease 87:203.
blight. Strandberg, J. O. and White, J. M. 1978. Cercospora apii
damage of celery – Effects of plant spacing and growth on
raised beds. Phytopathology 68:223–226.
Causal agent
Early blight is caused by the fungus Cercospora apii.
The pathogen produces hyaline, multicelled, filiform
spores that measure 22–290 x 3.5–4.5 μm and are
borne on clusters of brown conidiophores. Cercospora
apii is seedborne in celery. This pathogen appears to be
primarily a pathogen of celery and celeriac, though
C. apii has been reported to infect lettuce and the orna-
mental plant bells-of-Ireland (Moluccella laevis). The
relationship between these different isolates is
unknown.
Disease cycle
Both seed and infected celery debris are important
F UNGAL D ISEASES
sources of inoculum. Cercospora apii can survive as

mycelium on seed for more than 2 years. It is favored by
warm (15–30º C) temperatures and long periods of leaf
wetness or high relative humidity. Sporulation is
greatest when there have been at least 10 hours of leaf
wetness. Spores are released during the morning as
A PIACEAE 85
Fusarium oxysporum f. sp. apii 52 Discolored 52

FUSARIUM YELLOWS vascular tissue of
Fusarium yellows
Introduction and significance of celery.
Fusarium yellows is the most important soilborne
disease of celery in North America and parts of Europe.
Susceptible cultivars can be severely damaged and
unharvestable. From the 1930s through 1959,
Fusarium yellows was controlled by using resistant
cultivars. However, race 2 of the pathogen subsequent-
ly occurred, overcame this resistance, and caused sub-
stantial damage. Race 2 is now established throughout
the USA. Though race 2 tolerant cultivars are now
available, the disease continues to be an important
concern.

Affected plants are severely stunted and foliage turns
bright yellow(51). The internal vascular and pith tissue
of crowns and roots takes on a dark red to brown dis-
coloration (52). This vascular discoloration rarely Causal agent
extends far up into the attached petioles. As disease Fusarium yellows is caused by the soilborne fungus
progresses, the central pith of the crown and root will Fusarium oxysporum f.sp. apii. Pathogen morphology
break down, become colonized by secondary decay and colony characteristics are similar to other
organisms, and turn soft and rotted. The pathogen F. oxysporum fungi. The fungus forms one- or two-
infects large roots and causes them to become gray, celled, oval to kidney-shaped microconidia on
water-soaked, and soft (53). Severely affected plants can monophialides, and four- to six-celled, fusiform, curved
collapse and die. macroconidia. Microconidia measure 5–12 x 2–4 μm,
51 53
F UNGAL D ISEASES
51 Decline and stunting of celery plants infected with 53 Dark, decayed celery root infected with Fusarium
Fusarium yellows. yellows.
while macroconidia range from 25–45 x 3–5 μm (four- Cerkauskas, R. F. and Chiba, M. 1991. Soil densities of Fusarium
oxysporum f.sp. apii race 2 in Ontario, and association
celled) to 35-60 x 3–5 μm (six-celled). Macroconidia between celery cultivar resistance and photocarcinogenic
are usually produced in cushion shaped structures furocoumarins. Canadian Journal of Plant Pathology
13:305–314.
called sporodochia. Chlamydospores are also formed.
Correll, J. C., Puhalla, J. E., and Schneider, R. W. 1986.
The pathogen is usually readily isolated from sympto- Identification of Fusarium oxysporum f.sp. apii on the basis
matic vascular tissue. Semi-selective media like of colony size, virulence, and vegetative compatibility.
Komada’s medium can help isolate the pathogen if Phytopathology 76:396–400.
Elmer, W. H. and Lacy, M. L. 1987. Effects of inoculum densities
secondary rot organisms are present. This pathogen is
of Fusarium oxysporum f.sp. apii in organic soil on disease
apparently host specific to celery. Two distinct races expression in celery. Plant Disease 71:1086–1089.
have been documented. Race 1 affects only self- Elmer, W. H., Lacy, M. L., and Honma, S. 1986. Evaluations of
blanching cultivars; race 2 was first recorded in celery germ plasm for resistance to Fusarium oxysporum f. sp.
apii Race 2 in Michigan. Plant Disease 70:416–419.
California in 1978 and affects both self-blanching and
Elmer, W. H. and Lacy, M. L. 1987. Effects of crop residues and
green cultivars. There is some diversity between race 2 colonization of plant tissues on propagule survival and soil
isolates. For example, isolates from Ohio appear to be populations of Fusarium oxysporum f. sp. apii Race 2.
significantly more virulent than California isolates.
Hart, L. P. and Endo, R. M. 1978. Reappearance of Fusarium
yellows of celery in California. Plant Disease Reporter
Disease cycle 62:138–142.
The pathogen is soilborne and can survive for many Lacy, M. L., Berger, R. D., Gilbertson, R. L., and Little, E. L.
1996. Current challenges in controlling diseases of celery.
years in soil as resilient chlamydospores. Chlamydo- Plant Disease 80:1084–1091.
spores germinate in response to celery root exudates Opgenorth, D. C. and Endo, R. M. 1985. Abiotic factors and
and infect the roots. The pathogen then invades the chlamydospore formation in Fusarium oxysporum f. sp. apii.
vascular system and spreads through the plant. Transactions of the British Mycological Society 84:740–742.
Orton, T. J., Durgan, M. E., and Hulbert, S. D. 1984. Studies on
Fusarium yellows is favored by warmer temperatures inheritance of resistance to Fusarium oxysporum f. sp. apii in
(20–32º C) and dry soils. Under field conditions, celery. Plant Disease 68:547–578.
symptoms can appear 30 to 40 days after planting. This Puhalla, J .E.1984. Races of Fusarium oxysporum f. sp. apii in
disease is caused only by primary inoculum that is California and their genetic interrelationships. Canadian
Journal of Botany 62:546–550.
soilborne and is therefore considered a monocyclic Toth, K. F. and Lacy, M. L. 1991. Increasing resistance in celery
disease. to Fusarium oxysporum f. sp. apii with somaclonal variation.
Control
Do not plant susceptible celery cultivars into fields
having a history of Fusarium yellows. Therefore, Phoma apiicola
maintain good records and monitor where the disease PHOMA CROWN AND ROOT ROT
occurs. Prevent introduction of the pathogen into unin-
fested fields by completing production procedures in Introduction and significance
clean fields before entering known infested areas. If This disease, caused by Phoma apiicola, occurs in
equipment and vehicles have been in infested fields, North America and Europe and affects celery, celeriac,
clean such equipment prior to entering other areas. The and fennel. Carrot, caraway, parsley, and parsnip are
most important management step is to use resistant or reported to be susceptible to this pathogen, but are also
tolerant cultivars. Few celery cultivars have complete are infected by P. complanata. Yet another species,
resistance to this pathogen, so tolerant cultivars may P. rostrupii, has been reported on carrot from Russia
still develop some symptoms. and Ukraine, where it is an important seedborne disease
F UNGAL D ISEASES
and causes a dry brown root rot. Overall, Phoma crown

References and root rot is considered a minor disease, though
Awuah, R. T., Lorbeer, J. W., and Ellerbrock, L. A. 1986. losses occur both in the field and in storage. Phoma
Occurrence of Fusarium yellows of celery caused by Fusarium problems on celeriac are known as scab or rust, and
oxysporum f.sp. apii Race 2 in New York and its control.
Plant Disease 70:1154–1158. recently have become more damaging in the UK.
A PIACEAE 87
Symptoms and diagnostic features Pythium spp.

The roots and crowns of celery show light brown DAMPING-OFF,
lesions that turn black and spread to the petiole bases. PYTHIUM ROOT ROT
With decline of the petioles, yellowing and death of the
outer leaves follows. Leaf spot symptoms are rarely Introduction and significance
seen. Early root infection results in stunted growth and Apiaceae are affected by various Pythium species
possible plant death. On celeriac, the roots develop a throughout most production areas. Poor sanitation at
dry brown rot. The presence of black pycnidia in rotted nurseries and adverse growing conditions are usually
tissue is an important diagnostic feature, as symptoms responsible for the most severe problems. Disease
can resemble those caused by licorice rot or black rot. severity differs depending on the particular region. In
the UK, celery seedlings are very susceptible to
Causal agent damping-off, though in California this disease is rare.
Phoma crown and root rot is caused by the fungus P.
apiicola. On rotted tissues the pathogen produces black, Symptoms and diagnostic features
spherical pycnidia (measuring up to 250 μm in Poor emergence and collapse of seedlings soon after
diameter) that have cylindrical necks and produce rod- emergence are characteristic of damping-off. Infection
shaped, hyaline conidia that measure 3–14 x 1–2 μm. can spread rapidly within transplant trays, resulting in
patches of dead plants. Roots are initially water-soaked
Disease cycle and later develop reddish-brown lesions (54). In the
The pathogen is seedborne, so the disease can be field, transplants can become infected from soilborne
initiated on transplants prior to being field planted. inoculum. In such situations, poor or stunted growth is
Phoma apiicola can survive in infested debris for several the most obvious symptom. Affected plants have
years. Conidia are splashed by rain or overhead chlorotic foliage, brown roots, and reduced feeder roots
sprinkler irrigation and infect plants directly or through
wounds. The optimum temperature for activity is Causal agent
16–18º C, but under wet conditions disease develop- Damping-off and Pythium root rot are caused by
ment can take place at much lower temperatures. several Pythium species, including the following:
P. artotrogus, P. debaryanum, P irregulare, P.
Control mastophorum, P. paroecandrum, P. ultimum. Pythium
Rotate crops for at least 2 years away from Apiaceae paroecandrum also causes a root rot of parsley. These
crops. Use seed that does not have significant levels of oomycete organisms are common soil inhabitants that
the pathogen. Fungicide sprays may give some control. survive by means of resilient oospores. Most species
produce sporangia, which mature and release infective
References swimming zoospores.
Hewett, P. D. 1970. Phoma apiicola on celery seed. Plant
54
Williams, P. H. and Wade, E. K. 1967. Scab of celeriac. Plant
Disease Reporter 51:427–429.
F UNGAL D ISEASES
54 Dark, rotted celery roots affected by Pythium.

Disease cycle Sclerotinia sclerotiorum

Oospores germinate and grow in response to seed and PINK ROT
root exudates. Infection and disease development
require wet soil conditions that allow for zoospore Introduction and significance
movement and contact with host roots. Severe infection Pink rot is the name given to Sclerotinia disease on
occurs in low lying or poorly drained areas. Disease celery. Sclerotinia occurs wherever celery is grown and
symptoms can appear rapidly on small seedlings, but losses can be high. Sclerotinia scerlotiorum has a wide
for larger transplants the foliar symptoms may not host range and can be difficult to manage. Sclerotinia
appear for several weeks. Established celery plants are minor also occurs on Apiaceae crops such as celery and
generally not affected by these pathogens. The fennel, but is less prevalent than S. sclerotiorum.
pathogen can contaminate trays, equipment, bench
tops, and other surfaces and become problematic in Symptoms and diagnostic features
transplant production systems. Symptoms on celery can develop at any stage of growth
and in storage. If celery transplants are grown in
Control seedbeds in the ground, a watery rot can develop where
Practice thorough sanitation in greenhouse transplant plants are in contact with the soil. Infected seedlings
environments. Regularly clean and disinfect transplant soon collapse. The pathogen can grow from diseased
trays, planters, bench tops, and other equipment and seedlings to neighboring plants. Airborne ascospores
containers that come in contact with transplants. Use can land on celery transplants grown in trays inside
pathogen-free rooting medium and irrigation water. greenhouses and cause brown, foliar blighting and
Use soilless, peat-based rooting media. Set the growing collapse of plants (55). Fluffy white mycelium and black
conditions so that rapid germination and growth of sclerotia usually form on diseased plants (56).
celery transplants is enhanced. Avoid applying excess For field planted celery, Sclerotinia species infect the
water and nutrients. In the field, rotate with non-host base of the petioles and cause a soft, brown spreading
crops, though such strategies will not eradicate soil- lesion that usually has a pink color or border (57). Pink
borne pathogens such as Pythium. Place transplants in rot develops rapidly and plants soon rot and collapse.
fields that are properly prepared and leveled and that Another feature of this disease is a foliar blight that is
drain well. In some production regions, such as the UK, initiated by airborne ascospores and results in brown,
fungicides may be required at planting. soft decay of foliage. Aerial infections often follow
damage to young foliage caused by the calcium defi-
Refrences ciency disorder known as blackheart. In most cases,
Hershman, D. E., Varney, E. H., and Johnston, S. A. 1986. Sclerotinia damage occurs as crops near maturity and
Etiology of parsley damping-off and influence of temperature the plant canopy becomes extensive. Pink rot may
on disease development. Plant Disease 70:927–930.
resemble bacterial soft rot (58); however, bacterial soft
McCracken, A. R. 1984. Pythium paroecandrum associated with
a root rot of parsley. Plant Pathology 33:603–604. rot causes extensive water soaking of tissues, an
Starr, J. L. and Aist, J. R. 1977. Early development of Pythium extremely mushy decay of petioles, and a very strong
polymorphon on celery roots infected by Meloidogyne hapla. disagreeable odor.
Vazquez, M .R., Davis, R. M., and Greathead, A. S. 1996. First
report of Pythium mastophorum on celery in California. Causal agent
Plant Disease 80:709. On celery, pink rot is primarily caused by Sclerotinia
sclerotiorum, though the small sclerotial species,
S. minor, can also infect celery. Sclerotinia sclerotiorum
F UNGAL D ISEASES
can infect the flowering stalks of parsley seed crops.

Fennel is susceptible to both pathogens. For detailed
descriptions of these pathogens, see the bean white
mold section in the chapter on legume diseases.
A PIACEAE 89
Disease cycle 56 Fungal growth 56

For detailed descriptions of the disease cycles, see the on celery petioles
bean white mold section in the chapter on legume caused by
diseases. Ascospores of S. sclerotiorum require Sclerotinia
exogenous nutrients prior to infecting healthy tissues; sclerotiorum.
this phenomenon is demonstrated on celery when the
physiological condition blackheart predisposes foliage
to infection.
Control
For an integrated approach to Sclerotinia control, see
the bean white mold section in the chapter on legume
diseases.
References
Budge, S. P. and Whipps, J. M. 1991. Glasshouse trials of
Coniothyrium minitans and Trichoderma species for the
biological control of Sclerotinia sclerotiorum in celery and
lettuce. Plant Pathology 40:59–66. 57 Celery petioles 57
Clarkson, J. P., Staveley, J., Phelps, K., Young, C. S., and Whipps, infected with
J .M. 2003. Ascospore release and survival in Sclerotinia Sclerotinia
sclerotiorum. Mycological Research 107:213–222.
sclerotiorum.
Griffin, M. J. 1985. Evaluation of dicarboximide fungicides for
control of pink rot (Sclerotinia sclerotiorum) of glasshouse
celery. Tests of Agrochemicals and Cultivars No. 6 (Annals of
Applied Biology 106, Supplement):48–49.
Koike, S. T. 1999. Stem and crown rot of chervil, caused by
Sclerotinia sclerotiorum, in California. Plant Disease
83:1177.
Koike, S. T., Daugovish, O., and Downer, J. A. 2006. Sclerotinia
petiole and crown rot of celery, caused by Sclerotinia minor,
in California. Plant Disease 90: In press.
Reyes, A. A. 1988. Suppression of Sclerotinia sclerotiorum and
watery soft rot of celery by controlled atmosphere storage.
58 Bacterial soft 58
55
rot: Decayed
petioles of soft rot
of celery (compare
with pink rot,
above).
F UNGAL D ISEASES
55 Celery transplants infected by ascospores of

Sclerotinia sclerotiorum.
Septoria apiicola conditions, spores ooze out of the pycnidia and form
LATE BLIGHT white, curled filaments on leaf surfaces. Symptoms on
celeriac are similar to those on celery.
Late blight is probably the most important foliar disease Causal agent
of celery worldwide and is capable of causing complete Late blight is caused by the fungus Septoria apiicola. On
crop loss in extreme cases. Problems are usually related plant tissue the pathogen is readily identified by its
to seedborne infection and disease severity therefore black pycnidia that are immersed in plant tissues.
varies greatly from season to season. This celery Pycnidia are ostiolate, measure 75–195 μm in diameter,
pathogen also affects celeriac. Septoria blight of parsley and contain hyaline, multicelled, filamentous conidia
is caused by a different species, S. petroselini. Late blight (22–56 x 2–2.5 μm). No perfect stage has been
of Apiaceae plants is unrelated to late blight disease, reported. The pathogen is seedborne. Celery and
caused by Phytophthora infestans, of tomato and celeriac are not susceptible to the Septoria blight
potato. pathogen of parsley, S. petroselini.
Symptoms and diagnostic features Disease cycle

Initial symptoms are small, chlorotic leaf spots that Infested seed is usually the most important source of the
measure less than 5 mm in diameter. These lesions soon pathogen. The pathogen can survive for 2 to 3 years on
become brown and necrotic and contain small, discrete, seed when storage conditions are dry and cool
black fruiting bodies (pycnidia) of the fungus (59). The (5 –15º C). Under ambient conditions, survival on seed
leaf spots sometimes have chlorotic margins. Spots appears to be about one year. Storage conditions
usually are angular in shape. In the field, older, lower suitable for celery seed also favor survival of S. apiicola.
foliage is infected first and the symptoms move up onto Spores penetrate through leaf stomata and epidermis,
younger foliage with time. As the disease develops, leaf producing leaf spots in 7 to 8 days under optimum con-
spots increase in number, the spots coalesce, and the ditions. Disease severity increases with rising tempera-
entire leaf can turn brown and take on a blighted tures over the range of 5–25º C. Increasing leaf wetness
appearance. The petioles are also susceptible and duration, from 72 to 96 hours, also increases disease
develop grayish-brown, irregularly shaped lesions that severity. Leaf wetness duration for at least 24 hours at
harbor numerous pycnidia (60). Diseased petioles are 20º C provides optimal conditions for disease develop-
not marketable and must be trimmed off the harvested ment. Severe epidemics are associated with prolonged
celery. If crops are subject to rain or sprinkler irrigation, periods of rain and season-long overhead sprinkler irri-
disease spread can be rapid and result in extensive gation. Late blight development, as the name implies,
damage to the crop. Because the pathogen is seedborne, occurs mostly after canopy closure and as crops near
symptoms can be found on transplants. Under humid maturity.
59 60
F UNGAL D ISEASES
59 Leaf infections of late blight of celery. 60 Petiole infections of late blight of celery.
A PIACEAE 91
Control Thanatephorus cucumeris

Use seed that does not have significant levels of the (anamorph = Rhizoctonia solani)
pathogen. Before planting seed for transplants, treat CRATER SPOT
with hot water (30 minutes at 48–49º C), aerated
steam, or fungicides. An effective chemical treatment is Introduction and significance
soaking seed in a 0.2% aqueous suspension of thiram This disease affects the petioles of celery and parsley and
for 24 hours at 30º C. Store infested seed for at least 2 causes disfiguring blemishes, which necessitates extra
years to significantly reduce viable seedborne inoculum. trimming at harvest. The disease occurs sporadically,
Inspect transplants and do not use any that show but when it appears significant damage can result. This
symptoms. Avoid planting consecutive celery crops so disease should not be confused with crater rot of carrot
that diseased crop residue can break down. Destroy that is caused by Rhizoctonia carotae.
volunteer celery or celeriac plants. After transplants are
established in the field, irrigate crops with furrow or Symptoms and diagnostic features
drip irrigation. Do not walk through or drive Symptoms are confined to the lower portions of petioles
equipment through diseased fields prior to entering near the soil and range from small (3–8 mm in
healthy fields, as inoculum can adhere to clothing and diameter), pale brown water-soaked spots to large red-
equipment. Apply fungicides as preventative measures brown sunken lesions up to 5 cm in diameter (61).
prior to plant infection. There is some progress in using Lesions occur on both the outer and inner surfaces of
predictive models to schedule sprays, and leaf wetness the petiole; lesions on the outer petioles are more rec-
durations of 12 hours or more have been used as a tangular because of the prominent veins in the tissue
threshold for treatment in North America. Resistant that delimit the lesion (62). The disease produces a dry,
cultivars in commercial lines are not yet available.
References 61
Ataga, A. E., Epton, H. A. S., and Frost, R. R. 1999. Interaction
of virus-infected celery and Septoria apiicola. Plant Pathology
48:620–626.
Edwards, S. J., Collin, H. A., and Isaac, S. 1997. The response of
different celery genotypes to infection by Septoria apiicola.
Gabrielson, R. L. and Grogan, R. G. 1964. The celery late blight
organism, Septoria apiicola. Phytopathology 54:1251–1257.
Green, K. R., O’Neill ,T. M., and Wilson, D. 2002. Effect of leaf
wetness duration and temperature on the development of leaf
spot (Septoria apiicola) on celery. Proceedings of the BCPC
Conference – Pests & Diseases 2002 1:225–230.
Kavanagh, T. and Ryan, E. W. 1971. Methods of assessment of
celery leaf spot (Septoria apiicola) in relation to fungicide 61 Crater spot lesions at base of celery plant.
evaluation. Annals of Applied Biology 68:263–270.
Lacy, M. L. 1994. Influence of wetness periods on infection of
celery by Septoria apiicola and use in timing sprays for 62
control. Plant Disease 78:975–979.
Mathieu, D. and Kushalappa, A. C. 1993. Effect of temperature
and leaf wetness duration on the infection of celery by
Septoria apiicola. Phytopathology 83:1036–1040.
Maude, R. B. and Shuring, C. G. 1970. The persistence of
Septoria apiicola on diseased celery debris in soil. Plant
F UNGAL D ISEASES
Mudita, I. W. and Kushalappa, A. C. 1993. Ineffectiveness of the
first fungicide application at different incidence levels to
manage Septoria blight in celery. Plant Disease 77:
1081–1084.
Sheridan, J. E. 1966. Celery leaf spot: sources of inoculum.
Annals of Applied Biology 57:75–81. 62 Close-up of crater spot lesions of celery.
firm rot, though secondary organisms sometimes Celery mosaic virus

colonize lesions and cause soft rots. Symptoms are CELERY MOSAIC
usually detected close to harvest.
Causal agent Celery mosaic virus (CeMV) occurs in production areas
Crater spot is caused by the basidiomycete fungus all over the world and can cause significant damage in
Thanatephorus cucumeris. The anamorph stage, R. extreme cases. Carrot, celeriac, celery, cilantro, dill,
solani, is more commonly observed. This pathogen is a parsley, and parsnip are all affected.
true soil inhabitant, survives in soil as a saprophyte, and
has a very broad host range. For a description of R. Symptoms and diagnostic features
solani, see the carrot section on crown rot in this Younger leaves show vein clearing, chlorotic spotting,
chapter. It appears that some R. solani isolates from and interveinal mottling (63, 64). Older leaves exhibit
celery can infect diverse crops such as bean, cotton, and narrowing, twisting, and cupping of the leaflets. The
tomato; likewise, isolates from sugar beet and potato petioles have a green mottle or streaking, but do not
can cause crater spot. The white or gray white mat of have the necrotic spotting characteristic of Cucumber
mycelium of the teleomorph T. cucumeris can mosaic virus infection. Infection of young plants can
sometimes be seen on the lower parts of celery petioles. cause stunting and horizontal, prostrate growth of the
outer petioles. Crinkle strains cause raised green blisters
Disease cycle and crinkling of leaves.
Rhizoctonia solani persists in organic matter and as
sclerotia in soil. Infection is particularly favored by
warm, moist soil conditions. However, in the UK 63
problems can occur on late season crops when temper-
atures are cool and when cultivation moves soil into
close contact with celery petioles. The T. cucumeris
stage may not be involved in disease development.
Control
Do not plant celery in fields where there are fresh or
partially decomposed crop residues that provide sub-
strates for R. solani. Avoid planting transplants too
deeply into the soil, as these are more likely to develop
severe crater spot. Fields should be well drained and not
kept overly wet. Avoid moving soil into and around
the plant crowns during cultivation and weeding 63 Celery leaves infected with celery mosaic virus.
operations. Where problems occur regularly, apply
fungicides. Rotate celery with non-host crops such as 64
cereals to reduce soil populations of R. solani. However,
short crop rotations will not eradicate populations of
soilborne R. solani.
References
Houston, B. R. and Kendrick, J. B. 1949. A crater spot of celery
V IRAL D ISEASES
petioles caused by Rhizoctonia solani. Phytopathology

39:470–474.
Pieczarka, D. J. 1981. Shallow planting and fungicide application
to control Rhizoctonia stalk rot of celery. Plant Disease 65:
879–880.
64 Celery leaves infected with celery mosaic virus.
A PIACEAE 93
Causal agent 65 Celery petioles 65

CeMV is a potyvirus and is made up of filamentous infected with
rods measuring approximately 750 x 15 nm and single- Cucumber mosaic
stranded RNA genomes. CeMV is transmitted in a non- virus.
persistent manner by over 20 different aphid species.
Two distinct strains, common and crinkle leaf mosaic,
are recognized.
Disease cycle
There are many wild Apiaceae hosts, including cow
parsley (Anthriscus sylvestris), poison hemlock (Conium
maculata), wild celery (Apium graveolens), and wild
parsnip (Pastinaca sativa). The virus can be acquired by
aphids after only 5–30 seconds of feeding, but infectivi-
ty is lost within 24 hours. Symptoms appear within days
of inoculation. There is no seed transmission.
Control 66 Celery petioles

66
Avoid planting celery in areas were the virus is known infected with
to cause significant disease. Control weed hosts and Cucumber mosaic
spray for the aphid vectors. Control in high-risk areas virus.
of the USA relies on an annual celery-free period of
at least one month. Follow general suggestions for
managing virus diseases (see Part 1).
References
D’Antonio, V., Falk, B., and Quiros, C. F. 2001. Inheritance of
resistance to celery mosaic virus in celery.
Purciful, D. E. and Shepard, J. F. 1967. Western celery mosaic
virus in Florida celery. Plant Disease Reporter 51:502–505.
Sutabutra, T. and Campbell, R. N. 1971. Strains of celery mosaic
virus from parsley and poison hemlock in California. Plant
Disease Reporter 55:328–332.
CUCUMBER MOSAIC that produces a crinkled effect. When young plants are
infected, they may show leaf yellowing, together with
Introduction and significance vein necrosis and distinctive elongated, necrotic, or
Cucumber mosaic virus (CMV) occurs worldwide in translucent sunken lesions on the petioles (65, 66).
many crops and weeds. Celery and other Apiaceae
crops are infected only occasionally. Causal agent
CMV has one of the widest host ranges of any
V IRAL D ISEASES
Symptoms and diagnostic features pathogen, with over 800 reported plant (crop and
Affected plants show outward and downward curling weed) hosts. CMV is a cucumovirus with virions that
of young petioles that gives the center of plants a are isometric (29 nm in diameter) and contain three
conspicuous flattened appearance. Leaves have vein single stranded RNAs. Various strains exist, with the
clearing and dark green, thickened interveinal tissue type strain and the calico strain occurring in celery.
Disease cycle BLACKHEART

The virus is transmitted by many different aphid species
in a non-persistent, stylet-borne manner. Aphids can Introduction and significance
acquire the virus in less than a minute and transmit it Blackheart is a physiological disorder of celery that is
immediately, but they remain infective for only a few similar to tipburn of lettuce, spinach, and other leafy
hours. CMV is not reported to be seedborne in celery. vegetables. If environmental conditions favor develop-
ment of this abiotic disorder, significant quality loss
Control can take place. In addition, some pathogens such as
Control is difficult to achieve because of the numerous Sclerotinia sclerotiorum readily colonize blackheart-
sources of CMV in other crops and weeds, such as affected tissue, causing extensive decay and further
chickweed (Stellaria media). Follow general suggestions plant damage.
for managing virus diseases (see Part 1).
References Symptoms initially develop exclusively on the margins
Bruckart, W. L. and Lorbeer, J. W. 1976. Cucumber mosaic virus of developing leaf tips deep within the celery head. Such
in weed hosts near commercial fields of lettuce and celery. symptoms consist of light to dark brown speckling,
lesions, and necrosis. As the plant grows, the affected
Douine, L. and Devergne, J. C. 1979. Recensement des espèces
végétables sensibles au virus de la mosaïque du concombre foliage grows up and out of the inner plant whorl and
(CMV). Etudes bibliographiques. Annales de becomes visible. Leaf tips continue to die back and the
Phytopathologie 11:439–475.
brown tissue expands into the rest of the leaflets (67).
Lord, K .M., Epton, H. A. S., and Frost, R. R. 1988. Virus
infection and furcoumarins in celery. Plant Pathology
37:385–389. Causal factor
Pemberton, A. W. and Frost, R. R. 1986. Virus diseases of celery Blackheart develops when the margins of young leaves
in England. Annals of Applied Biology 108:319–331.
contain low calcium levels. Conditions that favor rapid
Tomlinson, J. A. and Carter, A. L. 1970. Studies on the seed
transmission of cucumber mosaic virus in chickweed plant growth may trigger this disorder. Such predispos-
(Stellaria media) in relation to the ecology of the virus. Annals ing conditions include warm temperatures and high
of Applied Biology 66:381–386. fertilization rates. Ascospores of the pink rot pathogen
(Sclerotinia sclerotiorum) can land on blackheart-
affected foliage and cause a soft, brown rot having
67 Blackheart 67
characteristic white mycelium and black sclerotia.
symptoms on
young celery Control
foliage. Plant celery cultivars that are not prone to blackheart.
Avoid applying excessive amounts of fertilizer, and
irrigate with drip irrigation systems. Drip irrigation
systems provide more even irrigation rates and help
reduce blackheart risk. Foliar calcium supplements
have limited benefit.
References
Gubbels, G. H. and Carolus, R. L. 1971. Influence of
A BIOTIC D ISORDERS
atmospheric moisture, ion balance, and ion concentration on

growth, transpiration, and blackheart of celery. Journal of the
American Society for Horticultural Science 96:201–204.
A PIACEAE 95
DAUCUS CAROTA (CARROT)
Xanthomonas campestris pv. carotae Causal agent

BACTERIAL LEAF BLIGHT Bacterial leaf blight is caused by the bacterium
Xanthomonas campestris pv. carotae. The pathogen
Introduction and significance can be isolated on standard microbiological media and
This common bacterial disease occurs in most carrot produces yellow, mucoid, slow growing colonies
producing areas. Damaging outbreaks are associated typical of most xanthomonads. The pathogen is host
with high rainfall or use of overhead irrigation. specific to carrot. Other bacterial problems of carrots
are postharvest soft rots of roots caused by Pseudo-
Symptoms and diagnostic features monas marginalis, P. viridiflava, Erwinia carotovora
The first symptoms of this disease are angular yellow ssp. carotovora, E. chrysanthemi, and other species.
leaf spots that later develop into irregularly shaped,
brown, water-soaked spots with yellow halos (68). Disease cycle
These lesions dry out and become brittle. Older lesions The pathogen is mostly dispersed between plants by
sometimes appear black. Lesions develop particularly splashing rain and overhead irrigation water, though
at the leaf margins. Formation of a gummy exudate and some spread occurs by insects and passing animals and
browning of the petioles also occurs. The pathogen can machinery. Considerable numbers of bacteria must be
cause lesions and a blight of the flower umbels and present on the leaf surface before symptoms occur.
flower stalks; a yellow exudate can ooze from such Xanthomonas campestris pv. carotae is seedborne but
lesions. Bacterial leaf blight symptoms may resemble also survives in soil in association with infested carrot
those of other foliar diseases of carrot such as Alternaria debris. The severity of epidemics is related to the
leaf blight and Cercospora leaf blight. Examination by amount of infested seed. Under Californian conditions,
microscope and lab analysis are required to differenti- 1 x 107 colony forming units/g seed are required for
ate these various foliar blights. severe epidemics to occur. Lower numbers of contami-
nated seed may still produce significant disease but
would require especially favorable temperatures and
rainfall. Optimum temperatures for disease develop-
ment are 25–30º C.
68
Control
pathogen. Grow seed crops in dry regions without
using overhead irrigation to reduce the risk of seed-
borne inoculum. Treat infected seed with hot water.
Copper sprays may partially reduce disease severity if
treatments are applied from an early stage of plant
development. Rotate carrots with non-susceptible
crops on a 2- or 3-year cycle to eliminate infested crop
debris.
References
Cubeta, M. A. and Kuan, T. L. 1986. Comparison of MD5 and
XCS media and development of MD5A medium for
detecting Xanthomonas campestris pv. carotae in carrot seed.
Phytopathology 76:1109.
68 Leaf spots of bacterial leaf blight of carrot.
Godfrey, S. A. C. and Marshall, J. W. 2002. Identification of cold- If carrot seedlings are infected shortly after
tolerant Pseudomonas viridiflava and P. marginalis causing
severe carrot postharvest bacterial soft rot during refrigerated emergence, as might be the case if inoculum is
export from New Zealand. Plant Pathology 51:155–162. seedborne or soilborne, such seedlings can die. Affected
Kuan, T.L., Minsavage, G. V., and Gabrielson, R. L. 1985. seedlings have a gray or black rot of the upper root at
Detection of Xanthomonas campestris pv. carotae in carrot
seed. Plant Disease 69:758–760.
soil level, similar to that caused by Pythium species.
Meng, X. Q., Umesh, K. C., Davis, R. M., and Gilbertson, R. L. There are, however, few reports of infected roots in
2004. Development of PCR-based assays for detecting harvested, stored carrots. Alternaria pathogens of other
Xanthomonas campestris pv. carotae, the carrot bacterial leaf
Apiaceae crops include A. petroselini and A. smyrnii on
blight pathogen, from different substrates. Plant Disease
88:1226–1234. celery and parsley, and A. selini on parsley.
Umesh, K. C., Davis, R. M., and Gilbertson, R. L. 1998. Seed
contamination thresholds for development of carrot bacterial Causal agent
blight caused by Xanthomonas campestris pv. carotae. Plant
Disease 82:1271–1275. Alternaria leaf blight is caused by Alternaria dauci.
Williford, R. E. and Schaad, N. W. 1984. Agar medium for Conidia of A. dauci are brown and club-shaped. The
selective isolation of Xanthomonas campestris pv. carotae main conidial body measures 50–100 x 12–24 μm, and
from carrot seeds. Phytopathology 74:1142. Abstract.
has seven to eleven transverse septa and one or more
longitudinal septa per segment. Each spore has one very
long, septate, hyaline or pale brown, apical beak that
Alternaria dauci measures 50–250 x 2–5μm.
ALTERNARIA LEAF BLIGHT
Introduction and significance 69

Alternaria leaf blight is one of the most important foliar
diseases of carrot and occurs worldwide. Severe
epidemics reduce carrot root size and yields, and addi-
tional losses occur when weakened and diseased foliage
cannot be pulled by top-lifting machines, leaving roots
in the ground. In European regions with cool climates,
serious epidemics only develop in seasons with above-
average rainfall.

Initial symptoms are greenish-brown, water-soaked,
angular spots (69). These spots become dark brown to
black and may have a yellow halo. Lesions often occur
on or near the edge of older leaflets. Extensive spotting
results in an overall general browning and yellowing of
the entire leaf. As lesions enlarge and coalesce, the leaf
may die. Severely affected crops exhibit large patches
where the foliage has a scorched or blighted appear-
ance. Dark, rectangular, elongated lesions are produced
on the petioles. The pathogen also affects flowers,
F UNGAL D ISEASES
bracts, and developing seeds in carrot seed plants.

Alternaria leaf blight symptoms may resemble those of
other foliar diseases of carrot such as bacterial leaf
blight and Cercospora leaf blight. Examination by
microscope and lab analysis are required to differenti-
ate these various foliar blights. 69 Leaf spots of Alternaria leaf blight of carrot.
A PIACEAE 97
Disease cycle References

Spores can germinate in 2 hours on wet leaves and Ben-Noon, E., Shtienberg, D., Shlevin, E., and Dinoor, A. 2003.
infect via stomata. Sporulation and infection can occur Joint action of disease control measures: a case study of
Alternaria leaf blight of carrot. Phytopathology
over a broad temperature range (8–30º C), though the 93:1320–1328.
optimum is 25º C. Completion of the disease cycle from Ben-Noon, E., Shtienberg, D., Shlevin, E., Vintal, H., and Dinoor,
infection to sporulation requires only 8 to 10 days, A. 2001. Optimization of chemical suppression of Alternaria
dauci, the causal agent of Alternaria leaf blight of carrot.
which allows epidemics to develop rapidly. The Plant Disease 85:1149–1156.
pathogen is seedborne and is found in the seed mericarp Chelkowski, J. and Visconti, A. (eds). 1992 .Topics in Secondary
and on the seed surface. It can survive on seed for Metabolism – Volume 3. Alternaria: Biology, Plant Diseases
several years and on plant debris for several months. and Metabolites. Elsevier, Amsterdam, 573pp.
Farrar, J. J., Pryor, B. A., and Davis, R. M. 2004. Alternaria
Infested crop residues may be an important source of diseases of carrot. Plant Disease 88:776–784.
inoculum, especially if carrots are grown in successive Gillespie, T. J. and Sutton, J. C .1979. A predictive scheme for
years. Where adjacent crops are grown sequentially, timing fungicide applications to control Alternaria leaf blight
there can be significant spread of wind-borne inocula of carrots. Canadian Journal of Plant Pathology 1:95–99.
Maude, R. B. 1966. Studies on the etiology of black rot,
from the older to the newer crop. Stemphylium radicinum (Meir, Drechsl & Eddy) Neerg., and
leaf blight, Alternaria dauci (Kuhn) Groves & Skolko, on
Control carrot crops; and on fungicide control of their seedborne
infection phases. Annals of Applied Biology 57:83–93.
Maude, R. B., Drew, R. L. K., Gray, D., Petch, G. M., Bujalski,
pathogen. Where there is a low level of seedborne W., and Nienow, A. W. 1992. Strategies for control of seed-
infection, treat carrot seed with hot water or fungicides. borne Alternaria dauci (leaf blight) of carrots in priming and
The development of fungicide-resistant strains has process engineering systems. Plant Pathology 41:204–214.
Netzer, D. and Kenneth, R. G. 1969. Persistence and
reduced the effectiveness of dicarboximide seed treat- transmission of Alternaria dauci (Kuhn) Groves & Skolko in
ments. Because carrot cultivars differ in susceptibility, semi-arid conditions in Israel. Annals of Applied Biology
plant those having more tolerance or resistance. Reduce 63:289–294.
soilborne infection by rotating carrots with non-hosts. Pryor, B. M., Strandberg, J. O., Davis, R. M., Nunez, J. J., and
Gilbertson, R. L. 2002. Survival and persistence of Alternaria
Avoid placing newer carrot fields adjacent to older, dauci in carrot cropping systems. Plant Disease
possibly diseased fields. Regularly monitor carrot crops 86:1115–1122.
for Alternaria leaf blight symptoms and apply fungi- Strandberg, J. O. 1977. Spore production and dispersal of
Alternaria dauci. Phytopathology 67:1262–1266.
cides in a timely manner. A predictive scheme for
Strandberg, J. O. 1987. Isolation, storage and inoculum
Alternaria leaf blight management has been developed production for Alternaria dauci. Phytopathology
in Canada. This system uses leaf-wetness duration and 77:1008–1012.
temperature to calculate infection indices. These indices Strandberg, J. O. 1988. Establishment of Alternaria leaf blight on
carrots in controlled environments. Plant Disease 72:
indicate risk of slight, moderate, or severe infection. For 522–526.
example, severe infection is likely with greater than 72 Strandberg, J. O. 1988. Detection of Alternaria dauci on carrot
hours leaf wetness at 7º C, or greater than 12 hours leaf seeds. Plant Disease 72:531–534.
wetness at 16–20º C. The use of infection indices will Wijnheijmer, E. H. M., Brandenburg,W. A., and Ter Borg, S. J.
1990. Interaction between wild and cultivated carrots
require validation for local conditions. Gibberellic acid (Daucus carota L.) in the Netherlands. Euphytica
has been used to stimulate carrot foliar growth and may 40:147–154.
be another means for managing Alternaria leaf blight. Zimmer, R.C. and McKeen, W. 1969. Interaction of light and
temperature on sporulation of carrot foliage pathogen
Alternaria dauci. Phytopathology 59:743–749.
F UNGAL D ISEASES
Alternaria radicina Symptoms and diagnostic features

BLACK ROT Initial symptoms are small, brown leaf spots having
chlorotic halos that later enlarge to form black lesions.
Introduction and significance These lesions are similar to those caused by Alternaria
Although this disease is important as a storage disease dauci, though they tend to be more prominent and
of carrots, it also causes seedling damping-off, foliar cause dark brown or black lesions at the base of the
and crown infection, and an umbel blight. Occasionally petiole. Emerging seedlings show weakening and black-
extensive crop loss occurs, though the importance of ening of the crowns and upper roots (70). In the field,
black rot has decreased where carrots are maintained crown symptoms usually consist of black lesions that
and stored in situ in the field rather than harvested and extend below soil level (71, 72, 73). Secondary black
kept in cold storage. Black rot is found in all the main lesions also develop on the taproot, particularly if there
carrot-production areas. The disease also affects other is any splitting or damage. In postharvest storage,
important Apiaceae crops such as parsnip. A. radicina causes dry, black, sunken lesions that have
sharply defined margins. Root-to-root spread can occur
during prolonged storage.
70 72
70 Weakened carrot crowns caused by black rot. 72 Blackening of internal carrot crown and upper root
tissue caused by black rot.
71 73
F UNGAL D ISEASES
71 Diseased carrot crown affected by black rot. 73 Black rot symptoms on parsnip.
A PIACEAE 99
Causal agent References

Black rot is caused by the fungus Alternaria radicina. Benedict, W. G. 1977. Effect of soil temperature on the pathology
The spores of A. radicina are borne singly or in chains of Alternaria radicina on carrots. Canadian Journal of Botany
55:1410–1418.
of two, are ellipsoid to oval, measure 20–50 x 10–25
Chelkowski, J. and Visconti, A. (eds), 1992. Topics in Secondary
μm, and have seven to eight lateral septa. Each spore Metabolism – Volume 3. Alternaria: Biology, Plant Diseases
may also have one or two longitudinal septa per and Metabolites. Elsevier, Amsterdam, 573pp.
segment. The conidia lack the long beaks of many other Farrar, J. J., Pryor, B. A., and Davis, R. M. 2004. Alternaria
diseases of carrot. Plant Disease 88:776–784.
Alternaria species. Alternaria radicina also affects the
Maude, R. B. 1966. Studies on the etiology of black rot,
crowns, petiole bases, and roots of celery and celeriac, Stemphylium radicinum (Meir, Drechsl & Eddy) Neerg., and
and causes foliar symptoms in caraway, dill, fennel, leaf blight, Alternaria dauci (Kuhn) Groves & Skolko, on
carrot crops; and on fungicide control of their seedborne
parsley, and parsnip. infection phases. Annals of Applied Biology 57:83–93.
Pryor, B. M. and Gilbertson, R. L. 2001. A PCR-based assay for
Disease cycle detection of Alternaria radicina on carrot seed. Plant Disease
Alternaria radicina is commonly seedborne and is 85:18–23.
Pryor, B. M., Davis, R. M., and Gilbertson, R. L. 1994. Detection
found on the surface and in the pericarp and testa of and eradication of Alternaria radicina on carrot seed. Plant
seed. The pathogen survives in crop residues and also Disease 78:452–456.
persists in the soil in the absence of debris for at least 8 Pryor, B. M., Davis, R. M., and Gilbertson, R. L. 1998. Detection
years. A. radicina produces microsclerotia that function of soil-borne Alternaria radicina and its occurrence in
California carrot fields. Plant Disease 82:891–895.
as survival structures. Disease development is favored Pryor, B. M., Davis, R. M., and Gilbertson, R. L. 2000. A
by warm (greater than 20º C) temperatures and toothpick inoculation method for evaluating carrot cultivars
prolonged wet conditions. Growth of this pathogen for resistance to Alternaria radicina. HortScience
35:1099–1102.
occurs over the range -0.5–30 ºC, but optimum tem-
perature is 28 ºC. Crops can be affected at any stage,
but senescent leaves are most susceptible. Infections on
petioles are followed by crown infections.
Control
pathogen. For low levels of seed infection, treat with hot
water or fungicides. Plant resistant cultivars. Implement
crop rotations to reduce soilborne inoculum. Foliar
fungicides used for Alternaria leaf blight should have
some effect on the spread of black rot, but specific rec-
ommendations for field use have not been developed.
For stored crops, carefully handle carrots during har-
vesting and washing to avoid damage to roots.
Maintain cool temperatures (0–1 ºC) and high relative
humidity during storage.
F UNGAL D ISEASES
Athelia arachnoidea Causal agent

(anamorph = Rhizoctonia carotae) Crater rot is caused by the fungus Rhizoctonia carotae.
CRATER ROT The hyphae of R. carotae are hyaline and narrower
(4–5 μm) than most other Rhizoctonia spp. and have
Introduction and significance clamp connections at most septa. Indeed, because of
This problem is a storage disease of carrots, but little is these morphological characters, this stage of the
known about its activity in fields. Most records of this pathogen is not considered a true Rhizoctonia species.
disease are from western Europe and North America. The fungus forms sclerotia that initially are white but
This disease should not be confused with crater spot of later mature and are brown, measure 1–3 mm diameter,
celery that is caused by Rhizoctonia solani. and consist of aggregates of mycelium. The sclerotia are
produced in clusters on the surface of the carrot. The
Symptoms and diagnostic features role of the basidiomycete perfect stage, Athelia arach-
Typical symptoms develop after several weeks of low noidea, in disease development is not known.
temperature storage and consist of small, 5–10 mm in
diameter, sunken lesions or pits on the carrot surface. Disease cycle
Over time the root develops patches of white, flattened Mycelium spreads from root to root even in cold
mycelium (74). Brown sclerotia may also form on the storage (1–3º C). High humidity and free moisture
stored carrot. Secondary bacterial rots and gray mold favors disease development. The pathogen is soilborne
may develop on affected roots and lead to general and some infection is thought to occur in the field prior
breakdown and soft rot of roots. to harvest. Mycelium on the crown or roots is thought
to initiate infection during cold storage. The pathogen
is also able to survive in wooden storage bins.
74
Control
Carefully handle and wash carrots prior to cold storage.
Maintain sufficiently cold temperatures, but avoid
overly wet storage conditions. Disinfest storage con-
tainers; line with polyethylene liners. Careful monitor-
ing of carrots in storage will allow problems to be
detected at an early stage and affected crops to be
removed before serious problems develop.
References
Adams, G. C. and Kropp, B. R. 1996. Athelia arachnoidea, the
sexual state of Rhizoctonia carotae, a pathogen of carrot in
cold storage. Mycologia 88:459–472.
Derbyshire, D. M. and Crisp, A. F. 1978. Studies on treatments to
prolong storage life of carrots. Experimental Horticulture
30:23–28.
Jensen, A. 1971. Storage diseases of carrots, especially
Rhizoctonia crater rot. Acta Horticulturae 20:125–129.
Punja, Z. K. 1987. Mycelial growth and pathogenesis by
Rhizoctonia carotae on carrot. Canadian Journal of Plant
F UNGAL D ISEASES
Ricker, M. D. and Punja, Z. K. 1991. Influence of fungicide and

chemical salt dip treatments on crater rot caused by
Rhizoctonia carotae in long term storage. Plant Disease
75:470–474.
74 Crater rot of stored carrots showing white fungal

growth.
A PIACEAE 101
Athelia rolfsii (anamorph = Sclerotium rolfsii) White stringy mycelium forms on infected roots (75)
SOUTHERN BLIGHT and also on adjacent soil. Small (1–2 mm diameter),
brown, spherical sclerotia appear on infected tissues
Introduction and significance and mycelium. Sclerotia are produced in 5 to 6 days
Southern blight is important on a wide range of culti- when temperatures are optimal (27–30º C). Plant-to-
vated plants, including Apiaceae vegetables such as plant spread occurs when the mycelium grows over the
carrot, celery, parsley, and parsnip. It is most damaging soil surface and contacts adjacent plants.
in tropical and sub-tropical regions. Southern blight is
of limited importance in southern Europe and is not Causal agent
established in the UK. Southern blight is caused by the soilborne pathogen
Athelia rolfsii. This basidiomycete fungus is usually
Symptoms and diagnostic features present in the field in its anamorph stage, Sclerotium
This pathogen can cause water-soaked leaf lesions if rolfsii; the role of the basidiomycete stage in disease
foliage is in contact with the soil, leading to yellowing development is not clear. Sclerotium rolfsii produces
and wilting of foliage. Direct infection of the carrot root abundant white mycelium, and hyphae have clamp
is more important and results in a pale brown, soft rot connections. The diagnostic spherical, tan to light
of the taproot. In advanced stages of the disease, the brown sclerotia form readily in culture. Basidiospores
woody core of the root may be pulled out of the ground may be produced by some isolates, are hyaline and
or the whole root may rot away, leaving a hole in the measure 6–12 x 1.0–1.7 μm.
ground that is lined with mycelium and root tissue.
Disease cycle
The pathogen is soilborne and can survive for many
years in soil as sclerotia. S. rolfsii is a soil saprophyte
75
and can colonize organic substrates. Disease occurs
when temperatures are above 15º C. Wet conditions
and acid soils are conducive to disease development.
Control
Implement crop rotation, though this strategy will be
only partially effective because of the wide host range
and soilborne nature of this pathogen. Growing veg-
etables during the cooler months may reduce damage.
Fungicides and soil amendments are generally not very
effective. Soil fumigation and heat treatments can be
effective and may be affordable for high value crops.
References
Gurkin, R. S. and Jenkins, S. F. 1985. Influence of cultural
practices, fungicides, and inoculum placement on southern
blight and Rhizoctonia crown rot of carrot. Plant Disease
69:477–481.
Okabe, I. and Matsumoto, N. 2003. Phylogenetic relationship of
Sclerotium rolfsii (teleomorph Athelia rolfsii) and S. delphinii
based on ITS sequences. Mycological Research 107:164–168.
F UNGAL D ISEASES
Punja, Z. K. 1985. The biology, ecology and control of

Sclerotium rolfsii. Annual Review of Phytopathology
23:97–127.
Punja, Z. K., Carter, J. D., Campbell, G. M., and Rossell, E. L.
1986. Effects of calcium and nitrogen fertilizers, fungicides,
75 Mycelium and sclerotia on carrot root infected with
and tillage practices on incidence of Sclerotium rolfsii on
southern blight. processing carrots. Plant Disease 70:819–824.
Cercospora carotae with a paler center (77). Severely blighted foliage is

CERCOSPORA LEAF BLIGHT weakened and snaps off during mechanical harvesting.
In seed crops, early infection may prevent seed devel-
Introduction and significance opment, while later infection results in infested seed.
This is one of the more important foliar diseases of The pathogen does not infect carrot roots. Cercospora
carrots, particularly in parts of North America. leaf blight symptoms may resemble those of other foliar
Cercospora leaf blight was first confirmed in the UK in diseases of carrot such as bacterial leaf blight and
2005. Yield losses occur because of early damage to Alternaria leaf blight. Examination by microscope and
foliage and when weakened and diseased foliage cannot lab analysis are required to differentiate these various
be pulled by top-lifting machines, leaving carrot roots foliar blights.
in the ground.
Causal agent
Symptoms and diagnostic features Cercospora leaf blight is caused by the fungus
The first symptoms are small necrotic leaf flecks that Cercospora carotae. The pathogen produces hyaline,
measure 1–3 mm in diameter and tend to be angular in multicelled, filiform spores that measure 40–110 x 2.2–
shape (76). These small flecks enlarge to form gray to 2.5 μm and are borne on clusters of brown conidio-
tan spots (3–5 mm diameter) having chlorotic halos. As phores. Sporulation on the lesions causes these spots to
lesions increase in number and coalesce, leaves can take on a pale gray appearance. This pathogen appears
wither and die. Petiole lesions are elliptical and brown to be host specific to carrot and other Daucus species.
77 Petiole lesions
76 77
of Cercospora leaf
blight of carrot.
F UNGAL D ISEASES
76 Leaf spots of Cercospora leaf blight of carrot.

A PIACEAE 103
Disease cycle Erysiphe heraclei, Leveillula spp.

The pathogen grows over the temperature range POWDERY MILDEW
7–37º C, with an optimum of 19–28º C. Spore germi-
nation requires a minimum 12 hours of leaf wetness at Introduction and significance
20–30º C. The optimum temperature for infection is Powdery mildews are commonly found on many
28º C. Spores penetrate leaves via stomata and Apiaceae plants. Erysiphe heraclei infects carrot, celery,
symptoms appear in as few as three days under ideal chervil, dill, parsley, and parsnip (see also pages 118 and
conditions, usually occuring first on the younger 126). Leveillula lanuginosa or L. taurica has been
foliage. Young leaves of late planted crops are particu- reported from warmer regions in the Mediterranean,
larly susceptible to inoculum from older nearby crops. Asia, and Africa on carrot, caraway, celery, coriander,
Seed, infested carrot debris, and wild Daucus plants are dill, fennel, and parsley. In western Europe, attacks
potential inoculum sources. Spores are airborne and show considerable seasonal variation and are often of
also dispersed by rain or overhead irrigation. limited importance. In Mediterranean countries, early
attacks are more important and can cause significant
Control yield losses.
pathogen. Rotate carrots so that infected crop residues Symptoms and diagnostic features
decay. Plant resistant cultivars. Use fungicides if The first signs of powdery mildew caused by E. heraclei
available. Research indicates that fungicide treatments usually appear on the older leaves and consist of
should be initiated when 50% of the middle leaves are scattered white colonies having superficial, radiating
affected; additional applications are needed at 7–10-day fungal growth typical of most powdery mildews (78).
intervals if the temperature exceeds 16º C and leaf Subsequently the younger leaves become affected and
wetness exceeds 12 hours. general colonization of the leaf surface ensues. Severe
infection causes some leaf twisting and deformity and
References early senescence of the foliage. For powdery mildew
Carisse, O. and Kushalappa, A. C. 1992. Influence of interrupted caused by Leveillula species, symptoms are angular,
wet periods, relative humidity, and temperature on infection chlorotic leaf spots. White sporulation usually occurs
of carrots by Cercospora carotae. Phytopathology 82:
602–606. mainly on the corresponding undersides of these spots.
Carisse, O., Kushalappa A. C., and Cloutier, D. D. 1993.
Influence of temperature, leaf wetness, and high relative
humidity duration on sporulation of Cercospora carotae on
carrot leaves. Phytopathology 83:338–343.
78
Carisse, O. and Kushalappa, A. C. 1990. Development of an
infection model for Cercospora carotae on carrot based on
temperature and leaf wetness duration. Phytopathology
80:1233–1238.
Kushalappa, A. C., Boivin, G. and Brodeur, L. 1989. Forecasting
incidence thresholds of Cercospora blight in carrots to initiate
fungicide application. Plant Disease 73:979–983.
F UNGAL D ISEASES
78 Powdery mildew of carrot infected by Erysiphe

heraclei.
Causal agents Control

Erysiphe heraclei is an ectophytic powdery mildew with Maintain good crop growth through adequate fertilizer
cylindrical conidia measuring 25–45 x 12–21 μm and and irrigation programs. Mulching may reduce drought
borne singly. Cleistothecia are not always observed, but stress and likewise reduce powdery mildew severity. Use
when present measure 80–120 μm, have long coralloid resistant cultivars when available. Fungicides such as
appendages, and enclose asci with three to five asco- sulfur or triazole products may be effective.
spores. Each ascospore is 18–30 x 10–16 μm. In
contrast, Leveillula species are endophytic powdery References
mildews. Because the Leveillula perfect stage is Citrulli, M. 1975. The powdery mildew of parsley caused by
sometimes not observed, the fungus is often called by its Leveillula lanuginosa. Phytopathologia Mediterranea
14:94–99.
conidial anamorph name (Oidiopsis). Leveillula lanug-
Koike, S. T. and Saenz, G. S. 1994. Occurrence of powdery
inosa has cylindrical conidia measuring 40–80 x 13–20 mildew on parsley in California. Plant Disease 78:1219.
μm with distinctive swellings near each end of the spore. Koike, S. T. and Saenz, G. S. 1997. First report of powdery
Cleistothecia of this species measure 170–250 μm and mildew caused by Erysiphe heraclei on celery in North
America. Plant Disease 81:231.
have short hyaline or yellow appendages and numerous
Netzer, D. and Katzir, R. 1966. Combined control of Alternaria
asci with two ascospores (30–35 x 15–20 μm). blight and powdery mildew in carrot. Plant Disease Reporter
Leveillula taurica forms lanceolate primary conidia 50:594–595.
(30–80 x 12–22 μm) and more cylindrical secondary Palti, J. 1975. Erysiphaceae affecting umbelliferous crops, with
special reference to carrot, in Israel. Phytopathologia
conidia; its cleistothecia are 140–250 μm in diameter Mediterranea 14:87–93.
with short hyaline or light brown appendages and Soylu, E. M. and Soylu, S. 2003. First report of powder mildew
contain asci with two ascospores (25–40 x 15–23 μm). caused by Erysiphe heraclei on dill (Anethum graveolens) in
Turkey. Plant Pathology 52:423.
Disease cycle
The disease cycle can be completed in 7 days under
optimum conditions. High humidity and moderate
temperatures favor infection. Crops become more sus-
ceptible with age and carrots become more susceptible
7 weeks after planting. Disease severity is increased by
drought stress and is reduced by rain or overhead irri-
gation. The Leveillula pathogens are mainly associated
with dryer production areas. If cleistothecia are
produced, these structures enable pathogen survival
between crops. The cleistothecia have been recorded as
contaminants in carrot seed, but it is not known if seed
transmission occurs. There may be some host special-
ization, but isolates appear to be able to infect a number
of host species. Wild and volunteer Apiaceae species
and weeds are potential sources of conidial inoculum.
Growing powdery mildew hosts throughout the year
enables the pathogen to survive and spread from crop
to crop.
F UNGAL D ISEASES
A PIACEAE 105
Helicobasidium brebissonii Symptoms and diagnostic features

(anamorph = Rhizoctonia crocorum) Patches of severely affected carrots may appear in early
VIOLET ROOT ROT autumn when the foliage turns yellow and wilts. Dense,
felted, purple to white fungal growth may be present on
Introduction and significance the crowns of affected plants and also on soil surfaces
This disease occurs worldwide and is an important adjacent to such plants (79). Soil adheres to roots when
problem of carrot in Europe, New Zealand, Tasmania, they are harvested and an extensive, dark purple
and parts of North America. The pathogen has a wide mycelial growth is present on the surface of affected
host range and affects other major crops such as sugar roots (80, 81). Severely affected roots usually exhibit
beet, potato, and asparagus. Of vegetable root crops, some soft rot symptoms due to secondary decay
carrot is perhaps the most susceptible to violet root rot. organisms. More typically, violet root rot is detected on
Other Apiaceae vegetables can be affected and include washed roots of plants having healthy foliage (82). The
parsley, parsnip, and celeriac in the UK. Affected roots affected roots show patches of purplish black mycelium
are unmarketable and even slight infection can induce and small dark spots that are 150–200 μm in diameter.
an unpleasant flavor to the commodity. These spots are infection cushions that form after host
79 81
79 Growth of violet root rot pathogen around carrot 81 Violet root rot of parsnip.
crown.
80 82
F UNGAL D ISEASES
80 Violet root rot of carrot. 82 Severe violet root rot on parsley roots.
penetration. When large areas of the root have been and bindweed (Convolvulus spp.) are important
colonized, the dense fungal growth on washed roots has alternate hosts. There are some reports that grass
a leathery appearance. Mycelial growth is slow, so weeds, clover, and alfalfa are also hosts. The production
fungal signs are rarely found on young seedlings. of other vegetable crops may contribute to soil
inoculum. These crops include asparagus, bean, beet,
Causal agent celery, crucifers, fennel, rhubarb, and sweet potato.
Violet root rot is caused by the basidiomycete fungus Rapid disease development is associated with mild con-
Helicobasidium brebissonii. The anamorph is tradi- ditions in autumn. The pathogen is active over a wide
tionally named Rhizoctonia crocorum, though recent range of temperatures (5–30º C) and has a temperature
taxonomic research may result in a name change. optimum of 20º C.
Rhizoctonia crocorum is the primary stage that causes
the disease and produces coarse mycelial strands (up to Control
1 mm diameter) that enables it to spread through soil Rotate crops using non-host plants. In the UK, a
and infect new host plants. Sclerotia form mainly rotation of 3 to 4 years between root crops seems to
around the small lateral roots and are usually less than provide satisfactory control for this disease on sugar
5 mm in diameter. The presence of dark violet brown beet. However, longer rotations may be required for
pigmentation and a hyphal diameter of 4–8 μm carrots. Practice thorough weed control, particularly
separates this pathogen from R. solani, which has for perennial weeds. When violet root rot is detected in
brown hyphae that measure 5–10 μm. H. brebissonii is a crop, harvest the crop early to prevent further spread
slow-growing and difficult to isolate. Attempt isolations and losses. Crop residues and wash water from packing
by placing tissues from actively developing lesions onto houses can harbor the pathogen; do not return these
malt extract agar. The Helicobasidium perfect stage materials to land scheduled for carrot production. The
usually produces basidiospores only in the spring. pathogen may also survive animal digestive systems and
There are taxonomic and etiological questions be carried in manure from stock fed on diseased roots.
regarding Helicobasidium isolates from different parts Avoid moving infested soil between fields by thorough-
of the world. Some research indicates that H. mompa ly cleaning farm machinery after operations in infested
(from east Asia and pathogenic on apple and other fields. For acid soils, apply lime to raise soil pH to about
woody and herbaceous plants), H. compactum (from 7.0. Resistant cultivars are not available.
tropical and sub-tropical regions and synonymous with
H. mompa), and H. brebissonii ([= H. purpureum] References
from Europe and North America) may all be one Asher, M. 2001. Root rots: is there a problem? British Sugar Beet
species. In England, this hypothesis is supported by Review 69:18–21.
Dalton, I. P., Epton, A. S., and Bradshaw, N. J. 1981. The
observations that violet root rot could be detected on
susceptibility of modern carrot cultivars to violet root rot
carrots grown in an apple orchard that was infected caused by Helicobasidium purpureum. Journal of
with violet root rot. Recent molecular studies indicate Horticultural Science 56:95–96.
that Helicobasidium is involved in a complex life cycle Lutz, M., Bauer, R., Begerow, D., and Oberwinkler, F. 2004.
Tuberculina –Thanatophyton/Rhizoctonia crocorum –
with Tuberculina species, which are parasites of rust Helicobasidium: a unique mycosparasitic-phytoparasitic life
fungi. The Helicobasidium/Rhizoctonia crocorum strategy. Mycological Research 108:227–238.
organism appears to be a stage in the life cycle of Moore, R. T. 1987. The genera of Rhizoctonia-like fungi:
Ascorhizoctonia, Ceratorhiza gen. nov., Epulorhiza gen. nov.,
Tuberculina. Moniliopsis, and Rhizoctonia. Mycotaxon 29:91–99.
Uetake, Y., Arakawa, M., Nakamura, H., Akahira, T., Sayama,
Disease cycle A., Cheah, L.H., Okabe, I., and Matsumoto, N. 2002.
F UNGAL D ISEASES
This pathogen is soilborne and occurs where root crops Genetic relationships among violet root rot fungi as revealed
by hyphal anastomosis and sequencing of the rDNA ITS
have been grown intensively. It is capable of long-term regions. Mycological Research 106:156–163.
survival and disease can recur after a 10 to 20 year Valder, P.G. 1958. The biology of Helicobasidium purpureum
absence of root crops. The fungus survives by means Pat. Transactions of the British Mycological Society
41:283–308.
of sclerotia and weed hosts. Perennial weeds such
as sowthistle (Sonchus spp.), thistles (Cirsium spp.),
A PIACEAE 107
Mycocentrospora acerina Disease cycle

LICORICE ROT The fungus survives in soil for at least two years by
means of chlamydospores. Mycocentrospora acerina
Introduction and significance may persist in soil longer when other susceptible hosts
Licorice rot is a storage disease of carrot and celery in are present. It has a wide host range of over 90 species,
temperate regions. The same pathogen also causes including crops such as beet, pea, and many common
black canker on parsnip and anthracnose of caraway. weeds. It can infect plants at all stages of growth and is
In the field, the licorice-rot pathogen can occasionally saprophytic on decaying plant residues. The fungus is
be found growing in large root lesions caused by cavity favored by cool conditions, and solar radiation inhibits
spot. In the UK, its importance has declined as carrots spore production. Chlamydospores on the surface of
are now frequently maintained and stored in situ under flooded soil can produce conidia that are then dispersed
straw in the field rather than harvested and kept in cold by water movement. There is little spread in storage and
storage. intact tissues are resistant to infection. Inoculum may
spread during postharvest rinsing if wash water is not
Symptoms and diagnostic features adequately chlorinated and changed.
Symptoms usually develop around the crown or root
tips after 5 to 6 weeks of storage, but may occur on Control
other parts of the taproot. Infected areas consist of Rotate carrots and other Apiaceae crops with non-host
watery, dark brown, or black lesions that are sunken plants on a 3- to 4-year cycle. Carefully handle carrots
and penetrate deep into the root (83). Lesions do not during harvesting and washing procedures. Store
have a discrete margin, unlike those caused by carrots in clean, cool, and humid conditions. For
Alternaria radicina, and rotted tissues usually contain carrots with wounds, a short incubation period of high
diagnostic chains of chlamydospores. On celery, the temperatures and high humidity prior to long-term
symptoms are sunken, elongated, black lesions at the storage should be beneficial.
base of the petioles and are referred to as black crown
rot. On various hosts including carrot, this pathogen
also causes dark brown or black leaf lesions that are
similar to those caused by various other pathogens.
Causal agent
Licorice rot is caused by the fungus Mycocentrospora
acerina. The pathogen produces distinctive conidia that
measure 60–250 x 10–12 μm, are needle-shaped, 83
strongly curved, and have whip-like terminal
appendages and lateral appendages (resembling a germ
tube) on the basal cell. The conidia have 4 to 24 trans-
verse septa. Conidia usually form under humid condi-
tions during storage. Their production under field
conditions is stimulated by rainfall and occurs over a
wide range of temperatures (2–25º C). Conidia are
dispersed by splashing water over short distances,
usually less than 9 meters. Hyphae are hyaline, but may
F UNGAL D ISEASES
appear pinkish when developing on lesions under damp

conditions. The chlamydospores are ovate to spherical,
dark brown, thick-walled single cells measuring
15–20 μm and produced within the mycelium.
83 Licorice rot canker on parsnip root.

References Pythium violae, P. sulcatum

Davies, W. P. and Lewis, B. G. 1980. The inter-relationship CAVITY SPOT
between the age of carrot roots at harvest and infection by
Mycocentrospora acerina in storage. Annals of Applied
Biology 95:11–17. Introduction and significance
Davies, W. P., Lewis, B. G., and Day, J. R. 1981. Observations on Cavity spot is an important disease of carrots in Europe,
infection of stored carrot roots by Mycocentrospora acerina. Australia, USA, and other temperate regions. The
disease results in regular and significant economic
Day, J. R., Lewis, B. G., and Martin, S. 1972. Infection of stored
celery plants by Centrospora acerina. Annals of Applied losses. Modest infection levels of 10 to 20% affected
Biology 71:201–210. roots can lead to rejection of the entire harvest because
Derbyshire, D. M. and Crisp, A. F. 1978. Studies on treatments to it is not economically feasible to remove diseased roots
prolong storage life of carrots. Experimental Horticulture
30:23–28.
on the grading line. Cavity spot has been recognized
Evenhuis, A. 1997. Effect of root injury on lesion development of since 1961 when it was described on carrot and parsnip
caraway roots infected by Mycocentrospora acerina. in the USA. However, the cause of the problem
European Journal of Plant Pathology 103:537–544. remained unidentified until the late 1980s.
Evenhuis, A., Verdam, B. and Zadoks, J. C. 1997. Splash
dispersal of conidia of Mycocentrospora acerina in the field.
Plant Pathology 46:459–469. Symptoms and diagnostic features
Hermansen, A .1992. Weeds as hosts of Mycocentrospora Symptoms are usually first detected about 12 weeks
acerina. Annals of Applied Biology 121:679–686. after planting. The first symptoms are small, pale
Le Cam, B., Rouxel, F., and Villenueve, F. 1993. Post-harvest
pathogens on cold stored carrots: Mycocentrospora acerina,
yellow or water-soaked elliptical spots on the root
the major spoilage fungus. Agronomie 13:125–133. surface. A section through such lesions will reveal a
Lewis, B. G., Davies, W. P., and Garrod, B. 1981. Wound-healing small cavity just a millimeter or so below the periderm,
in carrot roots in relation to infection by Mycocentrospora or outer skin of the root. Cavity spot infections are par-
acerina. Annals of Applied Biology 99:35–42.
Wall, C. J. and Lewis, B. G. 1978. Quantitative studies on
ticularly evident when there has been rotting and disin-
survival of Mycocentrospora acerina conidia in soil. tegration of the surface layer of the lesion, revealing an
Transactions of the British Mycological Society 71:143–146. open sunken cavity that usually ranges from 4 – 13 mm
Wall, C. J. and Lewis, B. G. 1980. Infection of carrot leaves by wide. If roots are washed carefully before examination,
Mycocentrospora acerina. Transactions of the British
Mycological Society 75:163–165. the cavity spot lesion may still have remains of the
Wall, C. J. and Lewis, B. G. 1980. Survival of chlamydospores periderm over or around the edge of the lesion (84).
and subsequent development of Mycocentrospora acerina in
soil. Transactions of the British Mycological Society
75:207–211.
84
F UNGAL D ISEASES
84 Carrot roots showing periderm tissue extending

over cavity spot lesions.
A PIACEAE 109
Cavity spot lesions often have a grayish or black 85 Root lesions of

85
margin (85, 86). Lesions increase in size as secondary cavity spot of
organisms colonize damaged tissue and may become carrot.
several centimeters in diameter. Diagnosis of cavity spot
can be complicated by the presence of a number of soil
fungi in the lesions, including Pythium intermedium,
P. sylvaticum, Fusarium spp. and Cylindrocarpon
destructans. As lesions enlarge and coalesce, large areas
of the root may be covered with a shallow, soft rot.
On parsnip, lesions referred to as cavity spot are
small, slightly sunken, and red-brown. When lesions are
sectioned, the red-brown discoloration of the tissue
penetrates several millimeters into the root. Lesions
penetrate deeper in parsnip than carrot roots because
parsnip roots do not produce a wound reaction that
limits fungal invasion. Formal confirmation of a cavity
spot pathogen for parsnip is still needed. However,
because experiments demonstrated that metalaxyl 86 Close-up of 86
treatments controlled cavity spot symptoms on parsnip, root lesions of
it was believed that an oomycete pathogen may be cavity spot of
involved. carrot.
Causal agent
Cavity spot is caused by the soil oomycetes Pythium
violae and P. sulcatum. Pythium violae is often the
dominant pathogen, though P. sulcatum is important at
some sites. Both pathogens are slow-growing in culture
and difficult to isolate unless cavity spot lesions are
young. Corn meal agar containing pimaricin (100 mg
/liter) and rifampicin (= rifamycin; 30 mg/liter) is a
useful medium for isolating these organisms. In culture,
P. violae grows slowly at 5 to 7 mm per day at 25º C; in
contrast, non-pathogenic, fast growing Pythium species
can grow at rates of 25 to 30 mm per day at 25º C.
Oogonia of P. violae average 29.5 μm diameter (range
16–34 μm), with the inner oospores measuring 11–28 Disease cycle
μm. Pythium sulcatum produces aplerotic oospores After P. violae initiates root infection, the pathogen
averaging 14.5 μm diameter. Pythium violae has a grows within the carrot root for 3 to 4 days before a
wider host range than P. sulcatum and affects common host resistance reaction is stimulated and wound
weeds, ryegrass, and wheat. This wide host range periderm tissue, containing lignin and suberin, is
appears to explain observations that cavity spot can formed beneath the lesion. This results in a dark discol-
occur even if there is no history of carrot production. oration around the edge of the cavity spot lesion.
F UNGAL D ISEASES
87
timing is critical, so apply fungicides at planting or
shortly after crop emergence. Applications made later
than 6 weeks after planting are less effective. However,
there are recent indications of rapid breakdown of
metalaxyl in soil, resulting in lack of acceptable control.
Avoid planting carrots in sites with poor drainage.
Irrigate carrots carefully so that flooding and excess
water do not occur. Avoid sites with acid soil pH, or
amend such soils by applying calcium carbonate lime
and adjusting soil pH to 7–7.5. Deep cultivation
between carrot rows has reduced cavity spot develop-
ment in some situations. Harvest crops early if cavity
87 After peeling of canning carrots, cavity spot lesions spot has started to appear.
appear as raised gray areas.
References
Davison, E. M. and McKay, A. G. 1999. Reduced persistence of
metalaxyl in soil associated with its failure to control cavity
spot of carrots. Plant Pathology 48:830–835.
Wound periderm is resistant to the peeling process used
El-Tarabily, K. A., Hardy, G. E. St J., Sivasithamparam, K.,
for canning carrots, resulting in cavity lesions that Hussein, A. M., and Kurtboke, I. D. 1996. Microbiological
remain as raised mounds on peeled roots (87). The differences between limed and unlimed soils and their
relationship with cavity spot of carrot (Daucus carota L.)
cavity is formed when cells of the secondary phloem, caused by Pythium coloratum in Western Australia. Plant and
periderm, and pericycle collapse following enzyme pro- Soil 183:279–290.
duction by the pathogen. Other, fast growing Pythium Farrar, J. J., Nunez, J. J., and Davis, R. M. 2002. Repeated soil
species appear to be less effective at circumventing host applications of fungicide reduce activity against cavity spot in
carrots. California Agriculture 56(2):76–79.
resistance and inducing tissue collapse. However, these Guba, E. F., Young, R. E., and Ui, T. 1961. Cavity spot disease of
other species are capable of producing larger quantities carrot and parsnip roots. Plant Disease Reporter
of cell wall degrading enzymes than P. violae, enabling 45:102–105.
them to invade and extend lesions initiated by P. violae. Gladders, P. and McPherson, G. M. 1986. Control of cavity spot
in carrots with fungicides. Aspects of Applied Biology
P. violae is favored by soil temperatures below 20º C. 12:223–233
Cavity spot is unlikely to spread between roots kept in Hiltunen, L. H. and White, J. G. 2002. Review paper: Cavity
cold storage. spot of carrot (Daucus carota). Annals of Applied Biology
113:259–268.
Cavity spot is usually most prevalent in acid (pH 5 or
Liddell, C. M., Davis, R. M., Nuñez, J. J., and Guerard, J. P.
lower) soils and where there is poor drainage or 1989. Association of Pythium species with carrot root
compacted soil. Development of cavity spot is favored dieback in the San Joaquin Valley of California. Plant Disease
by wet, anaerobic conditions that reduce host vigor and 73:246–249.
Lyshol, A. J., Semb, L., and Taksdal, G. 1984. Reduction of
increase root exudates; such exudates stimulate germi- cavity spot and root dieback in carrots by fungicide
nation of Pythium oospores in soil. applications. Plant Pathology 33:193–198.
Schrandt, J.K., Davis, R. M., and Nuñez, J. J. 1994. Host range
Control and influence of nutrition, temperature, and pH on growth of
Pythium violae from carrot. Plant Disease 78:335–338.
Rotate carrots with at least 5 years between carrot or Vivoda, E., Davis, R. M., Nuñez, J. J., and Guerard, J. P. 1991.
parsnip crops. Longer rotations may be required if Factors affecting the development of cavity spot of carrot.
cavity spot had been severe. Serological tests (ELISA) of Plant Disease 75:519–522.
F UNGAL D ISEASES
soil for the cavity spot pathogen are available in the UK White, J. G. 1988. Studies on the biology and control of cavity
spot. Annals of Applied Biology 113:259–268.
and may be used for risk assessment. Use cultivars with White, J.G., Stanghellini, M. E., and Ayoubi, L. M. 1988.
moderate to good levels of resistance to cavity spot. Variation in the sensitivity to metalaxyl of Pythium spp.
Fungicides, particularly the phenylamide chemical isolated from carrots and other sources. Annals of Applied
Biology 113:269–277.
metalaxyl (and related isomer mefenoxam), were very
effective as spray treatments for many years. Treatment
A PIACEAE 111

88
WHITE MOLD, COTTONY ROT,
WATERY SOFT ROT

White mold or cottony rot of carrots is perhaps most
important as a storage rot. Sclerotinia sclerotiorum
occurs commonly on harvested carrots in temperate
regions, but it usually only becomes apparent when
roots are stored under warm humid conditions for
several days. The other white mold species, S. minor,
has occasionally been reported on carrots in the USA
and Japan. White mold infects most Apiaceae crops,
especially causing economic damage in celery and 88 Close up of Sclerotinia growing near carrot crown.
fennel. Sclerotinia sclerotiorum can also cause blights
and seed stalk dieback on Apiaceae crops such as celery
and parsley. 89

The first symptoms are small, 5–10 mm in diameter,
water-soaked, brown lesions on leaves, crowns, or the
upper exposed shoulders of taproots (88). Senescent
foliage in contact with the soil is particularly suscepti-
ble to initial infections. White mycelial growth can be
found on senescent leaves and other parts of the carrot
when the soil is moist and humidity is high. The
pathogen can spread extensively between plants via the
mats of senescing lower foliage. As the pathogen
develops, the white mycelium produces small mounds
of hyphae that later become hard, black sclerotia (89).
Infection of leaves can lead to root rots in the field. The 89 Sclerotia of Sclerotinia sclerotiorum forming on
roots develop a soft rot and sclerotia occur on and carrot roots.
around the taproots. On stored roots, S. sclerotiorum
produces extensive, fluffy white mycelium, and under- 90
lying tissues become soft and rotted (90). In contrast,
bacterial soft rots are slimy and lack this white mycelial
growth.
Causal agents
White mold is caused by two species of the ascomycete
fungus Sclerotinia: S. sclerotiorum and S. minor. For
detailed descriptions of these pathogens, see the bean
F UNGAL D ISEASES
white mold section in the chapter on legume diseases.
90 Harvested carrots showing white mold infections.

Disease cycle Streptomyces scabies

The disease cycle is similar to that described for white SCAB
mold on other vegetables such as bean and lettuce. For
detailed descriptions of the disease cycles, see the bean Introduction and significance
white mold section in the chapter on legume diseases. This disease is occasionally a serious problem in carrot
Even though optium temperatures for this pathogen are and can make fresh market crops unmarketable.
15–20º C, some activity continues even during cold Parsnip may also be affected. Scab is a familiar problem
storage of carrots at 0º C. Storage losses can be high on potato, radish, beet, and turnip.
because of extensive mycelial spread from root to root.
Control Symptoms on carrot are raised, brown, corky lesions on
For an integrated approach to white mold control, see the taproot. Lesions measure 0.5–2 cm and are often
the bean white mold section in the chapter on legume elongated horizontally across the carrot root. Sunken
diseases. Handle carrots carefully at all stages of har- lesions are also produced (91).
vesting and washing. Clean and disinfect storage con-
tainers between batches of carrots. Fungicides are Causal agent
generally no longer used as pre-storage treatments. The pathogen is considered to be the actinomycete
Maintain storage and shipment conditions at tempera- Streptomyces scabies. Actinomycetes are Gram-positive
tures of 0º C and provide at least 95% relative humidity. bacteria that can form branching filaments and are
Inspect stored carrots so that problems can be identified common soil inhabitants. However, recent research on
at an early stage and losses minimized by promptly potato has identified several species of Streptomyces
disposing affected carrots. that cause common scab, so the etiology of scab disease
may be more complex. Streptomyces acidiscabies has
References been reported from the USA and S. europeiscabiei from
Cheah, L. H., Page, B. B. C., and Shepherd, R.1997. Chitosan carrot in France and The Netherlands. Scab isolates
coating for inhibition of Sclerotinia rot of carrots. New from carrot are able to infect potato and radish.
Zealand Journal of Crop and Horticultural Science 54:63–70.
Clarkson, J. P., Staveley, J., Phelps, K., Young, C. S., and Whipps,
J. M. 2003. Ascospore release and survival in Sclerotinia Disease cycle
sclerotiorum. Mycological Research 107:213–222. Streptomyces scabies is a soil organism that invades the
Finlayson, J. E., Rimmer, S. R., and Pritchard, M. K. 1989. root through root openings such as sites of lateral root
Infection of carrots by Sclerotinia sclerotiorum. Canadian
Journal of Plant Pathology 11:242–246. emergence or wounds. The pathogen causes localized
Kora, C., McDonald, M. R., and Boland, G. J. 2003. Sclerotinia death of cells and the formation of corky tissue. This
rot of carrot: an example of phenological adaptation and wound reaction results in the scab symptoms. Infection
bicyclic development by Sclerotinia sclerotiorum. Plant
Disease 87:456–470.
is favored by alkaline soils, dry conditions, and warm
temperatures (optimum 20º C, with little activity below
11º C). Carrot is thought to be susceptible to infection
for only 2 to 3 weeks during development, beginning
when roots start to thicken (when root diameter is
greater than 2 mm). This infection period is equivalent
to 475 to 625 degree days after planting. At this stage,
the periderm grows through the epidermis and the
resulting small wounds are vulnerable to infection.
F UNGAL D ISEASES
Control
Rotate carrots with crops that are not susceptible to
scab; however, crop rotations are not entirely successful
because Streptomyces spp. survive in soil for very long
periods. Irrigate to maintain adequate soil moisture,
A PIACEAE 113
Thanatephorus cucumeris
91
(anamorph = Rhizoctonia solani)
CROWN AND ROOT ROT

This disease is occasionally a problem in North
America. In the UK, the name crown rot has been used
for both external symptoms associated with Fusarium
spp. and for the internal symptoms caused by virus
infections (e.g. Parsnip yellow fleck virus, see descrip-
tion and symptoms on page 124). Therefore, clarifica-
tion will be necessary when this common term is used.
91 Carrot root showing scab symptoms. Symptoms and diagnostic features

This disease causes the crowns and lower portions of
petioles to develop dry, dark brown, sunken lesions.
Such infections can also occur further down the root.
especially during the early stages of crop growth. There Symptoms on the taproot may resemble the lesions
are indications of differences in cultivar susceptibility, caused by the cavity spot pathogen (Pythium species).
so plant more tolerant varieties if these can be identified. The disease results in premature senescence and death
After harvest, corky tissue on raised scab lesions may be of foliage. Root infections may be colonized by second-
dislodged during washing operations, so low levels of ary soil fungi and soft rot bacteria. The mycelium of R.
infection may escape detection. solani occasionally may be present on the crown under
certain conditions. The pathogen also causes damping-
References off and root rot of carrot seedlings (92).
Bouchek-Mechiche, K., Pasco, C., Andrivon, D., and Jouan, B.
2000. Differences in host range, pathogenicity to potato
cultivars and response to soil temperature among
Streptomyces species causing common and netted scab in
France. Plant Pathology 49:3–10.
92
Goyer, C. and Beaulieu, C. 1997. Host range of Streptomyces
strains causing common scab. Plant Disease 81:901–904.
Hanson, L. E. and Lacy, M. L. 1990. Carrot scab caused by
Streptomyces spp. in Michigan. Plant Disease 74:1037.
Janse, J. D. 1988. A Streptomyces species identified as the cause
of carrot scab. Netherlands Journal of Plant Pathology
94:303–306.
Lambert, D. H. 1991. First report of additional hosts for the acid
scab pathogen Streptomyces acidiscabies. Plant Disease
75:750.
Schoneveld, J. A. 1994. Effect of irrigation on the prevention of
scab in carrots. Acta Horticulturae 354:135–144.
Wanner, L. A. 2004. Field isolates of Streptomyces differ in
pathogenicity and virulence on radish. Plant Disease
88:785–796.
F UNGAL D ISEASES
92 Brown lesions of crown and root rot on carrot

seedlings.

Crown rot is caused by the basidiomycete fungus Davis, R. M. and Nuñez, J. J. 1999. Influence of crop rotation on
Thanatephorus cucumeris. On plants the anamorph the incidence of Pythium- and Rhizoctonia-induced carrot
root dieback. Plant Disease 83:146–148.
stage, Rhizoctonia solani, is more often observed. This
Grisham, M. P. and Anderson, N. A. 1983. Pathogenicity and
pathogen is a true soil inhabitant, survives in soil as a host specificity of Rhizoctonia solani isolated from carrots.
saprophyte, and has a broad host range. Rhizoctonia Phytopathology 73:1564–1569.
solani has no asexual fruiting structures or spores and Mildenhall, J. P. and Williams, P. H. 1973. Effect of soil
temperature and host maturity on infection of carrot by
produces characteristically coarse, brown, approxi- Rhizoctonia solani. Phytopathology 63:276–280.
mately right-angle branching hyphae. The hyphae are Sumner, D. R., Phatak, S. C., and Carling, D. E. 2003. First
distinctly constricted at branch points, and a cross wall report of Rhizoctonia solani AG–2–4 on carrot in Georgia.
with dolipore septum is deposited just after each
branch. Hyphal cells are multi-nucleate. Small, tan to
brown, loosely aggregated clumps of mycelia function Thielaviopsis basicola, Chalaropsis thielavioides
as sclerotia that enable the fungus to withstand unfa- BLACK MOLD
vorable conditions. The teleomorph T. cucumis is not
often observed, and its role in disease development is Introduction and significance
not known. Rhizoctonia solani isolates are divided into These two fungi cause postharvest problems when
distinct groups, called anastomosis groups (AGs), that washed carrot roots are not stored properly. Thielavi-
have differing virulence levels and in some cases opsis may occasionally cause problems on seedlings and
preferred host ranges. The groups affecting carrots are mature crops in the field. Many crops in the UK will
mainly AG 2-2 and AG 4, and occasionally AG 1. In the have some black mold contamination. In North
US, AG 2-4 was confirmed on carrot in Georgia. America these diseases are more prevalent on muck
soils than on mineral soils.
Disease cycle
Crown rot develops when temperatures are above Symptoms and diagnostic features
18º C and soils are moist. Spread from plant to plant Superficial light to dark gray fungal growth develops on
can occur if there is a full leaf canopy. Lesion develop- the surface of the affected carrot root (93). As disease
ment on roots continues during storage. Problems tend progresses, the growth becomes black and irregular in
to be most severe on organic soils and are favored by outline. Root tissue below such mycelium remains rel-
warm and wet conditions close to harvest. In the UK, atively firm unless secondary bacterial organisms
during the 1980s, Rhizoctonia root rot of seedlings was colonize the lesions.
particularly damaging in autumn-sown carrots that
were overwintered under polythene covers, resulting in Causal agents
a high proportion of deformed roots. This growing Black mold is caused by two soilborne fungi.
practice is no longer used and planting in early winter Thielaviopsis basicola (synonym Chalara elegans) is the
has reduced root rot problems. more common of the two organisms and affects a range
of vegetables including legumes and tomato. It survives
Control in the soil by means of thick walled chlamydospores
Allow sufficient time for crop residues to break down in which are rectangular, dark brown, measure 7–12 x
soil, thereby reducing soil inoculum prior to carrot 10–17 μm, and form in chains of four to eight cells.
planting. Crops such as alfalfa and legume cover crops These chains readily fragment into single cells. T.
appear to increase risks of Rhizoctonia problems, so basicola also produces hyaline, rectangular endoconi-
F UNGAL D ISEASES
avoid these rotation crops if this disease is a concern. dia that measure 7–17 x 2.5–4.5 μm and are exuded in
Avoid cultivating or related procedures late in the crop long chains. Chalaropsis thielavioides produces ovoid,
cycle because such practices can deposit infested soil dark brown chlamydospores which measure 14–19 μm
onto the crown or petioles. Fungicides may provide and are borne singly or in short chains. This pathogen
some control of the disease. In stored carrots, maintain likewise produces long chains of hyaline, rectangular
temperatures close to 0º C. endoconidia measuring 8–15 x 2.5–4.5 μm.
A PIACEAE 115
Uromyces graminis, U. lineolatus

93
RUST

Rust diseases are a minor problem in carrot and other
Apiaceae vegetables, but they are common on wild
Apiaceae. Little is known about this disease and moni-
toring is advisable if Apiaceae crops are introduced into
new areas of production.

93 Black mold on carrot caused by Thielaviopsis. Early symptoms of rust consist of chlorotic, irregularly
shaped leaf lesions. Such lesions later develop typical
raised pustules, often forming mostly on the undersides
Disease cycle of infected leaves. The leaf epidermis covering the
Both these fungi are common soilborne organisms. pustules will rupture and release aeciospores (94).
Occasionally there may be symptoms of root infection
in the field prior to harvest, but this phase of the disease Causal agents
is associated with damage to the root. Black mold is Two heteroecious rust fungi affect carrot; these rusts
more often associated with roots damaged during har- produce different spore types on two distinct host
vesting, washing, and grading. Black mold is particu- plants. Uromyces graminis produces aecia on Apiaceae
larly a problem when roots are not cooled rapidly and plants such as carrot and fennel, and uredinia and telia
stored at 5º C. Washed, pre-packed carrots are most on grass hosts (Melica spp.). This pathogen occurs in
vulnerable because of the high humidity in the bags. Asia, Mediterranean regions, Russia, and South
America. Uromyces lineolatus (= U. scirpi) has aecidia
Control on Apiaceae and uredinia and telia on club-rush
Avoid black mold by carefully handling roots to (Scirpus spp.); it is found in wet and marshy areas in
minimize damage during harvesting and postharvest Europe and North America.
handling. Cool carrots quickly to remove field heat. Autoecious rusts complete their life cycle on one host
Chlorinate and change wash water regularly to reduce plant and include Puccinia angelicae on angelica, P.
spread of inoculum. Fungicide dips are no longer used nitida on parsley, P. pimpinellae on fennel or anise, and
for controlling black mold, though other chemicals P. apii on celery.
such as potassium sorbate and propionic acid have
shown good activity against T. basicola.
94
References
Derbyshire, D. M. and Shipway, M. R. 1978. Control of post-
harvest deterioration in vegetables in the UK. Outlook on
Agriculture 9:246–252.
Paulin-Mahady, A. E., Harrington, T. C., and McNew, D. 2002.
Phylogenetic and taxonomic evaluation of Chalara,
Charlaropsis, and Thielaviopsis anamorphs associated with
Ceratocystis. Mycologia 94:62–72.
Punja, Z. K., Chittaranjan, S., and Gaye, M.M. 1992.
F UNGAL D ISEASES
Development of black root rot caused by Chalara elegans on

fresh market carrot. Canadian Journal of Plant Pathology
14:299–309.
Punja, Z. K. and Gaye, M.M. 1993. Influence of postharvest
handling practices and dip treatments on development of
black root rot on fresh market carrots. Plant Disease
77:989–995. 94 Rust aecia on carrot petioles.
Control Symptoms and diagnostic features

Investigate rust outbreaks to determine possible sources When young carrot plants are affected, growth is
of inoculum; such information may allow for the elim- stunted and there is pronounced reddening, chlorotic
ination of alternate rust hosts near the crop. Apply mottling, and overall yellowing of the foliage (95).
fungicides if available. There may be twisting of the lower leaves. Roots are
severely stunted (96) and some plants may die. Young
References parsley plants show reddening of the older leaves and a
Wilson, M. and Henderson, D. M. 1996. British Rust Fungi. general yellowing of the foliage, and plants may become
Cambridge University Press, Cambridge, 384 pp. stunted (97). Infection of older carrot and parsley plants
produces milder symptoms and plants may be symp-
tomless when temperatures are above 24º C. In general,
Carrot red leaf virus, Carrot mottle virus
leaf discoloration of all Apiaceae plants may be caused
CARROT MOTLEY DWARF by a variety of factors, so virus tests are required to
confirm CMD disease.
Carrot motley dwarf (CMD) is a sometimes damaging Causal agents
disease of carrots grown in temperate regions. The CMD disease is caused by a co-infection of two viruses:
disease occurs primarily in the USA (California) but is Carrot red leaf virus (CRLV), which is a polerovirus
also common in the UK. CMD also affects parsley, with isometric particles (25 nm in diameter), and Carrot
cilantro, and dill. mottle virus (CMoV), an umbravirus having single
95
V IRAL D ISEASES
95 Carrot field affected with carrot motley dwarf.

A PIACEAE 117
stranded RNA but lacking a protein coat. Both viruses 96

can infect plants individually, but CMD disease is only
produced when both viruses are present. When present
as single viruses, only CRLV can be transmitted by the
aphid vector. CMoV cannot be vectored by the aphid
unless this virus is accompanied by the helper virus
CRLV; the CRLV proteins encapsidate the RNA of
CMoV, enabling transmission by aphids. The mixture
of viruses is transmitted by the willow carrot aphid
(Cavariella aegopodii) in a persistent manner. CMD is
restricted to cultivated and wild Apiaceae, and the
viruses are not seedborne.
Disease cycle
For carrot, disease spreads when these viruses are
vectored between successive or nearby carrot crops.
Presence of the aphid vector and CMD disease in over- 96 Stunted carrots infected with carrot motley dwarf.
wintered and volunteer carrots is an important source Healthy plant is on the right.
of the problem for newly planted carrots. Wild
Apiaceae, such as wild carrot (Daucus carota) and cow 97
parsley (Anthriscus sylvestris), are also potential sources
of CMD viruses.
Control
In some regions, control has been achieved by planting
spring crops at least 1.5 km away from overwintered
crops. In California, reducing the number of carrot
fields that are kept intact through the winter has signif-
icantly reduced disease occurrence in new, spring
planted carrots. Remove volunteer and weed hosts
before new crops emerge. Carrot cultivars vary in their
response to CMD, so use more tolerant cultivars if
available.
References 97 Carrot motley dwarf causing yellowing and

Morton, A., Spence, N. J., Boonham, N., and Barbara, D. J. reddening of parsley foliage.
2003. Carrot red leaf associated RNA in carrots in the United
Kingdom. Plant Pathology 52:795.
Waterhouse, P. M. and Murant, A. F. 1983. Further evidence on
the nature of the dependence of carrot mottle virus on carrot
red leaf virus for transmission by aphids. Annals of Applied
Biology 103:455–464.
Watson, M. T. and Falk, B. W. 1994. Ecological and
epidemiological factors affecting carrot motley dwarf
development in carrots grown in the Salinas Valley of
V IRAL D ISEASES

Watson, M. T., Tian, T., Estabrook, E., and Falk, B. W. 1998.
A small RNA resembling the beet western yellows luteovirus
ST9-associated RNA is a component of the California carrot
motley dwarf complex. Phytopathology 88:64–170.
PASTINACA SATIVA (PARSNIP)
Erysiphe heraclei
98
POWDERY MILDEW

Powdery mildew is probably the most important foliar
disease of parsnip in the UK. Powdery mildew is more
damaging to parsnip than to carrot or celery. Early
attacks can cause significant yield losses.

The symptoms usually appear first on the petioles and
leaf blades of older foliage. The superficial white fungal
growth is similar to that of other powdery mildews. In 98 Early symptoms of powdery mildew on underside of
the UK, little infection is seen until crop canopies close parsnip leaf.
over in July. Younger leaves become infected as disease
progresses. When powdery mildew is severe, both 99
upper and lower leaf surfaces are affected and develop
yellowing and early loss of the foliage (98, 99).
Causal agent
Powdery mildew is caused by the ascomycete Erysiphe
heraclei. For a description of this pathogen, see the
carrot section on powdery mildew in this chapter (page
103). There may be some host specialization, but
isolates appear to be able to infect a number of
Apiaceae host species.
Disease cycle 99 Powdery mildew of parsnip.

Overlapping parsnip plantings, volunteer parsnip, and
weed hosts are potential sources of infection. The References
disease cycle can be completed in 7 days under Palti, J. 1975. Erysiphaceae affecting Apiaceae crops, with special
optimum conditions. High humidity and moderate reference to carrot, in Israel. Phytopathologia Mediterranea
14:87–93.
temperatures favor infection. Crops become more sus-
ceptible with age. Disease severity is increased by
drought stress and is reduced by rain or overhead
irrigation. Itersonilia pastinacae, I. perplexans
ITERSONILIA CANKER,
Control BLACK CANKER
Apply fungicides such as sulfur or triazole products if
F UNGAL D ISEASES
severe disease is a possibility. Such materials are strictly Introduction and significance
protectants and must be applied prior to significant Itersonilia or black canker is an important disease of
disease development. Avoid over-fertilizing because parsnip in the UK, North America, and Australia. The
high nitrogen rates can result in succulent foliage that is pathogen also affects dill and wild Apiaceae plants.
very susceptible to powdery mildew. Affected parsnip roots are unmarketable.
A PIACEAE 119
Symptoms and diagnostic features ballistospores are discharged and will fall onto the agar.
Infected parsnip develops dark brown, black, or purple- On Waksman albumen agar, I. pastinacae produces
black lesions located around the crown, upper root, and chlamydospores and exhibits slower, more irregular
especially around the bases of lateral roots (100). growth than I. perplexans, which does not produce
Lesions are usually superficial and extend only a few chlamydospores.
millimeters deep. Advanced lesions lose their smooth
surface layer and have coarse exposed tissues. Second- Disease cycle
ary organisms are prevalent in advanced cankers. Foliar The pathogen survives in soil by means of chlamydo-
symptoms consist of small (1–2 mm diameter), brown spores and in crop residues. Airborne ballistospores are
spots with yellow halos. Spots coalesce into larger produced, released during the morning as humidity
necrotic areas. Petioles and inflorescences are also decreases, and land on susceptible tissues. Itersonilia
affected. Root symptoms usually begin late in the canker increases significantly when leaf senescence
summer and continue to develop as long as crops starts, so infection in young crops is uncommon. Spores
remain in the ground. Late harvested crops can washed from leaves make contact with crown and
therefore be severely affected. Other pathogens cause upper root tissues, leading to canker lesions. Cankers
cankers on parsnip and laboratory tests are required to are associated with extended periods of rainfall.
identify the pathogens, which include the following: Optimum temperatures are about 20º C. The pathogen
Mycocentrospora acerina, Alternaria radicina, Cylin- may be seedborne.
drocarpon destructans, Sclerotinia sclerotiorum.
Control
Causal agent Rotate parsnip with non-host crops and control wild
Black canker is caused by the basidiomycete fungus Apiaceae plant hosts. Use seed that does not have sig-
Itersonilia. Two species, I. perplexans and I. pastinacae, nificant levels of the pathogen. Select and plant cultivars
are implicated in this disease. Some researchers believe that are resistant to black canker. Protect roots by
the two species are synonymous. In culture, Itersonilia covering crowns and exposed upper-root tissues with
produces low growing, slimy colonies. Hyphae have soil. Regularly sample and examine parsnip roots as the
clamp connections at septa and produce short sterig- crop nears maturity so that affected fields can be
mata that bear spores. Spores are kidney shaped ballis- harvested early. Fungicide sprays for preventing root-
tospores that measure 11.4–20.0 x 7.2–11.4 μm and canker symptoms are not effective.
are forcibly discharged from the sterigmata. Thick
walled chlamydospores, measuring 9–13 x 13–20 μm, References
are produced by some isolates. Itersonilia has a yeast Channon, A. G. 1963. Studies on parsnip canker. I. The causes of
phase that appears in culture under certain conditions. the disease. Annals of Applied Biology 51:1–15.
Channon, A. G. 1963. Studies on parsnip canker. II.
Itersonilia can be isolated from diseased tissue by sus-
Observations on the occurrence of Itersonilia pastinacae and
pending tissue samples directly over agar surfaces; related fungi on the leaves of parsnips and in the air within
parsnip crops. Annals of Applied Biology 51:223–230.
Channon, A. G. 1964. Studies on parsnip canker. III. The effect
of sowing date and spacing on canker development. Annals of
100
100 Parsnip root Applied Biology 54:63–70.
infected with Channon, A. G. 1965. Studies on parsnip canker. VI. Cercospora
Itersonilia. acerina (Hartig) Newhall – a further cause of black canker.
Annals of Applied Biology 56:119–128.
Channon, A. G. 1969. Infection of the flowers and seed of
parsnip by Itersonilia pastinacae. Annals of Applied Biology
F UNGAL D ISEASES
64:281–288.
Channon, A. G. and Thomson, M. C. 1981. Parsnip canker
caused by Cylindrocarpon destructans. Plant Pathology
30:181.
Koike, S. T. and Tjosvold, S. A. 2001. A blight disease of dill in
California caused by Itersonilia perplexans. Plant Disease
85:802.
Phloeospora herclei
101
PHLOEOSPORA LEAF SPOT

Phloeospora leaf spot is generally a minor leaf disease
of parsnip. In the UK severe infection usually occurs on
late summer and autumn parsnip crops. A Phloeospora
disease also has been reported from New Zealand.

The first symptoms are small (1–2 mm) pale green or
brown leaf spots. As disease develops, leaf spots
increase in number, spots coalesce to form large necrotic
blotches (2–5 cm), and infected leaf tissue becomes gray 101 Necrotic leaf blotches of Phloeospora leaf spot of
brown (101). The disease spreads rapidly through the parsnip.
crop, causing extensive leaf death and defoliation (102).
No root symptoms have been reported. Severely
102
affected leaf tissue has tiny black fruiting bodies called
acervuli. Spore tendrils ooze from acervuli and form
characteristic white patches on leaf surfaces (103).
Causal agent
Phloeospora leaf spot is caused by the fungus
Phloeospora herclei. Fruiting bodies are minute, cup-
shaped structures called acervuli. Conidia are formed in
these structures and are curved, one to four septate
(though most are single septate), and measure 50–80 x
3.5–5 μm. The early literature probably confused
P. herclei with Ramularia pastinaceae. The Phloeospora
leaf spot disease reported from New Zealand is attrib-
uted to P. crescentium. However, P. herclei and P. cres- 102 General necrosis of parsnip foliage caused by
centium may be the same organism. Phloeospora leaf spot.
Disease cycle 103

Little is known about the epidemiology of this
pathogen. Inoculum is spread by splashing water and
direct contact between leaves. Phloeospora herclei
probably survives on infected debris and on weed hosts
such as hogweed (Heracleum sphondylium).
Control
Specific control measures have not been developed.
F UNGAL D ISEASES
References
Laundon, G. F. 1970. Records of fungal plant diseases in New
Zealand. New Zealand Journal of Botany 8:51–66.
Riley, E. A. 1952. Leaf spot of parsnip caused by Phloeospora
103 White spore masses of Phloeospora leaf spot of
crescentium (Barth.) n. comb. Mycologia 44:213–215.
parsnip.
A PIACEAE 121
Phoma complanata Causal agent

PHOMA CANKER Phoma canker is caused by Phoma complanata.
Colonies are light to olivaceous gray, have even
Introduction and significance margins, and produce dense aerial mycelium. Pycnidia
This disease has increased in importance since it was measure 35–49 μm in diameter and have thick walls.
first reported in Canada in 1984. The pathogen is host Conidia are hyaline, guttulate, and variable in shape.
specific to parsnip and related weeds, such as cow Conidia dimensions are 5–9 x 2–3.5 μm (mean 7.4 x
parsnip (Heracleum lanatum). Field diagnosis of 2.4 μm), though large (27 x 8 μm) one-septate spores
Phoma canker is difficult because several pathogens occur in older cultures or lesions.
produce similar symptoms and more than one causal A second pathogen, Phomopsis diachenii, can be
agent may be present on diseased plants. In the UK, P. confused with the Phoma canker organism. Reddish
complanata may now be the most important cause of brown leaf spots with deep purple margins measure
parsnip root cankers. 10–20 mm in diameter and contain black pycnidia.
Microscopic examination shows that P. diachenii, like
Symptoms and diagnostic features most Phomopsis species, produces both filiform and
If present, leaf spots are circular, brown, and often have oval spores.
yellow halos. As disease develops, leaf spots coalesce
and result in a general yellowing, necrosis, and blighting Disease cycle
of foliage. Pycnidia appear in leaf lesions about two Leaf spots and petiole lesions of Phoma canker appear
weeks after infection. Dark brown to black lesions may 4 to 5 days after infection, and disease rapidly pro-
develop on petioles, resulting in leaves that twist and gresses if favorable conditions are present. Insects are
bend over. Large, dark brown to black cankers form on reported to contribute to secondary spread. Root
parsnip crowns and on the sides of taproots (104). infection occurs when spores are washed down from
These cankers can enlarge and affect much or all of the the infected foliage. In the UK, foliar symptoms may be
crown tissue. Cankers result in splitting or cracking on absent even though root cankers are present; in these
the upper portion of the root. Careful examination of situations, the source of infection is likely to be
the surfaces of cankers will reveal pycnidia embedded soilborne inoculum. Phoma complanata is seedborne
in these tissues (105). Pycnidia ooze a white or creamy and can reduce seedling establishment. Diseased roots
spore exudate. Affected roots are reported to have a contain elevated levels of furocoumarins. These sub-
sweet cinnamon odor. stances are photocarcinogens, so take precautions to
prevent skin contact when handling parsnip roots.
104 105
F UNGAL D ISEASES
104 Root symptoms of Phoma canker of parsnip. 105 Decayed parsnip root with pycnidia of the Phoma
canker pathogen.
Control Plasmopara umbelliferarum,

Rotate crops so that a 4-year break occurs between (P. crustosa/P. nivea)
parsnip plantings. Use seed that does not have signifi- DOWNY MILDEW
cant levels of the pathogen. Choose and plant cultivars
that are known to have tolerance or reduced suscepti- Introduction and significance
bility to this pathogen. Monitor and sample crops Downy mildew occurs on parsnip, but in the UK severe
regularly so that harvest can be scheduled early if crop damage is rare. It also occurs on carrot, celery,
Phoma canker starts to appear. Application of fungi- chervil, fennel, and parsley. Downy mildew isolates
cides may help control foliar symptoms; however, affecting carrot are reported only in Europe.
chemicals are not effective at preventing disease caused
by soilborne inoculum. Symptoms and diagnostic features
Symptoms are yellow, angular shaped leaf blotches. The
References lesions soon turn brown and leaves develop a ragged
Cerkauskas, R. F. 1985. Canker of parsnip caused by Phoma appearance as the centers of lesions fall out. White
complanata. Canadian Journal of Plant Pathology sporulating growth develops on the undersides of the
7:135–138.
lesions (106). Young, succulent growth is most suscep-
Cerkauskas, R. F. 1987. Phoma canker severity and yield loss in
parsnip. Canadian Journal of Plant Pathology 9:311–318. tible to infection and leaves with multiple lesions turn
Cerkauskas, R. F. 1987. Phoma canker of parsnips. Ministry of yellow and senesce (107).
Agriculture Fisheries and Food, Ontario, Canada. Leaflet 87-
041, 3pp.
Causal agent
Cerkauskas, R. F. and Mc Garvey, B. D. 1988. Fungicidal control
of Phoma canker of parsnips. Canadian Journal of Plant Downy mildew is caused by an oomycete in the genus
Pathology 10:252–258. Plasmopara. This produces monopodial branched
sporangiophores that emerge from leaf stomates.
Smaller branches that bear sporangia are arranged at
right angles to the supporting branches. Sporangia are
ovoid, hyaline, have a single pore on the distal ends, and
measure 23–27 x 17–19 μm. Oospores are produced
within infected tissues and seeds. The nomenclature of
the various downy mildews that infect Apiaceae is
under review. Some researchers believe the names
P. crustosa and P. nivea are not valid, and propose that
P. umbelliferarum be used as the pathogen name.
106 107
F UNGAL D ISEASES
106 Parsnip leaf infected with downy mildew. 107 Necrotic leaf tissue of parsnip caused by downy
mildew.
A PIACEAE 123
Disease cycle 108

Infection is favored by cool, wet conditions. Free
moisture is required for sporangia to germinate and
release zoospores through the distal pore. These
swimming spores then invade the leaf via stomata.
Control
Control measures are not usually required. Rotate to
non-host crops to reduce the risk of infection from
soilborne oospores. When symptoms appear early in
the season, apply fungicides.
References
Constantinescu, O. 1990. The nomenclature of Plasmopara
parasitic on Umbelliferae. Mycotaxon 43:471-477. 108 Leaf lesions caused by Ramularia leaf spot of
parsnip.
Ramularia pastinacae
109
RAMULARIA LEAF SPOT

This leaf spot disease is commonly found on parsnip.
However, economic impact is usually limited.

This disease is characterized by small (3–7 mm in
diameter), pale brown leaf spots with darker margins
and chlorotic halos (108). The centers of the older
lesions often fall out, resulting in shot-hole symptoms
(109). The undersides of active lesions support white
sporulation.
109 Shot hole symptoms of Ramularia leaf spot of
Causal agent parsnip.
Leaf spot is caused by the fungus Ramularia pastinacae.
Conidiophores emerge from leaf tissues in fascicles.
Conidia are hyaline, cylindrical, and zero to four
septate, though most spores are bicellular. Conidia
measure 14–42 x 3–5 μm.
Control
Disease cycle Broad-spectrum fungicides used for other diseases
There has been little investigation of this disease, but should provide some control of this problem. Rotate to
warm and wet conditions favor infection. The disease non-hosts to avoid carry over of this pathogen to sub-
F UNGAL D ISEASES
occurs in small foci and then spreads to cause a more sequent parsnip plantings. Plow in crop residues soon
general infection of the crop. after harvesting, and control volunteer parsnip plants.
Parsnip yellow fleck virus during sedimentation. It is transmitted in a semi-

PARSNIP YELLOW FLECK persistent manner for a period of 1 to 4 days by adults
of several aphid species: willow carrot aphid (Cavariella
Introduction and significance aegopodii), C. pastinaceae, and possibly others. A
Parsnip yellow fleck virus (PYFV) is widespread, infects helper virus, Anthriscus yellows virus (AYV), is required
many Apiaceae plants, and occasionally causes severe for aphid transmission of PYFV. There are two recog-
losses in carrot crops in the Netherlands and in the UK. nized serotypes of PYFV: the parsnip serotype infects
This is the most common virus disease of parsnip in celery, parsnip, and cow parsley (Anthriscus sylvestris);
Europe. the anthriscus serotype infects carrot, chervil, cilantro,
and dill.
On carrots, symptoms are browning and death of the Disease cycle
youngest leaves of seedlings, followed by death of these An interesting dynamic exists between these two
plants (110, 111). Plants that continue to live can show viruses, the various Apiaceae hosts, and the aphid
stunting, early leaf senescence, and distortion and elon- vectors. Only plants that are susceptible to both viruses
gation of the top part of the root. Roots can show can act as virus reservoirs. The major crops – carrot,
internal discoloration and external black spotting celery, and parsnip – are all immune to AYV, the helper
(112). In carrot seed crops, plants can decline prema- virus. Therefore, within plantings of these host plants
turely. For parsnip, the first symptoms are bold yellow there is no plant-to-plant spread of the problem.
veins and vein netting. Foliage later shows yellow However, weed hosts such as cow parsley (A. sylvestris)
flecking and a yellow green mosaic (113, 114). It is and hogweed (Heracleum sphondylium) are hosts to
possible that the problem known as ‘crown rot,’ which both viruses and therefore can be sources of both
has resulted in serious losses in northwest England since pathogens.
the mid-1980s, was caused by PYFV (115).
Control
Causal agent Avoid planting susceptible crops in areas were the virus
PYFV is a sequivirus and has isometric particles that are is known to cause significant disease. Control weed
30 nm in diameter and separate into two components hosts and spray for the aphid vectors.
111
111 Death of
110
carrot growing
point caused by
Parsnip yellow
fleck virus.
V IRAL D ISEASES
110 Leaf necrosis, death of the growing point, and loss

of carrots caused by Parsnip yellow fleck virus.
A PIACEAE 125
References 112
Elnager, S. and Murant, A. F. 1976. Relations of the semi-
persistent viruses parsnip yellow fleck and anthriscus yellows
with their vector Cavariella aegopodii. Annals of Applied
Biology 84:169-181.
Hemida, S. K. and Murant, A. F. 1989. Particle properties of
parsnip yellow fleck virus. Annals of Applied Biology
114:87–100.
Runham, S. R., Town, S. J., and Gladders, P. 1995. Evaluation of
fungicides against crown-rot disorder of carrots. Tests of
Agrochemicals and Cultivars: Annals of Applied Biology 126
(Supplement) 16: 12–13.
Van Dijk, P. and Bos, L. 1985. Viral dieback of carrot and other
Apiaceae caused by the Anthriscus strain of parsnip yellow
fleck virus, and its distinction from carrot motley dwarf.
Netherlands Journal of Plant Pathology 91:169–187.
112 Black spotting on carrot roots associated with
Parsnip yellow fleck virus.
113
113 Mosaic symptoms on parsnip caused by Parsnip

yellow fleck virus.
114 115
V IRAL D ISEASES
114 Parsnip yellow fleck virus causing yellow spotting 115 Crown rot and root core discoloration of carrot
on parsnip leaf. caused by Parsnip yellow fleck virus.
PETROSELINUM CRISPUM (PARSLEY)
Erysiphe heraclei, Leveillula lanuginosa Phytophthora spp., Pythium spp.

POWDERY MILDEW ROOT ROT
116
Root rots caused by Phytophthora and Pythium
pathogens are important field problems in parsley.
These diseases have been reported from Europe, North
America, and Australia. In parsley, losses of more than
50% can occur.

The first symptoms of Phytophthora root rot are leaf
yellowing and wilting of foliage several weeks after
planting. Plants are stunted and finally collapse and die
(117, 118). The main parsley roots have orange-brown
lesions that enlarge and rot. Pythium root rots result in
stunted plants and decayed feeder roots.
116 Powdery mildew on parsley leaves.
Causal agents
On parsley, powdery mildew produces dense, white Several species of Phytophthora infect parsley, including
growth on leaves (116). Severe attacks cause yellowing P. cryptogea in California, P. parasitica in Hawaii, and
and early senescence of the older leaves. The primary P. primulae in the UK. Carrots are affected by other
powdery mildew pathogen is Erysiphe heraclei. Phytophthora species, including P. cactorum, P. crypto-
Leveillula lanuginosa is a second type of powdery gea, P. megasperma, P. parasitica, P. porri, and P.
mildew affecting parsley and causes angular yellow primulae. Pythium paroecandrum and perhaps other
blotches on the upper leaf surface; white sporulation is Pythium species affect parsley. Phytophthora and
found on both upper and lower leaf surfaces. For more Pythium pathogens are oomycete organisms, and most
details, see the carrot section on powdery mildew in this species produce sporangia and swimming zoospores.
chapter (page 103).
Disease cycle
References These pathogens are soilborne and are mostly favored
Citrulli, M. 1975. The powdery mildew of parsley caused by by wet, cool soil conditions. However, P. parasitica on
Leveillula lanuginosa. Phytopathologia Mediterranea carrots develops when temperatures are high (30–
14:94–99.
36º C). Some isolates show host specialization. For
Koike, S. T. and Saenz, G. S. 1994. Occurrence of powdery
mildew on parsley in California. Plant Disease 78:1219. example, P. parasitica from parsley infects coriander but
not carrot, celery, or tomato.
Control
Rotate with non-susceptible crops. Prepare the soil so
F UNGAL D ISEASES
that there is good drainage and reduced soil compac-

tion. Planting on raised beds may be helpful. Poorly
draining sites should be avoided. Fungicide treatments
of metalaxyl have been used in the UK.
A PIACEAE 127
Sclerotinia sclerotiorum
117
WHITE MOLD
White mold occurs on a number of Apiaceae crops,

including parsley. This pathogen is perhaps more
commonly found on parsley being grown for seed than
on parsley grown for market.
Infected seed stalks of parsley become light tan to
bleached in color. The leaves on affected stems initially
wilt (119). Eventually the entire stem dries up. White
mycelium may develop on the outside of such stems.
However, cutting into the seed stalk will usually reveal
profuse white mycelium and large black sclerotia in the
117 Collapsed parsley infected with Phytophthora central core of the stalk (120 ).
primulae. For more detail see the white mold section for carrot
and the pink rot section for celery.
118
119 Parsley 119

infected with
Sclerotinia sclero-
tiorum.
118 Phytophthora primulae root rot of parsley.
References
Davis, R. M., Winterbottom, C. Q., and Mirectich, S.M.1994. 120 Sclerotia of 120
First report of Phytophthora root rot of parsley. Plant Disease Sclerotinia
78:1122.
sclerotiorum
Hershman, D. E., Varney, E. H., and Johnston, S. A .1986.
Etiology of parsley damping-off and influence of temperature. forming inside
Plant Disease 70:927–930. parsley stem.
Hine, R. B. and Aragaki, M. 1963. Influence of soil temperature
on a crown rot disease of parsley caused by Phytophthora
parasitica. Phytopathology 53:1113–1114.
McCracken, A. R. 1984. Pythium paroecandrum associated with
root-rot of parsley. Plant Pathology 33: 603–604.
F UNGAL D ISEASES
Septoria petroselini 122 Parsley leaves

122
SEPTORIA BLIGHT infected with
Septoria blight.
This is a common and important foliar disease of
parsley in Europe, Asia, and North America. Severe
disease can render the parsley crop unmarketable.
Parsley is not susceptible to the late blight pathogen of
celery, Septoria apiicola.

Symptoms consist of irregularly shaped leaf spots that
initially are small and measure 2–5 mm in diameter. As
disease develops, the spots increase in number, coalesce,
and result in extensive blighting of the overall foliage
(121, 122). Leaf spots range in color from green-brown
to bleached white and tend to be angular in shape. The
presence of many tiny, dark fruiting bodies (pycnidia) in
the spots is a key characteristic sign of Septoria.
Causal agent Disease cycle

Septoria blight is caused by the fungus Septoria Septoria blight of parsley is a seedborne disease. There
petroselini. On plant tissue the pathogen is readily iden- is little research on the epidemiology of this pathogen.
tified by its black pycnidia that are immersed in plant However, the biology will be very similar to that of
tissues. Pycnidia are ostiolate, measure approximately S. apiicola; see the celery section on late blight in this
100 μm in diameter, and contain hyaline, multicelled, chapter (page 90). Rain and overhead irrigation spread
filamentous conidia (30–40 x 1–2 μm) that are mainly the pathogen in both transplant and field settings.
one to three septate. No perfect stage has been reported.
The pathogen is seedborne. Septoria petroselini does Control
not infect celery or celeriac. See the celery section on late blight in this chapter (page
90). As with celery, it is critical to use seed that does not
have significant levels of the pathogen. If rain or
121
overhead sprinkler water does not occur, it is often
possible to trim back symptomatic parsley plants and
harvest the subsequent healthy regrowth. Parsley
cultivars may vary in susceptibility; therefore, plant
tolerant cultivars if available.
References
Miller, S. A., Colburn, G. C., and Evans, W. B. 1999.
Management of Septoria leaf blight of parsley with fungicides
and efficacy of a disease predictive model. Phytopathology
83:S53 (Abstract).
F UNGAL D ISEASES
121 Parsley leaves infected with Septoria blight.

129
Asparagus officinalis Asparagus
ASPARAGUS (Asparagus officinalis) is a perennial monocot plant formerly included in the

Liliaceae (lily family) but now separately classed within the Asparagaceae. It is grown for its
immature, unexpanded shoots that are called spears. Spears originate from large
underground crowns that consist of fleshy rhizomes. Asparagus spears are only harvested for
a limited period during the spring season, after which the remaining spears are allowed to
grow, expand, and develop into the foliage, or fern, of the plant. The fern stage replenishes
crown energy and nutrients and allows the plant to grow and remain commercially
productive. Asparagus is grown as a perennial crop with a productive life of 5 to 15 years.
In addition to traditional green asparagus, there are purple spear varieties and white spears
that are cut while they are still below ground and have not formed chlorophyll.
Cercospora asparagi Disease cycle

CERCOSPORA BLIGHT Conidia are dispersed by wind or splashing water from
rain and sprinkler irrigations. Disease develops rapidly
Introduction and significance if warm, humid weather persists. Infected crop residue
This disease is most damaging in conjunction with high is the main source of inoculum.
temperatures and humidity, and problems occur in
parts of southern USA, South America, and Asia. Control
Damage is much less severe in cooler climates. Apply fungicide sprays. Avoid using overhead sprinkler
irrigation. At the end of the growing season, reduce
Symptoms and diagnostic features pathogen inoculum by managing the diseased fern. For
Pale brown to gray elliptical lesions that measure smaller acreages, the fern can be removed from the field
1–4 mm in diameter, with a red-brown or purple and destroyed. Otherwise, fern can be mowed or
margin, are produced on leaves and branches. Lesions chopped, and then buried by cultivation or re-ridging
appear before the canopy closes over the lower part of (earthing up) during the dormant period.
stems. As disease progresses, needles and smaller shoots
turn yellow, then brown, and dry. References
Conway, K. E., Motes, J. E., and Foor, C. J. 1990. Comparison of
Causal agent chemical and cultural controls for Cercospora blight on
asparagus and correlations between disease levels and yield.
Cercospora blight is caused by the fungus Cercospora Phytopathology 80:1103–1108.
asparagi. The pathogen produces hyaline, multicelled, Cooperman, C. J., Jenkins, S. F., and Averre, C. W. 1986.
filiform spores that measure 35–130 x 2.5–5 μm and Overwintering and aerobiology of Cercospora asparagi in
North Carolina. Plant Disease 70:392–394.
are borne on clusters of brown conidiophores.
Conidiophores arise from black stromata. Sporulation
F UNGAL D ISEASES
on the lesions causes these spots to take on a pale gray

appearance. This pathogen appears to be host specific
to asparagus.
Fusarium oxysporum f. sp. asparagi, Causal agents

F. proliferatum (teleomorph = Gibberella fujikuroi) Fusarium crown and root rot is caused by two species
FUSARIUM CROWN & ROOT ROT of Fusarium: F. oxysporum f. sp. asparagi and F. prolif-
eratum. For the first species, pathogen morphology and
Introduction and significance colony characteristics are similar to other F. oxysporum
Fusarium crown and root rot is implicated in the so- fungi. The fungus forms one- or two-celled, oval to
called ‘decline’ problem of asparagus. The decline kidney-shaped microconidia on monophialides, and
syndrome results in a progressive yield loss over a four- to six-celled, fusiform, curved macroconidia.
period of years. Other factors, such as virus infection, Microconidia measure 6–15 x 2.5–4.0 μm, while
are also thought to contribute to decline. Fusarium macroconidia range from 27–60 x 3.5–5.5 μm.
crown and root rot is recognized as an economically Macroconidia are usually produced in cushion-shaped
important problem worldwide. structures called sporodochia. Spherical chlamydo-
spores are also formed and are 10–11 μm in diameter.
Symptoms and diagnostic features Fusarium proliferatum produces microconidia and
Fusarium crown and root rot causes the fern foliage to macroconidia on polyphialides. An important identfi-
first turn chlorotic (123). Later the fern wilts, turns ciation feature is that microconidia are borne in long
brown, and dies (124). Internal tissues of lower stems chains and have distinctly truncated bases. Chlamydo-
and crowns have a red-brown discoloration, but remain spores are not formed. The pathogens can be isolated
firm and unrotted (125). Red-brown, oval lesions also from symptomatic vascular tissue. However, semi-
develop on asparagus roots and lower stems (126). selective media like Komada can help isolate them
Infected roots become dark, soft, and stringy. Plant because saprophytic organisms are often present in
growth is weakened and severely affected plants die. asparagus crowns and surrounding tissues. Fusarium
Postharvest decay of the spears may be caused by oxysporum f. sp. asparagi is apparently host specific to
various Fusarium spp., which results in reduced quality asparagus. Other Fusarium species can also be found in
and shelf-life. Seedling asparagus plants are stunted and asparagus crown and root tissue or sporulating at the
grow poorly, and foliage can be bright yellow. base of spears. Fusarium culmorum causes a foot and
stem rot of asparagus. Fusarium redolens f. sp. asparagi
has recently been separated from the F. oxysporum
group and also causes a crown and root rot.
123 124
F UNGAL D ISEASES
123 Yellowing of asparagus foliage caused by Fusarium 124 Dieback of asparagus foliage caused by Fusarium
wilt. wilt.
A SPARAGUS O FFICINALIS 131
Disease cycle 125

In addition to being a true soilborne pathogen able to
survive long periods of time in soil, the Fusarium wilt
pathogen is also seedborne. However, infected crowns
used for propagation are often the most important
sources of infection. The practice of propagating
asparagus by cutting up existing plant crowns allows
the pathogen to be distributed along with crown
divisions used to establish new plantings. Diseased
propagation crowns and infested seed result in new
plants being already infected. In the case of soilborne
inoculum, the fungus infects asparagus roots and then
grows systemically in the plant. If asparagus plants are
infected with viruses, root exudate release is increased 125 Vascular discoloration in asparagus crown infected
and soilborne Fusarium can be stimulated. A similar with Fusarium oxysporum.
interaction can occur when asparagus is replanted after
a previous asparagus crop; autotoxins released by the
126
previous asparagus crop’s residues increase nutrient
leakage from roots of the new crop.
Control
pathogen. Plant seed in propagation fields that do not
have a history of the problem, and which have not been
recently used for asparagus. If using crowns for propa-
gation, use only healthy, symptomless plants that are
taken from fields that do not have a history of this
disease. In some countries soil tests are used to detect
Fusarium prior to selecting uninfested propagation
sites. Maintain records so that asparagus is not planted
in fields having a history of this problem. Fungicide seed 126 Reddish lesions at base of spears caused by
treatments may help prevent infection of seedlings. Fusarium wilt.
Manage the crop to reduce stress on the plants. Practice
extended crop rotations, perhaps 5 or more years,
between asparagus plantings. Some cultivars such as References
UC 157 have some tolerance to this pathogen. An older Baayen, R. P., van den Boogert, P. H. J. F., Bonants, P. J. M., Poll,
practice consisted of applying salt (NaCl) to the beds of J. T. K., Blok, W. J., and Waalwijk, C. 2000. Fusarium
redolens f.sp. asparagi, causal agent of asparagus root rot,
infected plants. Though not widely practiced in the crown rot and spear rot. European Journal of Plant Pathology
USA, the application of salts helped reduce disease 106:907–912.
severity and associated crop loss. Blok, W. J. and Bollen, G. J. 1975. Host specificity and vegetative
compatibility of Dutch isolates of Fusarium oxysporum f. sp.
asparagi. Canadian Journal of Botany 75:383–393.
Blok, W. J. and Bollen, G. J. 1993. The role of autotoxins from
F UNGAL D ISEASES
root residues of the previous crop in the replant disease of

asparagus. Netherlands Journal of Plant Pathology 99,
Supplement 3:29–40.
Didelot, D., Nourrisseau, J. G., and Bouhot, D. 1996. Fusarium
root rot of asparagus: Development of a predictive test for
root rot. Proceedings of the VIII International Symposium on
Asparagus. Acta Horticulturae 415:373–375.
Elmer, W. H. 2004. Combining nonpathogenic strains of Helicobasidium brebissonii (anamorph = Rhizoctonia

Fusarium oxysporum with sodium chloride to suppress crocorum), Zopfia rhizophila
Fusarium crown and root rot of asparagus in replanted fields.
Plant Pathology 53:751–758. ROOT ROTS
Elmer, W. H. 2000. Incidence of infection of asparagus spears
marketed in Connecticut by Fusarium spp. Plant Disease
84:831–834. There are occasional problems with violet root rot,
Elmer, W. H. 1992. Suppression of Fusarium crown and root rot caused by Helicobasidium brebissonii, in asparagus.
of asparagus with sodium chloride. Phytopathology The anamorph, Rhizoctonia crocorum, is the primary
82:97–104.
stage that causes the disease and produces coarse
Elmer, W. H., Johnston, D. A., and Mink, G. I. 1996.
Epidemiology and management of the diseases causal to mycelial strands (up to 1 mm diameter) that enable it to
asparagus decline. Plant Disease 80:117–125. spread through soil and infect new host plants. Roots
Elmer, W. H. and Stephens, C. T. 1989. Classification of become covered with strands or dense mats of purple
Fusarium oxysporum f. sp. asparagi into vegetatively
mycelium. This pathogen is soilborne, occurs where
compatible groups. Phytopathology 79:88–93.
Elmer, W. H., Summerell, B. A., Burgess, L. W., and Nigh, E. L. root crops have been grown intensively, and spreads
1999. Vegetative compatibility groups in Fusarium from plant to plant. Because of the practice of growing
proliferatum from asparagus in Australia. Mycologia asparagus as a perennial, even low levels of soil infesta-
91:650–654.
tion can result in significant problems. Control relies on
Evans, T. A. and Stephens, C. T. 1989. Increased susceptibility to
Fusarium crown and root rot in virus-infected asparagus. avoiding infested sites. Where disease has occurred, do
Phytopathology 79:253–258. not replant asparagus. See the violet root rot section
Inglis, D. A. 1980. Contamination of asparagus seed by under carrot in the Apiaceae disease chapter (page 105).
Fusarium oxysporum f. sp. asparagi and Fusarium
moniliforme. Plant Disease 64:74–76. The fungus Zopfia rhizophila is common on the old
Johnston, S. A., Springer, J. K., and Lewis, G. D. 1979. Fusarium fleshy or dead roots of mature asparagus plants. It
moniliforme as a cause of stem and crown rot of asparagus produces numerous black perithecia on the root
and its association with asparagus decline. Phytopathology
69:778–780.
surface. Perithecia contain asci having two-celled,
Knaflewski, M. and Sadowski, C. 1990. Effect of chemical brown ascospores that measure 68–85 x 35–45 μm.
treatment of seeds on the healthiness of asparagus seeds and This fungus is generally regarded as a weak pathogen.
crowns. Acta Horticulturae 271:383–387. Plants growing in poorly drained areas are most likely
Nigh, E. L. 1990. Stress factors influencing Fusarium infection in
asparagus. Acta Horticulturae 271:315–322.
to be affected.
Nigh, E .L., Guerrero, C., and Stanghellini, M. E. 1997.
Evaluation of Fusarium infected asparagus spears for References
fumonisin mycotoxins. Proceedings of IX International Sadowski, C. 1990. The occurrence of Zopfia rhizophila
Asparagus Conference, 100–106. Rabenh. on asparagus roots in Poland. Acta Horticulturae
Schofield, P. 1991. Asparagus decline and replant problem in 271:377–381.
New Zealand. New Zealand Journal of Crop and
Horticultural Science 19:213–220.
Schofield, P., Nichols, M. A., and Long, P. G. 1996. The
involvement of Fusarium spp. and toxins in the asparagus
replant problem. Proceedings of the VIII International
Symposium on Asparagus. Acta Horticulturae 415:309–314.
Schreuder, W., Lamprecht, S. C., Marasas, W. F. O., and Calitz, F.
J. 1995. Pathogenicity of three Fusarium species associated
with asparagus decline in South Africa. Plant Disease
79:177–181.
F UNGAL D ISEASES
Phytophthora megasperma, Phytophthora spp.

127
PHYTOPHTHORA SPEAR AND
CROWN ROT

Phytophthora species are important pathogens of
asparagus in the Americas, Europe, Australia, and New
Zealand. Losses can exceed 50%. The disease appears
to be less important where white asparagus is produced.
Problems in England have appeared only recently.
Losses occur from reduced stands in new plantings,
lowered yields in established crops, and postharvest rot
of spears.

This is an early season disease. Emerging spears initially
develop small, light brown lesions. As disease progress- 127 White mycelium and spear infection of asparagus
es, lesions increase in size and can completely girdle the infected with Phytophthora.
spear. Spears often bend or twist at the infection site,
and eventually can collapse. Spear tissue becomes soft
and supports the growth of white mycelium (127). If
conditions dry after infection, diseased spears will germinating oospores. Zoospores swim in the soil
shrivel. Infected roots are initially water-soaked, then water and infect shoots and roots. Young spears are the
later brown and rotted. The pathogen can also infect most susceptible. The optimum temperatures for
asparagus crowns and causes a browning and softening infection are 10–12º C. Severe attacks are associated
of internal tissues. The soft tissue contrasts with dry rot with wet conditions and poor drainage. Later in the
symptoms caused by Fusarium. season when temperatures are 20–25º C and fern
growth is mature, there may be little disease. Infected
Causal agents crowns that are divided and used for propagation will
The main pathogen of Phytophthora spear and crown result in new plantings that already have the disease.
rot is the oomycete Phytophthora megasperma. Semi-
selective media, such as corn meal agar amended with Control
pimaricin, ampicillin, rifampicin, and PCNB, are Resistant cultivars are not yet available, though new
helpful for recovering Phytophthora. Phytophthora hybrids from New Zealand have partial resistance. Use
megasperma is homothallic and produces oogonia with seedlings and crown divisions that are disease-free.
mainly paragynous antheridia. Sporangia are non- Avoid fields that have a history of the disease or poorly
papillate, internally proliferating, and measure 35–60 x draining, heavy soils. Manage the field so that soils have
25–45 μm. Other Phytophthora pathogens of aspara- good structure and drain well. Apply fungicides, par-
gus include P. cactorum and P. cryptogea in California, ticularly phenylamide and fosetyl aluminum products.
and P. richardiae in Australia. All Phytophthora species
affecting asparagus are soilborne organisms. Asparagus References
isolates of P. megasperma may be a distinct species and Falloon, P. G. 1990. Field screening of asparagus for tolerance to
F UNGAL D ISEASES
could be renamed in the future. Phytophthora rot. Proceedings of the 7th International
Symposium on Asparagus. Acta Horticulturae 271:69–76.
Falloon, P. G. and Grogan, R. G. 1988. Isolation, distribution,
Disease cycle pathogenicity and identification of Phytophthora species on
Phytophthora species survive for long periods in soil by asparagus in California. Plant Disease 72:495–497.
means of oospores. Zoospores are released from spor- Falloon, P. G., Mullen, R. J., Benson, B. L., and Grogan, R. G.
1985. Control of Phytophthora rot with metalaxyl in
angia that are produced on infected host tissues or from established asparagus. Plant Disease 69:921–923.
Pleospora herbarum Introduction and significance

(anamorph = Stemphylium vesicarium) This disease is an important cause of yield loss in some
PURPLE SPOT production areas, notably New Zealand, USA, and
parts of Europe. In other areas, disease severity varies
128
and is dependent on wet weather in the latter part of the
growing season. Yield is reduced when purple spot
causes premature defoliation and diseased, unmarket-
able spears.

Two types of purple spot inoculum, ascospores and
conidia, cause similar symptoms. Small, elliptical
lesions that measure 2–6 mm in diameter develop on
the emerging spears. Lesions are often sunken and
brown with purple margins. These infection sites are
shallow and do not penetrate deeply into the spear.
However, the prominent lesions still reduce market-
ability of the product. Severe attacks result in large
numbers of lesions. Damage to spears from wind-
blown soil increases the degree of infection. On mature
fern, the symptoms are small white lesions with red-
brown margins that are on individual leaflets and stems
(128). Disease causes yellowing and defoliation of the
needles (129). Loss of the foliage can weaken the crown
and reduce yields in subsequent seasons.
Causal agent
The cause of purple spot is the ascomycete fungus
Pleospora herbarum. Spherical perithecia mature over
several months and produce yellow-brown ascospores
that have seven transverse septa and measure 38 x 18
128 Stem lesions of purple spot of asparagus. μm. The anamorph of this pathogen is Stemphylium
vesicarium. Conidia of S. vesicarium have verrucose
129
walls, are yellow-brown to olive-brown, measure
25–42 x 12–22 μm, and have one to six (usually three)
transeverse septa and one to three longitudinal septa.
The spores have a conspicuous basal scar. Conidia are
borne on mainly unbranched, yellow-brown to olive-
brown conidiophores that have a distinctly swollen
apical cell with a pore.
F UNGAL D ISEASES
129 Yellowing of asparagus leaves caused by

Stemphylium.
Disease cycle Puccinia asparagi

The pathogen survives on crop residues and fern debris, RUST
and produces perithecia that release ascospores in the
spring. Spear infection is associated with periods of wet Introduction and significance
weather during the harvest period. Symptoms may Rust occurs worldwide wherever asparagus is grown.
appear on spears in less than 24 hours after a rain. The disease is an important cause of early defoliation,
Infection occurs through stomata, and long periods and hence yield loss for subsequent years, in production
(greater than 16 hours) of surface wetness are required areas in North America and Europe. In the UK, rust
for severe infection to develop. This pathogen does not was of minor significance for many years, but it remains
persist in the soil. a threat as indicated by serious outbreaks in 1997.

Remove and dispose of fern residues prior to emergence After asparagus harvest is completed, subsequent
of spears in spring. Differences in cultivar susceptibility shoots are allowed to develop and grow into the foliage
may exist, so select more tolerant cultivars. Short or fern. Rust disease infects this fern foliage and causes
compact plants with low branches (for example, the dark to brown-red pustules on the stems and needles
culivar Cito) are generally more susceptible than tall (130). Rust can spread rapidly, causing extensive
erect types (cv. Jersey King). Apply protectant fungi-
cides, such as chlorothalonil, to the fern.
References
Evans, T. A. and Stephens, C. T. 1984. First report in Michigan of
the teleomorph of Stemphylium vesicarium, causal agent of
purple spot of asparagus. Plant Disease 68:1099.
130 Stem pustules 130
Falloon, P. G., Falloon, L. M., and Grogan, R. G. 1987. Etiology
and epidemiology of Stemphylium leaf spot and purple spot of rust of
of asparagus in California. Phytopathology 77:407–413. asparagus.
Hausbeck, M. K., Hartwell, J., and Byrne, J. M. 1997.
Epidemiology of Stemphylium leaf spot and purple spot in
no-till asparagus. Proceedings of IX International Asparagus
Conference, 48–53.
Johnson, D. A. 1990. Effect of crop debris management on
severity of Stemphylium purple spot of asparagus. Plant
Disease 74:413–415.
Johnson, D. A. and Lunden, J. D. 1986. Effects of wounding and
wetting duration on infection of asparagus by Stemphylium
vesicarium. Plant Disease 70:419–420.
Lacy, M. L. 1982. Purple spot: a new disease of young asparagus
spears caused by Stemphylium vesicarium. Plant Disease
66:1198–1200.
Meyer, M. P., Hausbeck, M. K., and Podolsky, R. 2000. Optimal
fungicide management of purple spot of asparagus and
impact of yield. Plant Disease 84:525–530.
Suberi, H. and Price, T. V. 2000. Infection of leaves by Alternaria
porri and Stemphylium vesicarium and disease development
in controlled environments. Plant Pathology 49:375–382.
Sutherland, P. W., Hallet, I. C., Parkes, S. L., and Templeton,
M. D. 1990. Structural studies of asparagus spear infection by
F UNGAL D ISEASES
Stemphylium. Canadian Journal of Botany 68:1311–1319.

131
Causal agent
Rust disease is caused by the basidiomycete fungus
Puccinia asparagi, an autoecious, macrocyclic rust. The
fungus forms uredinia pustules that release brown, one-
celled urediniospores that measure 19–30 x 18–25 μm.
Later in disease development, the same pustules will
form black, two-celled teliospores that measure 30–50
x 19–26 μm. Two other spore types, spermagonia and
aecidiospores, can also develop on yellowish lesions in
the spring but are often overlooked.
Disease cycle
Like most rust fungi, the life cycle is complex. Disease is
131 Dieback of asparagus foliage infected with rust. often initiated by teliospores that germinate to produce
intermediate spore types that eventually form aecidia.
Aecidiospores penetrate the asparagus host and result
132 132 Black in uredinia and urediniospores during the summer.
teliospores of rust Teliospores are produced in increasing numbers
of asparagus. towards the end of the season. Sporulation is optimal at
25–30º C. Spore germination requires surface moisture
for only 3 hours (optimum 9 hours) at 15º C. The com-
bination of warm days and cool nights with dew
formation is particularly favorable for rust develop-
ment.
Control
Remove and dispose of fern residues prior to emergence
of spears in spring. Remove volunteer asparagus plants
that might be infected. Apply fungicides such as triazole
products. Resistant cultivars are not yet available.
References
Beraha, L., Linn, M. B., and Anderson, H. W. 1960.
Development of asparagus rust pathogen in relation to
temperature and moisture. Plant Disease Reporter 44:82–86.
Blanchette, B. L., Groth, J. V., and Waters, L. 1982. Evaluation of
asparagus for resistance to Puccinia asparagi. Plant Disease
66:904–906.
Fantino, M. G., Granier, A., Solaini, J., and Di Carmine, D. 1990.
Four years of trials (1985–1988) on asparagus rust (Puccinia
asparagi D. C.) in Lazio. Acta Horticulturae 271:371–375.
Johnson, D. A. 1986. Two components of slow-rusting in
asparagus infected with Puccinia asparagi. Phytopathology
76: 08–211.
infection of the foliage (131). Later in the season, the
Johnson, D. A. and Lunden, J. D. 1992. Effect of rust on yield of
F UNGAL D ISEASES
pustules may become black as the teliospores are susceptible and resistant asparagus cultivars. Plant Disease
formed (132). Severe infection results in weakened 76:84–86.
plants and reduced yield. Mullen, R. J. and Viss, T. C. 1996. Control of asparagus rust in
the Sacramento-San Joaquin delta region of California.
Proceedings of the VIII International Symposium on
Asparagus. Acta Horticulturae 415:297–300
.
Asparagus virus 1, 2, 3,Tobacco streak virus range than AV-1 and includes other vegetables such as
ASPARAGUS VIRUSES beet, cucumber, basil, and bean. Yield loss estimates for
AV-2 alone are often 20–30%, but can be much higher.
Introduction and significance Single virus infections of AV-1 or AV-2 and virus com-
Asparagus is affected by several viruses including binations may increase nutrient exudate release from
Arabis mosaic virus, Cucumber mosaic virus, Straw- asparagus roots; this factor results in more severe
berry latent ringspot virus, Tobacco streak virus, and damage from Fusarium crown and root rot disease.
three asparagus viruses: Asparagus virus 1, Asparagus Asparagus virus 3 (AV-3) is a potexvirus. It is trans-
virus 2, and Asparagus virus 3. The extent of virus mitted mechanically and has filamentous, flexuous
problems on asparagus has not been thoroughly inves- particles 580 nm long. Tobacco streak virus (TSV) is an
tigated. At present the asparagus viruses 1, 2, and 3 ilavirus most prominent in North and South America
and Tobacco streak virus are considered the most and Australia. It is transmitted by thrips (Frankliniella
important. Asparagus virus 3 has only been reported occidentalis, Thrips tabaci) and mechanically. It may
from Japan. also be seedborne and transmitted to flowering plants
by pollen. In the USA, TSV has been associated with
Symptoms and diagnostic features plants that were infected by AV-2 from seed. It has a
Asparagus plants do not exhibit typical virus-like wider host range than AV-2 including beet, cucurbits,
symptoms when infected with these virus pathogens. lettuce, tomato, pea, basil, bean, and spinach.
Deformities, mosaic patterns, and other typical symp-
toms are not observed on diseased plants. However, Control
infected asparagus plants will have reduced vigor and AV-2 is the most important virus to control. Use seed,
yield fewer spears, especially if plants were infected at transplants, and divided crowns that do not harbor the
an early stage. Virus-infected plants may be more sus- virus. Disinfect cutting knives used in harvest, though
ceptible to other pathogens. this is not always feasible. Controlling the vectors will
not provide good control of AV-1 or TSV as these are
Causal agents and disease cycle acquired and transmitted rapidly. However, insect man-
Asparagus virus 1 (AV-1) is a potyvirus that has a agement should be practiced. Maintain good weed
750 nm flexuous particle and is worldwide in distribu- control if weed hosts are present.
tion. In the USA (Washington state), older plantings can
have 100% infection. It is transmitted in a nonpersist- References
ent manner by various aphid species, including Myzus Betaccini A, Giunchini, L., and Poggi Pollini, C. 1990. Survey on
persicae. AV-1 can be mechanically transmitted, but not asparagus virus diseases in Italy. Acta Horticulturae
271:279–284.
by plant-to-plant contact in the field. Weed hosts
Elmer, W. H. 2001. The economically important diseases of
include fat hen (Chenopodium album). AV-1 does not asparagus in the United States. Online. Plant Health Progress
cause obvious symptoms by itself, but yield losses of up doi:10.1094/PHP-2001-0521-01-RV.
to 30% have been claimed. Asparagus plants often Evans, T. A., DeVries, R. M., Wacker, T. L., and Stephens, C. T.
1990. Epidemiology of asparagus viruses in Michigan
carry a mixture of viruses; AV-1 in combination with asparagus. Acta Horticulturae 271:285–290.
AV-2 has caused much more severe yield loss (up to Falloon, P. G., Falloon, L. M. and Grogan, R. G. 1986. Survey of
70%) than either virus alone. California asparagus for asparagus virus I, asparagus virus II
and tobacco streak virus. Plant Disease 70:103–105.
Asparagus virus 2 (AV-2) has no known insect vector
Jaspers, M. V. and Falloon, P. G. 1996. Survey of asparagus
and is transmitted mechanically via sap on cutting crops in New Zealand for asparagus virus 2. Acta
knives, through seed, and by pollen. AV-2 is an ilarvirus Horticulturae 415:301–307.
with isometric particles and is widely distributed in Jaspers, M. V., Falloon, P. G., and Pearson, M. N. 1999. Long-
V IRAL D ISEASES
term effects of asparagus virus 2 infection on growth and

North America, New Zealand, and Europe. In New reproductivity in asparagus. Annals of Applied Biology
Zealand, the average incidence of AV-2 in a survey of 67 135:379–384.
fields was 44%. In the USA, seed infection in the late Uyeda, I. and Mink, G. I. 1981. Properties of asparagus virus II,
1980s averaged 22%, but this has now been largely a new member of the ilarvirus group. Phytopathology
40:832–846.
eliminated with virus-tested seed. AV-2 has a wider host
D ISEASES OF V EGETABLE C ROPS
138
Beta vulgaris Beet
THE PRIMARY VEGETABLES in the former Chenopodiaceae (goosefoot family) –

now a subfamily of the Amaranthaceae – include those grown as leafy vegetables and as root
commodities. Leafy commodities are primarily spinach (Spinacia oleracea) and Swiss chard
(Beta vulgaris subsp. cicla). The main root commodity is table beet or beetroot (Beta vulgaris).
However, young beet foliage is also harvested for market and is called leaf beet or spinach beet.
Cultivated beet and related commercial commodities are derived from Beta maritima
(sea beet) that originated in the Mediterranean and North African areas.
Table beet traditionally has been grown for its thick, edible red root. The red
root color comes from a combination of very stable purple (betacyanin) and yellow
(betaxanthin) pigments. Recently many more table beet choices are available as cultivars and
can have roots that are white, yellow, and other colors. Table beets are also grown for the foliage
and sold as beet greens. In production areas such as California, beet is planted in high density,
wide bed (2 m across) configurations, grown for only a few weeks, then harvested for the young,
tender foliage. This foliage is used as a fresh market commodity that is mixed with lettuce,
mustards, and other leafy vegetables and bagged as a ready-to-eat salad product.
Swiss chard is grown for its large leaves and prominent petioles.
Chard cultivars are likewise diverse, and various cultivars have white, red, yellow, or
orange-colored petioles. Like beets in California, Swiss chard is also grown for only a few weeks
and then harvested for a small, ‘baby leaf’ vegetable commodity.
As sugar beet (Beta vulgaris) is another closely related vegetable, information on sugar beet
should be consulted when considering diseases of spinach, Swiss chard, and table beet. Because
of the economic importance of spinach, spinach diseases are detailed in a separate chapter.
Aphanomyces cochlioides nearby infected seedlings. The pathogen invades the

DAMPING-OFF, hypocotyl and spreads into the petioles and cotyledons,
BLACK ROOT ROT often causing plants to collapse and die. Infected tissues
are initially brown and then turn black. As the fleshy
Introduction and significance tissues of the lower stem rot and dissipate, the
Damping-off and black root rot diseases affect table remaining central core of the hypocotyl dries out,
beet, Swiss chard, sugar beet, spinach, and a number of becoming dark, hard, and wire-like in appearance and
weeds including Chenopodium album. The disease is texture (133). If temperatures are above 15º C and the
known as ‘caida’ in South America. If conditions favor soil is wet, extensive areas of the crop could be lost
F UNGAL D ISEASES
the pathogen, there can be widespread stand loss. within a few days. On older plants the disease is called
black root rot. These larger plants develop root rots,
Symptoms and diagnostic features especially of the fine feeder roots, which result in
Pre-emergence losses are usually limited, but seedlings stunted growth, yellowing, and wilting. Roots are dark
that do emerge above ground become infected by in color. The shape of the swollen hypocotyl and upper
soilborne inoculum or mycelium spreading from taproot, the harvested beet, is distorted.
B ETA VULGARIS 139
133 Disease cycle

The pathogen is soilborne and persists for long periods
of time in the field. Oospores germinate and produce
zoosporangia, which subsequently release zoospores.
These zoospores swim to, and make contact with,
roots. Seedling infection becomes progressively more
severe as temperatures increase from 13 to 25º C.
Damage is limited if soil temperatures are below 15º C.
The pathogen can also survive on weed hosts.
133 Beet seedlings affected by Aphanomyces. Control

Resistant cultivars are widely used for sugar beet, where
susceptibility to A. cochlioides has been associated with
134
susceptibility to R. solani. Table beet appears to be less
sensitive to both pathogens. Rotate with non-host crops
such as small grains, soybean, and maize. Bean, clover,
and lucerne (alfalfa) may increase soil inoculum and
thereby cause problems for table beet. Select sites with
well-draining soils, prepare seedbeds so that water
drains well, and provide adequate potassium to the
crop. In Europe, plant early in the season so that
seedlings establish while soil temperatures are unfavor-
able for the pathogen. Conversely, late planting
increases the risk of attack. In the UK, seed treatment
134 Damping-off of red beet seedlings caused by with hymexazol has been widely used on sugar beet;
Pythium. this treatment is registered for table beet seed in some
countries.

Damping-off and black root rot diseases are caused by Byford, W. J. 1985. A comparison of fungicide seed treatments to
the oomycete Aphanomyces cochlioides. The life cycle improve sugar beet seedling establishment. Plant Pathology
34:463-466.
of this pathogen is probably similar to that described for
Payne, P. A., Asher, M. .J C., and Kershaw, C. D. 1994. The
A. euteiches. The sexual stage for homothallic A. incidence of Pythium spp. and Aphanomyces cochlioides
cochlioides develops when antheridia fuse with the associated with sugar beet growing soils of Britain. Plant
oogonium and an oospore is produced. Oospores are
Osburn, R. M. and Schroth, M. N. 1989. Effect of osmopriming
hyaline to yellow, measure 20–23 μm in diameter, and sugar beet seed on germination rate and incidence of Pythium
have less sculpturing of the internal wall than ultimum damping off. Plant Disease 73:21–24.
A. euteiches. Oospores are formed in rotted tissues and O’Sullivan, E. and Kavanagh, J. A. 1991. Characteristics and
pathogenicity of isolates of Rhizoctonia spp. associated with
are capable of surviving for many years in soil. The damping-off of sugar beet. Plant Pathology 40:128–135.
asexual stage consists of long, filamentous zoosporan- O’Sullivan, E. and Kavanagh, J. A. 1992. Characteristics and
gia that may be up to 3–4 mm long. Swimming primary pathogenicity of Pythium spp. associated with damping-off of
zoospores are released from the tips of the zoosporan- sugar beet. Plant Pathology 41:582–590.
F UNGAL D ISEASES
gia. These primary zoospores measure 6–15 μm and

may encyst and later germinate and release secondary
zoospores. A number of other soilborne pathogens
cause damping-off of beet, including the following:
Pleospora bjoerlingii, Pythium species (134), and
Rhizoctonia solani.
Cercospora beticola
135
CERCOSPORA LEAF SPOT

This disease occurs wherever table beets and Swiss
chard are grown and is one of the most important
diseases affecting plants in the chenopodium group.
The disease results in significant damage in warm
temperate areas, including southern Europe, the
Mediterranean region, Japan, Russia, and the USA.
Crop losses can exceed 40% on a root weight basis and,
in extreme cases, almost complete crop loss can occur.
The disease is particularly problematic when the crop is
grown for its foliage. 135 Cercospora leaf spot on beet.
Symptoms and diagnostic features Disease cycle

Circular leaf spots are small initially, up to 2 mm in Spores are splash and wind dispersed and may be
diameter, and can be very numerous. Spots have a pale carried in irrigation water. Sporulation, germination,
brown or off-white center with a reddish margin (135); and infection occur most rapidly at 25–35º C when
the latter is useful for distinguishing it from Ramularia night temperatures are above 16º C and relative
leaf spot. Spots expand in size, remain circular or humidity is above 90%. There is limited disease activity
oblong, and can result in extensive loss of foliage. The below 15º C. Leaf penetration occurs only via stomata.
centers of the spots become gray as the fungus produces Dry periods, of up to 6 hours during the day, enhance
dark mycelium and other structures within and on the infection compared with continuous wetness. Spots
leaf tissue. appear in 7 to 10 days after infection under optimal
conditions. Cercospora beticola overwinters as sclerotia
Causal agent in infected leaves and can survive in soil for up to 2
Cercospora leaf spot is caused by the fungus years. Initial inoculum comes from infested seed, weed
Cercospora beticola. The conidia are borne on hosts, and spores produced on infected crop residues.
unbranched brown conidiophores growing in clusters
from stomata. Conidia are hyaline, with three to 14 Control
septa, and are long and thread-like in shape. Conidia Use resistant cultivars if available. For sugar beet,
range in length from 78–228 μm, and are slightly specific and non-specific resistance has been identified.
tapered from base (4.4–6.3 μm width) to tip (1.6–3.2 Bury infected crop residues and destroy volunteer
μm width). Spore length and septation are influenced by plants. Do not plant vegetable production crops close
environmental conditions; spores may be up to 400 μm to seed crops. Use seed that does not have significant
long and have up to 27 septa. In leaf tissue the fungus levels of the pathogen. For infested seed, apply seed
makes dark mycelial clumps that are called sclerotia. A treatments. Apply fungicides prior to infection and
perfect stage has not been reported. Hosts include sugar symptom development. Isolates resistant to sterol
beet, table beet, Swiss chard, wild sea beet, spinach, and demethylation-inhibiting (DMI) fungicides have been
various Atriplex and Chenopodium weeds. The documented, so use products with different modes of
pathogen is seedborne. On sugar beet, various physio- action to reduce the risks of further resistance problems.
F UNGAL D ISEASES
logical races have been identified. In the UK, strobilurin plus triazole fungicide combina-
tions have recently been approved for use against
Cercospora on sugar beet. Disease prediction systems
are used in some countries to better time fungicide
applications.
B ETA VULGARIS 141

Calpouzos, L. and Stallknecht, G. F. 1967. Symptoms of The first signs of powdery mildew are scattered, small,
Cercospora leaf spot of sugar beets influenced by light radiating colonies consisting of superficial white fungal
intensity. Phytopathology 57:799–800.
growth. Such growth tends to start on the older leaves
Karaoglanidis, G. S. and Thanassoulopoulos, C. C. 2003. Cross-
resistance patterns among sterol biosynthesis inhibiting and occurs on both upper and lower leaf surfaces. As
fungicides (SBIs) in Cercospora beticola. European Journal of the disease develops, the entire leaf can become heavily
colonized with extensive patches of the white powdery
Karaoglanidis, G. S., Ioannidis, P. M., and Thanassoulopoulos,
C. C. 2002. Changes in sensitivity of Cercospora beticola fungus (136, 137). Older leaves with severe powdery
populations to sterol-demethylation-inhibiting fungicides mildew will turn yellow and can later senesce and die.
during a 4-year period in northern Greece. Plant Pathology Younger leaves can also be affected if disease in the field
51:55–62.
Moretti, M., Arnold, A., D’Agostini, A., and Farina, G. 2003.
is severe.
Characterization of field-isolates and derived DMI-resistant
strains of Cercospora beticola. Mycological Research Causal agent
107:1178–1188.
Powdery mildew is caused by the fungus Erysiphe
Pundhir, V. S. and Mukhopadhyay, A. N. 1987. Epidemiological
studies on Cercospora leaf spot of sugar beet. Plant Pathology betae. This pathogen is a typical powdery mildew
36:185–191. fungus having both sexual and asexual stages on beet
Wallin, J. R. and Loonan, D. V. 1971. Effect of leaf wetness and related hosts. Asexual conidia are produced
duration and air temperature on Cercospora beticola
infection of sugarbeet. Phytopathology 61:546–549.
basipetally in short chains arising from mycelium on the
leaf surface. Conidia are barrel-shaped, hyaline, and
variable in size depending upon environmental condi-
Erysiphe betae tions. Conidia are smaller (measuring 40 x 14 μm)
POWDERY MILDEW when temperatures and relative humidity are low and
larger (measuring 49 x 18 μm) when both factors are
Introduction and significance high. The sexual stage consists of a spherical cleisto-
This common disease occurs in Europe, the Middle thecium, that is initially yellow, later turns dark brown
East, and parts of the USA. It affects sugar beet, fodder to black, and measures 0.1 mm in diameter. Cleisto-
beet, table beet, and Swiss chard, as well as wild sea beet thecia have numerous simple or branched hyphal
(Beta maritima). Severe attacks can reduce yield by up appendages and contain four to six asci, each ascus
to 25% and table beet crops with badly diseased foliage bearing three to five ascospores. Ascospores measure
may be unmarketable. 20–30 x 14–16 μm.
136 137
F UNGAL D ISEASES
136 Beet leaf showing powdery mildew. 137 Beet severely affected by powdery mildew.
Disease cycle Peronospora farinosa f. sp. betae

Powdery mildew conidia have a high water content DOWNY MILDEW
(60%) that enables these spores to germinate at low
relative humidity. Germination occurs over a wide Introduction and significance
range of environmental conditions, with an optimum of This downy mildew affects sugar beet, mangold, Swiss
25º C and 70–100% relative humidity. Spores penetrate chard, wild sea beet, and table beet. Other forma
the leaf within a few hours and then produce hyphal speciales (f. sp.) affect different members of the
growth and chains of conidia. As conidia are dislodged Chenopodiaceae; for example, P. farinosa f. sp.
from the leaf and dispersed by winds, a new spore will spinaciae is the important downy mildew of spinach.
mature at the basipetal end of the conidial chain. Spores Beet downy mildew is found in almost all beet
are short-lived but may be transported in high altitude producing areas and is most common in mild climates
winds over long distances. Epidemics are associated such as coastal California and Oregon in the USA and
with dry weather alternating with periods of high in parts of Europe. Downy mildew has been associated
relative humidity and temperatures above 20º C. Plant with malformed roots of table beet in the UK. When
susceptibility increases with age, and damage is more downy mildew causes death of the apical growing
severe on drought-stressed plants because of leaf loss. point, plant growth is severely hampered and losses of
Frequent rains slow the progress of the disease. more than 50% can result.
Powdery mildew overwinters in buried roots (in Europe
these are called groundkeepers) and on volunteer beet Symptoms and diagnostic feature
and weed hosts. Cleistothecia can be found on crop Downy mildew can infect plants at any stage, and initial
debris, which is another means of overwintering. symptoms are chlorosis and distortion of the youngest
Cleistothecia release ascospores during rain. leaves. The pathogen grows systemically within the
young leaves and may invade the growing point,
Control resulting in reduced growth and a rosette of spindly,
Powdery mildew control relies on fungicides. Apply deformed, chlorotic leaves, which curl downwards
treatments at the onset of symptoms. Sulfur fungicides (138). Such leaves can be noticeably thickened and
and newer triazole products have been effective. After brittle. Under humid conditions, a dense, purple-gray
harvest, plow down and destroy crop residues, and growth appears on both upper and lower leaf surfaces.
remove volunteer plants. If possible, do not plant Individual downy mildew lesions can also develop on
vegetable beet in close proximity to sugar beet fields. A leaves. These lesions are chlorotic, irregular in shape,
disease forecasting system in the UK, based on the and later dry and turn brown. If the growing point has
number of ground frosts in February and March, helps been invaded, a dark heart rot of the crown may
guide control strategies in sugar beet. These forecasts develop. This heart rot can be difficult to recognize as a
could be useful to vegetable growers, as they provide an downy mildew symptom if the infected leaves have
indication of disease risk and inoculum pressure from senesced and dropped off the plant. If older plants are
sugar beet crops. infected, such plants can recover and produce addi-
tional leaves that are healthy. In seed crops, the main
References seed stalk is stunted and distorted, sepals and bracts are
Asher, M. J. C. and Williams, G. E. 1991. Forecasting the swollen, and the overall effect is a ‘witch’s broom’
national incidence of sugar beet powdery mildew from symptom.
weather data in Britain. Plant Pathology 40:10–107.
Hills, F. J., Chiarappa, L., and Geng, S. 1980. Powdery mildew of
sugar beet: Disease and crop loss assessment. Phytopathology
F UNGAL D ISEASES
70:680–682.
Ruppel, E. G., Hills, F. J., and Mumford, D. L. 1975.
Epidemiological observations on the sugarbeet powdery
mildew epiphytotic in western U. S. A. in 1974. Plant Disease
Reporter 59:283–286.
B ETA VULGARIS 143
Causal agent 138

Downy mildew is caused by the oomycete P. farinosa f.
sp. betae. The pathogen produces dichotomously
branched sporangiophores that emerge through
stomata. The sporangia are produced at the tips of the
sporangiophore branches, are hyaline to pale violet, and
measure 20–28 x 17–24 μm. Oospores measure
26–36 μm and under cool moist conditions are
produced in infected vegetative tissues and seed. The
pathogen was previously known as P. schachtii.
Disease cycle
The pathogen can be seedborne and therefore spread
from place to place in seed. About 1% of infested seeds 138 Beet leaves infected with downy mildew.
give rise to infected plants. Oospores in the soil
germinate to produce mycelium and then sporangia.
Overwintering mycelia in seed crops, weed hosts, and
volunteer plants also produce sporangia. Sporangia are
airborne and are carried by wind to host plants. For
severe epidemics to develop, cool, moist conditions
(optimum temperature is 8º C) are required. Sporangia
form at 5–22º C and 60–100% relative humidity
(optimum 12º C, 85% relative humidity) and germinate Pleospora bjoerlingii (anamorph = Phoma betae)
at 1–30º C (optimum 4–10º C). At least 6 hours of leaf BLACK LEG
wetness and cool temperatures (optimum 7–15º C) are
required for infection. There is little infection at tem- Introduction and significance.
peratures above 20º C. Black leg is an important disease of beet. The disease
occurs in most beet producing areas and is especially a
Control concern in Europe, North America, and Africa. The
Use seed that does not have significant levels of the pathogen causes symptoms on both roots and foliage.
pathogen. Use seed that has been produced in dry
regions that discourage downy mildew development. Symptoms and diagnostic features
Remove volunteer and weed plants that harbor the Symptoms on young plants include pre-emergence
pathogen. Destroy crop residues after harvest. There is damping-off, where seed and germinated seedlings die
some disease resistance available in sugar beet. Use before growing above ground. Damping-off symptoms
fungicides as required; protectant sprays of dithiocar- are indistinguishable from those caused by soilborne
bamates or phenylamides have given some control. pathogens Aphanomyces and Pythium. Young plants
that do emerge can develop black lesions on stem tissue
References that is in contact with soil. These lower stem symptoms
Byford, W. J. 1981. Downy mildews of beet and spinach. In: The are the reason for the common name of black leg. Foliar
Downy Mildews (Ed. D. M. Spooner) pp. 531–543. symptoms are pale brown leaf spots that can measure
Academic Press London.
up to 2 cm in diameter and contain concentric rings of
MacFarlane, J. W. 1968. Elimination of downy mildew as a
F UNGAL D ISEASES
major sugarbeet disease in the coastal valleys of California. the fungus fruiting bodies, or pycnidia. These spots are
Plant Disease Reporter 52:297–299. mostly found on the older leaves and may be centered
on rust pustules. In seed crops, the stems develop dark
streaks and lesions with gray centers. Severe infection
causes stems to break at the crown and roots to have a
dry black rot. Pedicels on the flowering stems can
develop lesions. Infected roots initially have water- may have systemic infections. Late in the season the
soaked lesions which turn brown and develop into pathogen can form the pseudothecia perfect stage and
deep, sunken black lesions containing gray white overwinter on crop residues. In the spring, pseudothe-
mycelium and pycnidia. Severely affected roots become cia produce airborne ascospores, which cause leaf spots
spongy and full of cavities (139). Root rot often in newly planted root crops and stem infections in seed
develops during storage of table beet. Root rot crops. At harvest, if beet foliage is closely trimmed to
symptoms may be confused with boron deficiency, the root or if roots are wounded, root rots can develop
which causes death of the growing point and allows during storage. Postharvest disease is favored by tem-
secondary rots to develop. peratures above 15º C but can take place at much lower
temperatures. If rain occurs close to seed crop harvest
Causal agent time, seedborne infection can be increased.
Black leg is caused by the ascomycete fungus Pleospora
bjoerlingii. The Pleospora form produces black pseudo- Control
thecia that measure 200–500 μm in diameter and have Use seed that does not have significant levels of the
one short apical papillum each. Pseudothecia develop pathogen. Seed treatments are a standard practice for
on rotted roots at the end of the season and on crop sugar beet and should also be considered for vegetable
residues that persist over the winter. In the spring the beet. A thiram seed treatment is now often used on table
pseudothecia produce brown ascospores that are 18–25 and sugar beet seed. Hot water seed treatment is
x 7–10 μm. The pathogen is usually encountered in its effective, but is not used commercially. Fungicide sprays
asexual stage Phoma betae. Black globose pycnidia, are rarely used on crops grown for root production, but
which are immersed in host tissue, produce hyaline, uni- may be useful for seed crops. Implement cultural
cellular conidia that measure 5–8 x 3–4.3 μm. practices such as crop rotation, burying crop residues
after harvest, and maintaining adequate levels of
Disease cycle phosphate, potash, manganese, and boron.
Phoma betae is a seedborne pathogen. Optimum con-
ditions for disease development are temperatures of References
14–18º C and periods of high humidity. The pathogen Bugbee, W. M. 1979. Pleospora bjoerlingii in the USA.
spreads between seedlings if conidia from diseased Phytopathology 69:277–278.
Bugbee, W. M. and Campbell, L. G. 1990. Combined resistance
seedlings are splashed by rain and sprinkler irrigation.
in sugar beet to Rhizoctonia solani, Phoma betae, and
Infected seedlings that survive and continue to grow Botrytis cinerea. Plant Disease 74:353–355.
Byford, W. J. and Gambogi, P. 1985. Phoma and other fungi on
sugar beet seed. Transactions of the British Mycological
Society 84:21–28.
139 Heiberg, B. C. and Ramsey, G. B. 1948. Phoma rot of garden
beets. Phytopathology 38:343–347.
Maude, R. B. and Bambridge, J. M. 1985. Effects of seed
treatments and storage on the incidence of Phoma betae and
the viability of infected red beet seeds. Plant Pathology
34:435–437.
Monte, E. and Garcia-Acha, I. 1988. Vegetative and reproductive
structures of Phoma betae in vitro. Transactions of the British
Mycological Society 90:233–245.
F UNGAL D ISEASES
139 Root lesions on beets caused by the black leg

pathogen, Phoma betae.
B ETA VULGARIS 145
Ramularia beticola
140
RAMULARIA LEAF SPOT

This disease is widespread in western and central
Europe and North America. Most research on this
problem has involved sugar beet and fodder beet, but
the problem also affects table beet, spinach beet, and
Swiss chard. Ramularia leaf spot is important in seed
crops, where it can cause severe defoliation in warm
and wet weather. Yield losses may reach 10 to 20%, but
such severity is unusual. The typical impact of the 140 Ramularia leaf spot of beet.
disease is to reduce the quality of the edible foliage.
141
Symptoms are pale brown, circular or irregularly
shaped leaf spots that range in size from 5 mm to more
than 10 mm in diameter (140, 141). The spots are
usually larger than those caused by Cercospora
beticola, and Ramularia infections lack the distinctive
red-brown margin of Cercospora lesions. In the UK,
symptoms first occur in June and tend to worsen as
crops near maturity in autumn. In seed crops, leaf spot
severity increases as temperatures rise in the spring.
Most leaf spots occur on the older leaves, and multiple
lesions lead to early death of the leaf. The undersides of 141 Ramularia leaf spot of beet.
the lesions usually have a fine white, granular appear-
ance because of the growth of the pathogen.
more than 2 years. Sources of inoculum are buried
Causal agent roots, piles of culled beets, overwintered spinach beet
Ramularia leaf spot is caused by the fungus Ramularia plantings, and overwintered seed crops. The pathogen
beticola. The pathogen produces clusters of hyaline may also be seedborne.
conidiophores that emerge from leaf stomata.
Conidiophores bear hyaline, cylindrical, mainly two- Control
celled conidia that measure 15 x 1.5 μm. Conidia form Resistant table beet cultivars have not been developed,
in short chains. There is no known teleomorph. but plant more tolerant selections if such can be identi-
Sporulation is usually present on leaf lesions and fied. Remove volunteer and weed hosts. Bury crop
appears as tiny white tufts of fungal growth. residues after harvest. Do not plant production crops
close to seed crops. Fungicides can provide some
Disease cycle control, though these materials are generally more
The fungus sporulates when relative humidity is above important for seed crops. Effective fungicides include
70% and temperatures are in the range of 5–20º C. dithiocarbamate and triazole products.
F UNGAL D ISEASES
Optimum temperatures for fungal growth are

16–17º C. After spores penetrate through leaf stomata, References
there is an incubation period of 16 days at 17º C before Byford, W. J. 1975. Ramularia beticola in sugar-beet seed crops
symptoms occur. This pathogen produces survival in England. Journal of Agricultural Science 85:369–375.
Byford, W. J. 1976. Experiments with fungicide sprays to control
structures called pseudosclerotia that are found in crop
Ramularia beticola in sugar-beet seed crops. Annals of
debris and soil. The fungus can persist in the soil for Applied Biology 82:291–297.
Streptomyces spp.
142
SCAB

Scab lesions on table beet can cause considerable reduc-
tions in quality, resulting in loss of marketable yield.

Scab causes irregularly shaped root lesions that vary in
size. Lesions coalesce and affect large areas on the beet
root. In some cases, the disease results in tumor-like out-
growths (142). Another disease, crown gall, caused by
the bacterium Agrobacterium tumefaciens, produces
similar symptoms consisting of large, rounded, swollen
root galls having an irregular rough surface. 142 Raised lesions on beet caused by scab disease.
Causal agent
The pathogen is considered to be the actinomycete References
Streptomyces scabies. Actinomycetes are Gram-positive Adams, M. J. and Lapwood, D. H. 1978. The period of
bacteria that can form branching filaments and which susceptibility of red beet to Streptomyces scab. Plant
are common soil inhabitants. Recent research on potato
Adams, M. J., Lapwood, D. H., and Rankin, B. 1976. The
has identified several species of Streptomyces that cause growth of red beet and its infection by Streptomyces spp.
common scab, so the etiology of scab disease may be Plant Pathology 25:147–151.
more complex. Potato and table beet are often grown in Adams, M. J., Lapwood, D. H., and Crisp, A. F. 1976. The
susceptibility of red beet cultivars to Streptomyces scab. Plant
the same rotation, so the same pathogen possibly infects Pathology 25:31–33.
both crops. Streptomyces species survive for long
periods in the absence of a host crop.
Disease cycle
Table beet is most susceptible to infection when the
hypocotyl starts to swell (called decortication), which
takes place about 5 weeks after planting. Infection
occurs through wounds or lenticels near the soil surface,
but sometimes roots and aerial parts are also infected.
Beets are only susceptible for a 2 to 3 week period, after
which tissues are suberized and become resistant to
infection. Infection is favored by light, sandy soils,
alkaline soil pH, warm temperatures (13–25º C), and
soil water potentials below –40 kPa ( = –0.4 bar).
Control
There are cultivar differences, so plant resistant or
F UNGAL D ISEASES
tolerant cultivars. Avoid planting susceptible crops in

known infested fields. Do not apply lime to infested
fields if beets will be planted, since disease severity is
reduced in acid soils. Implement a crop rotation scheme
that reduces the frequency of root crops. Maintain
adequate soil moisture during decortication.
B ETA VULGARIS 147
Uromyces betae
143
RUST

Rust occurs worldwide and affects sugar beet, fodder
beet, mangold, table beet, Swiss chard, and wild sea
beet (Beta maritima). In parts of Europe and Asia the
disease can be sufficiently severe to reduce yield. For
many crops rust is a minor problem, although it has
increased in prevalence in recent years.

Symptoms consist of typical orange, raised pustules that
measure 1–3 mm in diameter (143). Pustules develop
on both top and bottom leaf surfaces and are more con- 143 Rust pustules on beet.
spicuous on beet having green foliage than on red-
leaved beet. Necrotic tissue forms around the larger
pustules, especially when pustules develop in clusters or Disease cycle
rings. With severe rust, the leaves support extensive Inoculum consists of windborne spores from overwin-
numbers of pustules, are covered with the powdery tered seed crops, volunteer plants, and weed hosts. The
orange spores, and begin to turn yellow and die. Later pathogen may be seedborne. Urediniospores are the
in the season, the pustules become dark brown, partic- primary inoculum responsible for spread of the disease.
ularly on senescent foliage, as the brown teliospores are Optimal temperatures for urediniospore germination
produced. Severe attacks cause premature senescence of are in the range of 10–22º C. Teliospores are important
foliage and reduce both yield and quality. as overwintering structures that can survive on crop
residues and for up to a year on the soil surface.
Causal agent. Aecidiospores are produced in the spring and are a third
Rust is caused by the basidiomycete fungus Uromyces spore type capable of initiating infection, though they
betae. Like many rusts, there are multiple spore types are seen less frequently than the other spore stages. Rust
for this autoecious rust. Orange-brown to golden- development is favored by warm (15–22º C), moist
brown urediniospores are single-celled, oval in shape, conditions and is inhibited by dry conditions at higher
echinulate, have two to three equatorial pores, and temperatures.
measure 26–33 x 19–24 μm. Dark brown teliospores
are oval, smooth, with attached pedicels, measure Control
26–30 x 18–22 μm, with hyaline papilli covering the While resistant cultivars are available for the sugar beet,
single apical germ pores. An aecidial stage occurs in the no such varieties are yet developed for table beet.
spring when temperatures are 10–13º C. Aecidiospores Remove diseased volunteer and weed hosts. Do not
are slightly roughened (verruculose), measure 23–26 x plant production fields in close proximity to seed crops.
18–22 μm, and are produced in yellow, cup-shaped If available, apply fungicides.
aecidia. Optimum temperature for aecidiospore germi-
nation is 15º C. References
Punithalingam, E. 1968. CMI Descriptions of Pathogenic Fungi
F UNGAL D ISEASES
No. 177. Uromyces betae.

Beet curly top virus Introduction and significance

BEET CURLY TOP Virus diseases are of major economic importance in
sugar beet and related vegetables in the Amaranthaceae.
This plant family is subject to many virus pathogens,
144
but only a few viruses are consistent concerns for veg-
etables such as table beet and Swiss chard. Beet curly
top virus (BCTV) occurs in North and South America,
Asia, the Middle East, and the Mediterranean region.
This virus is an important pathogen of many crops such
as pepper, tomato, and chenopodium plants.

Symptoms consist of stunted plants and reduced
foliage. Leaves are severely rolled upwards, crinkled
(144, 145), and sometimes form enations which are
small, swollen growths visible on the lower leaf surface.
Taproots can become distorted and support prolifera-
tion of fine roots, resulting in a ‘hairy root’ symptom;
this root proliferation symptom can be misdiagnosed as
144 Curled leaves and stunted growth of sugar beet rhizomania. Phloem tissue can be necrotic when seen in
caused by Beet curly top virus. dissected roots.
145
Causal agent
BCTV is a geminivirus with isometric particles that
measure 18–22 nm in diameter and which occur singly
or in pairs. The BCTV genome is a single-stranded
circular DNA. BCTV is vectored in a persistent manner
by the beet leafhopper (Circulifer tenellus). Circulifer
opacipennis is a vector in the Mediterranean region. In
the plant, BCTV is restricted to the phloem tissue. On a
molecular level, researchers have compared strains of
BCTV from North America and the Middle East and
found them to be similar, providing evidence that these
various BCTV strains share a common origin.
Disease cycle
This virus infects many weed and crop hosts. Recent
research on curly top disease as it occurs in Amarantha-
145 Curled sugar beet leaves caused by Beet curly top ceae, Fabaceae, Solanaceae, and other crops indicates
virus. that the viral agent may differ depending upon the host
being considered. Curly top as a disease may actually be
caused by one of four different curly top virus species:
Beet curly top virus (BCTV), Beet mild curly top virus
V IRAL D ISEASES
(BMCTV), Beet severe curly top virus (BSCTV), and

Spinach curly top virus (SCTV). Research is on-going to
further determine the relationships of these various
viruses.
B ETA VULGARIS
149
Control Beet leaf curl virus

Follow general suggestions for managing virus diseases BEET LEAF CURL
(see Part 1).
References Beet leaf curl virus (BLCV) is a rhabdovirus that is
Briddon, R. W., Stenger, D. C., Bedford, I. D., Stanley, J., restricted to central Europe, where its hosts are beet,
Izadpanah, K., Markham, P. G. 1998. Comparison of a beet spinach, and bean.
curly top virus isolate originating from the old world with
those from the new world. European Journal of Plant
Pathology 104:77–84. Symptoms and diagnostic features
Duffus, J. E. 1983. Epidemiology and control of curly top Symptoms on beet are vein clearing of the youngest
diseases of sugarbeet and other crops. In: Plant Virus
Epidemiology, R. T. Plumb and J. M. Thresh (eds.). Blackwell
leaves, which curl as the veins fail to elongate. There is
Scientific, Oxford, pp. 297–304. proliferation of small leaves so that the plant has a
Soto, M. J. and Gilbertson, R. L. 2003. Distribution and rate of rosette-like appearance. Symptoms are more severe
movement of the curtovirus beet mild curly top virus (family when temperatures are high. Root growth is also
Geminiviridae) in the beet leafhopper. Phytopathology
93:478–484. reduced.
Wang, H., Gurusinghe, P. de A., and Falk, B. W. 1999. Systemic
insecticides and plant age affect beet curly top virus Causal agent and disease cycle
transmission to selected host plants. Plant Disease
83:351–355.
Virus particles are bacilliform and measure 225 x
80 nm. The vector is the adult beet lace bug (Piesma
quadratum) that can acquire the virus during its nymph
stages, but transmits it in a persistent manner as an
adult.
Control
Follow general suggestions for managing virus diseases
(see Part 1). Control has been achieved by early planting
of strips of beet around the edge of fields that attract
lacebugs as they move into crops from hedgerows. The
strips of beet are then plowed into the ground.
V IRAL D ISEASES
Beet mild yellowing virus

146
BEET MILD YELLOWING

The Polerovirus genus of viruses has three different
species that affect these crops. Beet mild yellowing virus
(BMYV) is the most important yellows virus on
Amaranthaceae hosts in the UK and Western Europe.
Beet western yellows virus (BWYV) is prevalent in the
USA and elsewhere and infects many other plants in
addition to beet, Swiss chard, and spinach. A third
polerovirus pathogen is Beet chlorosis virus (BCHV).
146 Symptoms on beet caused by Beet mild yellowing
Symptoms and diagnostic features virus.
Infected leaves develop a bright yellow to orange-yellow
color (146, 147) but lack the brown or red spotting 147
associated with Beet yellows virus (BYV). Older leaves
are thickened, brittle, and become extensively yellow.
Leaf veins and tissues adjacent to the veins may remain
green. This yellows symptom may be confused with
various nutrient deficiency symptoms, notably those
caused by nitrogen, iron, or magnesium deficiency.
Causal agent
Though BMYV and BWYV are serologically identical,
these two distinct viruses do not infect all the same
hosts, greatly complicating the etiology of this disease.
These three viruses all infect spinach and various beet 147 Patches of beets infected with Beet mild yellowing
species. However, while some American isolates of virus.
BWYV infect lettuce, BMYV strains from Europe
cannot infect this host.
BMYV and BWYV may be found in numerous crop Dewar, A. M. 1994. The Virus Yellows Warning Scheme – an
and weed plants, and the host list is extensive, including Integrated Pest Management system for sugar beet in the UK.
In: Individuals, Populations, and Patterns in Ecology. Leather,
over 150 documented plant species. All three viruses are S. R., Watts, A. D., Mills, N. J., and Walters, K. F. A. (eds), pp.
poleroviruses and are vectored by several aphid vectors, 173–185.
especially the green peach aphid (Myzus persicae), in a Dewar, A. M., Haylock, L. A., and Ecclestone, P. M. J. 1996.
Strategies for controlling aphids and virus yellows in sugar
persistent manner. There are reports that low levels of beet. Proceedings of the Brighton Crop Protection
seed transmission can occur. Conference – Pests & Diseases 1996 1:185–190.
Duffus, J. E. 1973. The yellowing virus diseases of beet.
Control Advances in Virus Research 18:347–386.
Duffus, J. E. and Russell, G. E. 1975. Serological relationships
Follow general suggestions for managing virus diseases between beet western yellows virus and beet mild yellowing
(see Part 1). Forecasts of yellows disease risk are virus. Phytopathology 65:811–815.
V IRAL D ISEASES
released annually in the UK for sugar beet growers; Smith, H. G. 1989. Distribution and infectivity of yellowing
these could be useful to vegetable growers as well. viruses in field-grown sugar beet plants. Annals of Applied
Biology 116:503–511.
Stevens, M., Smith, H. G., and Hallsworth, P. B. 1994. The host
range of beet yellowing viruses among common arable weed
species. Plant Pathology 43:579–588.
B ETA VULGARIS 151
Beet mosaic virus Beet necrotic yellow vein virus

BEET MOSAIC BEET NECROTIC YELLOW VEIN,
RHIZOMANIA
Beet mosaic virus (BtMV) is worldwide in distribution Introduction and significance
and is one of many viruses that can be found in Beet necrotic yellow vein virus (BNYVV) is a damaging
Chenopodium plants. virus that affects many plants in the Amaranthaceae.
The disease caused by BNYVV, rhizomania, occurs
Symptoms and diagnostic features virtually wherever beet and related plants are grown.
BtMV causes a pale green to yellow green mottle or
mosaic that is similar to other mosaic disease Symptoms and diagnostic features
symptoms. A backward curling of the leaf tip, when Leaves of infected plants show mild yellowing
present, is a characteristic feature. On spinach, young symptoms and an upright growth. There may be
leaves also curl backward. Spinach leaves develop wilting of leaves, occasional veinal yellowing, and
bright yellow flecks that merge to produce large necrotic lesions. The taproot is usually stunted and
chlorotic areas. Plants are stunted and leaves become shows constriction and rotting below soil level. The
necrotic. vascular rings in the root are brown and discolored. The
name rhizomania means ‘root madness,’ or ‘crazy root,’
Causal agent and disease cycle and refers to the extensive proliferation of lateral roots
BtMV is a potyvirus and has flexuous filamentous (148, 149).
particles measuring 690–770 x 13 nm. BtMV is trans-
mitted in a nonpersistent manner by several aphid 148
species, including Myzus persicae and Aphis fabae. The
pathogen host range is broad and includes many species
in diverse plant families. Several weeds are also
important hosts.
Control
(see Part 1).
References
Cockbain, A. J., Gibbs, A. J., and Heathcote, G. D. 1963. Some
factors affecting the transmission of sugar-beet mosaic virus 148 Proliferation of small feeder roots on sugar beet
and pea mosaic viruses by Aphis fabae and Myzus persicae.
Annals of Applied Biology 52:133–143. affected by rhizomania.
Rogov, V. V., Karasev, A. V., Agranovsky, A. A., and Gorbunova,
N. I. 1991. Characterization of an isolate of beet mosaic virus
from South Kazakhstan. Plant Pathology 40:515–523. 149
V IRAL D ISEASES
149 Rhizomania disease on beet.

Causal agent Beet pseudo-yellows virus

Different BNYVV strains have been documented, such BEET PSEUDO-YELLOWS
as the A type, B type, and the virulent P strain (named
after Pithiviers, France) that was discovered in France Introduction and significance
and recently detected in the UK. BNYVV is a furovirus Beet pseudo-yellows virus (BPYV) was first described
and has rod-shaped particles in three size ranges in California on greenhouse crops. However, the
(65–100, 270, or 390 x 20 nm). pathogen is now worldwide in distribution.
Disease cycle Symptoms and diagnostic features

BNYVV is vectored by Polymyxa betae, a soil inhabit- BPYV causes stunting and reduced growth. Mature
ing plasmodiophorid. Polymyxa betae may sometimes leaves show bright yellow spots that measure 1–1.5 cm
cause direct damage to young beet plants and can be in diameter; such leaves later become thickened and
considered a minor root pathogen. Transmission is brittle. The chlorosis caused by BPYV tends to be more
favored by warm soils with high moisture content, uniform with less greening along leaf veins than with
which favors vector activity and movement. Little BYV or the poleroviruses.
infection occurs below 10º C and the optimum temper-
ature for vector and virus multiplication is 25º C. Causal agent and disease cycle
BPYV is a closterovirus. This virus infects a wide range
Control of crops including beet, carrot, cucumber, lettuce,
Follow general suggestions for managing virus diseases pumpkin, spinach, strawberry, and numerous weeds.
(see Part 1). Do not plant susceptible hosts in fields The only known vector is the greenhouse whitefly
having a history of this problem. Do not allow infested (Trialeurodes vaporariorum), which transmits BPYV in
soil to be moved to uninfested fields. a semi-persistent manner.
References Control
Al musa, A. M. and Mink, G. I. 1981. Beet necrotic yellow vein Follow general suggestions for managing virus diseases
virus in North America. Phytopathology 71:773–776. (see Part 1).
Asher, M. J. C. 2002. The development of sugar-beet rhizomania
and its control in the UK. Proceedings of the BCPC
Conference – Pests & Diseases 2002 1:113–120. References
Barr, K. J. and Asher, M. J. C. 1992. The host range of Polymyxa Duffus, J. E. 1965. Beet pseudo-yellows, transmitted by the
betae in Britain. Plant Pathology 41:64–68. greenhouse whitefly (Trialeurodes vaporariorum).
Blunt, S. J., Asher, M. J. C., and Gilligan C. A. 1991. Infection of Phytopathology 55:450–453.
sugar beet by Polymyxa betae in relation to soil temperature. Wintermantel, W. M. 2004. Pumpkin (Cucurbita maxima and C.
Plant Pathology 40:257–267. pepo), a new host of beet pseudo-yellows virus in California.
Gerik, J. S. and Duffus, J. E. 1988. Differences in vectoring ability Plant Disease 88:82.
and aggressiveness of isolates of Polymyxa betae.
Hill, S. A. and Torrance, L. 1989. Rhizomania disease of sugar
beet in England. Plant Pathology 38:114–122.
Lennefors, B.-L., Lindsten, K., and Koenig, R. 2000. First record
of A and B type beet necrotic yellow vein virus in sugar beets in
Sweden. European Journal of Plant Pathology 106:199–201.
Payne, P. A. and Asher, M. J. C. 1990. The incidence of Polymyxa
betae and other fungal root parasites of sugar beet in Britain.
Tamada, T. and Baba, T. 1973. Beet necrotic yellow vein virus
V IRAL D ISEASES
from ‘rhizomania’ affected sugar beet in Japan. Annals of

Phytopathological Society of Japan 39:325–332.
Wisler, G. C., Lewellen, R. T., Sears, J. L., Liu, H.-Y., and Duffus,
J. E. 1999. Specificity of TAS-ELISA for beet necrotic yellow
vein virus and its application for determining rhizomania
resistance in field-grown sugar beets. Plant Disease
83:864–870.
B ETA VULGARIS 153

151
BEET WESTERN YELLOWS

species that affect these crops. Beet western yellows
virus (BWYV) is prevalent in the USA and elsewhere
and infects many other plants in addition to beet, Swiss
chard, and spinach. Beet mild yellowing virus (BMYV)
is the most important yellows virus on Amaranthaceae
hosts in the UK and Western Europe. A third polero-
virus pathogen is Beet chlorosis virus (BCHV).
151 Interveinal yellowing caused by Beet western
Symptoms and diagnostic features yellows virus on beet.
Infected leaves develop a bright yellow to orange-yellow
color but lack the brown or red spotting associated with
Beet yellows virus (BYV). Older leaves are thickened, Disease cycle
brittle, and become extensively yellow. Leaf veins and BWYV and BMYV may be found in numerous crop
tissues adjacent to the veins usually remain green (150, and weed plants, and the host list is extensive, including
151). This yellows symptom may be confused with over 150 documented plant species. All three viruses are
various nutrient deficiency symptoms, notably those poleroviruses and are vectored by several aphid vectors,
caused by nitrogen, iron, or magnesium deficiency. especially the green peach aphid (Myzus persicae), in a
persistent manner. There are reports that low levels of
Causal agent seed transmission can occur.
Though BWYV and BMYV are serologically identical,
these two distinct viruses do not infect all the same Control
hosts, greatly complicating the etiology of this disease. Follow general suggestions for managing virus diseases
These three viruses all infect spinach and various beet (see Part 1).
species. However, while some American isolates of
BWYV infect lettuce, BMYV strains from Europe References
cannot infect this host. Dewar, A. M. 1994, The Virus Yellows Warning Scheme – an
Integrated Pest Management system for sugar beet in the UK.
In: Individuals, Populations, and Patterns in Ecology. Leather,
S. R., Watts, A. D., Mills, N. J., and Walters, K. F. A. (eds), pp.
173–185.
Dewar, A. M., Haylock, L. A., and Ecclestone, P. M. J. 1996.
150 Strategies for controlling aphids and virus yellows in sugar
beet. Proceedings of the Brighton Crop Protection
Conference – Pests & Diseases 1996 1:185–190.
Duffus, J. E. 1973. The yellowing virus diseases of beet.
Advances in Virus Research 18:347–386.
Duffus, J. E. and Russell, G. E. 1975. Serological relationships
between beet western yellows virus and beet mild yellowing
virus. Phytopathology 65:811–815.
Smith, H. G. 1989. Distribution and infectivity of yellowing
viruses in field-grown sugar beet plants. Annals of Applied
V IRAL D ISEASES
Biology 116: 503–511.

Stevens, M., Smith, H. G., and Hallsworth, P. B. 1994. The host
range of beet yellowing viruses among common arable weed
150 Interveinal yellowing and necrotric spotting caused
by Beet western yellows virus on beet.
Beet yellows virus

152
BEET YELLOWS

Beet yellows virus (BYV) occurs throughout the world
on spinach and beets. In Europe, BYV and BMYV
together can cause significant losses on sugar beet.

Symptoms from BYV on table beet include mild
yellowing, vein clearing, or vein yellowing of the
younger leaves. Leaf necrosis can sometimes be associ-
ated with yellowing symptoms. However, BYV
probably does not cause such necrosis; the necrosis is
more likely due to decay caused by Alternaria and other 152 Beet yellows virus on beet.
secondary agents. Older leaves are thickened, brittle,
and turn yellow (152). Such leaves later develop red to
brown spots, which then gives the foliage a bronze References
color. Cold weather slows down the development of Duffus, J. E. 1973. The yellowing virus diseases of beet.
chlorosis, but increases necrotic symptoms. In spinach, Advances in Virus Research 18:347–386.
Smith, H. G. and Hallsworth, P. B. 1990. The effects of yellowing
young leaves show chlorotic spotting and vein clearing,
viruses on yield of sugar beet in field trials 1985–1987.
and subsequently turn yellow, necrotic, and distorted. Annals of Applied Biology 116:503–511.
The plants are stunted and may die if the growing point Smith, H. G. and Hinckes, J. A. 1987. Studies of the distribution
becomes necrotic. of yellowing viruses in the sugar beet root crop from 1981 to
1984. Plant Pathology 36:125–134.
Causal agent and disease cycle

BYV is a closterovirus having flexuous filamentous
particles that measure 1250 x 10 nm. At least 35 aphid
species have been reported as vectors, but the most
important are usually Myzus persicae and Aphis fabae.
The virus is transmitted in a semi-persistent manner and
is not retained after molting and passed to the progeny.
BYV has a very wide host range, including many of the
weed species infected by the polerovirus group.
Control
(see Part 1). Forecasts of yellows disease risk are
released annually in the UK for sugar beet growers;
these disease forecasts could be useful to vegetable
growers as well.
V IRAL D ISEASES
155
Brassicaceae Mustard family
MEMBERS OF THE BRASSICACEAE (mustard family) are among the most widely grown
vegetables and consist of over 300 genera. Brassicaceae plants are also commonly called
crucifers because the flowers have four petals that extend opposite each other and form the
shape of a square cross, hence are cruciform. The major vegetable group of Brassicaceae plants
are the Brassica oleracea or cole crops. Cole crops include the following familiar plants: kale and
collards (B. oleracea var. acephala), broccoli and cauliflower (both classified as B. oleracea var.
botrytis, though some taxonomists separate broccoli and name it B. oleracea var. italica),
cabbage (B. oleracea var. capitata), Brussels sprouts (B. oleracea var. gemmifera), kohlrabi
(B. oleracea var. gongylodes). In Europe broccoli is also called calabrese.
Other Brassica species vegetables include turnip (B. rapa), rutabaga or swede
(B. napus var. napobrassica), Chinese cabbage (B. pekinensis), broccoli raab or rappini (B. rapa
subsp. rapa), and pak-choi or bok choi (B. chinensis). Various leafy mustards are produced and
are classified as subspecies of B. juncea, B. campestris, B. alba, B. napus, and B. nigra.
Radish (Rhaphanus sativus) is a crucifer vegetable grown for the fleshy part of the
plant that is the stem hypocotyl and upper root. There is a great diversity in cultivars, ranging
from small, round varieties to very large, elongated types and colors that are red, white, green,
and even black. Other cultivars, such as R. sativus cv. longipinnatus, produce much larger roots
and are known as Chinese radish, mooli, or daikon.
Other Brassicaceae vegetables outside the Brassica genus include horseradish
(Armoracia rusticana), watercress (Nasturtium officinale), cress (Lepidium sativum), and rocket
salad or arugula (Eruca sativa). Many of these and other brassica vegetables are considered
specialty items; diseases of these plants are described in the Specialty Crops chapter.
Erwinia spp., Pseudomonas spp.

153
BACTERIAL HEAD/SPEAR ROT
OF BROCCOLI

This disease is highly dependent on weather and can
cause extensive losses of broccoli in California, the
southeast USA, and Europe (where broccoli is known
as calabrese). The disease occurs sporadically wherever

the crop is grown.

Initial symptoms consist of a dark, water-soaked decay
of the surfaces of small groups of florets in the broccoli
head, or spear (153). Later, infected portions of the head 153 Early infection of bacterial head rot of broccoli.
154
Control
Some differences in cultivar susceptibility exist, based
on architecture and exposure of the broccoli heads.
Broccoli heads having domed, and not flat, head shapes
are less likely to have severe head rot. Plant these less
susceptible cultivars, if available. Avoid planting
broccoli during the wet, rainy part of the year. Avoid
using overhead sprinklers, or schedule irrigations to
reduce the number of applications during head
formation. Increasing the interval between irrigations
from 2 to 8 days reduced head rotting by 50% in
Oregon. Protectant copper sprays have been used with
154 Advanced infection of bacterial head rot of some success under UK conditions, but such have not
broccoli. proven useful in California.
turn dark brown to black (154). The tissue becomes References

soft, collapses, and emits a bad odor. Secondary molds Canaday, C. H. and Wyatt, J. E. 1992. Effects of nitrogen
and bacteria cause further decay. Bacterial head rot fertilization on bacterial soft rot in two broccoli cultivars, one
resistant and one susceptible to the disease. Plant Disease
symptoms can resemble those of Alternaria head rot. 76:989–991.
With bacterial head rot, fungal sporulation is absent Canaday, C. H., Wyatt, J. E., and Mullins, J. A. 1991. Resistance
unless secondary molds colonize the diseased florets. in broccoli to bacterial soft rot caused by Pseudomonas
marginalis and fluorescent Pseudomonas species. Plant
Disease 75:715–720.
Causal agents Darling, D., Harling, R., Simpson, R. A., McRoberts, N., and
Bacterial head rot is caused by a complex of pathogenic Hunter, E. A. 2000. Susceptibility of broccoli cultivars to
bacteria including the following: Erwinia carotovora bacterial head rot: in vitro screening and the role of head
morphology in resistance. European Journal of Plant
subsp. carotovora, Pseudomonas fluorescens, P. mar- Pathology 106:11–17.
ginalis, P. viridiflava, and perhaps others. The roles of Hernandez-Anguiano, A. M., Suslow, T. V., Leloup, L., and
the different bacterial agents may differ. Some species, Kado, C. I. 2004. Biosurfactants produced by Pseudomonas
fluorescens and soft-rotting of harvested florets of broccoli
such as P. fluorescens, produce a surfactant-like and cauliflower. Plant Pathology 53:596–601.
chemical (viscosin) that allows bacteria to more readily Hildebrand, P. D. 1989. Surfactant-like characteristics and
penetrate the very waxy surface of broccoli florets. identity of bacteria associated with broccoli head rot in
Other bacteria do not make such substances and cannot Atlantic Canada. Canadian Journal of Plant Pathology
11:205–214.
reach broccoli tissues on their own. If multiple species Laycock, M. V., Hildebrand, P. D., Thibault, P., Walter, J. A., and
are present, the viscosin-producing species allow the Wright, J. L. C. 1991. Viscosin, a potent peptidolipid
non-producers to likewise penetrate the surface wax biosurfactant and phytopathogenic mediator produced by a
pectolytic strain of Pseudomonas fluorescens. Journal of
and infect the broccoli tissues. Agricultural Food Chemistry 39:483–489.
Ludy, R. L., Powelson, M. L., and Hemphill, D. D. 1997. Effect
Disease cycle of sprinkler irrigation on bacterial soft rot and yield of
broccoli. Phytopathology 81:614–618.
Severe disease is always associated with periods of cool
Robertson, S., Brokenshire, T., Kellock, L. J., Sutton, M., Chard,
temperatures and wet, foggy, or rainy weather when J., and Harling, R. 1993. Bacterial spear (head) rot of
crops begin to form the early broccoli flower heads. calabrese in Scotland: causal organisms, cultivar susceptibility
Frequent overhead sprinkler irrigation can promote this and disease control. Proceedings Crop Protection in Northern
Britain 1993:265–270.
disease. Infection is also tied with fluctuating day/night
Wimalajeewa, D. L. S., Hallam, N. D., Hayward, A. C., and
temperatures that allow water to condense on the Price, T. V. 1987. The etiology of head rot disease of broccoli.
heads. Excessive nitrogen applications increase disease Australian Journal of Agricultural Research 38:735–742.
severity. Secondary organisms are very often present on Wimalajeewa, D. L. S., Hayward, A. C., and Price, T. V. 1985.
Head rot of broccoli in Victoria, Australia, caused by
the diseased florets and this leads to rapid breakdown Pseudomonas marginalis. Plant Disease 69:177.
of tissues and difficulty in disease diagnosis.
B RASSICACEAE 157
Pseudomonas syringae pv. alisalensis Control

BACTERIAL BLIGHT Reduce or eliminate the use of overhead sprinkler irri-
gation. Do not plant a subsequent broccoli raab crop in
Introduction and significance fields having undecomposed, infested crop residues.
In California this disease is most often found on Copper applications provide only minimal protection
broccoli raab (Brassica rapa subsp. rapa) and more against this pathogen.
recently on broccoli and arugula. The disease is very
damaging to broccoli raab. This pathogen has also been References
detected in the eastern USA. This is a recently described Bull, C. T., Goldman, P., and Koike, S. T. 2004. Bacterial blight
disease and pathogen, and one that is gaining in impor- on arugula, a new disease caused by Pseudomonas syringae
pv. alisalensis in California. Plant Disease 88:1384.
tance on crops like broccoli raab.
Cintas, N. A., Koike, S. T., and Bull, C. T. 2002. A new pathovar,
Pseudomonas syringae pv. alisalensis pv. nov., proposed for
Symptoms and diagnostic features the causal agent of bacterial blight of broccoli and broccoli
raab. Plant Disease 86:992–998.
On broccoli raab (see chapter on Specialty Crops, page
Koike, S. T., Cintas, N. A., and Bull, C. T. 2000. Bacterial blight,
389), small, angular, water-soaked specks occur on a new disease of broccoli caused by Pseudomonas syringae in
leaves. These flecks expand, turn brown, and become California. Plant Disease 84:370.
surrounded by bright yellow borders. As disease Koike, S. T., Henderson, D. M., Azad, H. R., Cooksey, D. A., and
Little, E. L. 1998. Bacterial blight of broccoli raab: a new
develops, the affected areas enlarge and coalesce, disease caused by a pathovar of Pseudomonas syringae. Plant
causing large sections of the leaf to turn yellow, then Disease 82:727–731.
brown. With time the leaf can wilt and collapse,
resulting in blight-like symptoms. On broccoli, the
pathogen causes large, angular leaf spots that also begin
as water-soaked lesions that later turn tan to brown
(155).
Causal agent
Bacterial blight is caused by the bacterium Pseudo-
monas syringae pv. alisalensis.This pathogen appears to
be a new pathovar in the P. syringae group. The
pathogen is an aerobic, Gram-negative bacterium that
can be isolated on standard microbiological media.
Colonies are cream to light yellow in color, smooth, and
have a notably sticky consistency. When cultured on
King's medium B, this organism produces a diffusible 155
pigment that fluoresces blue under ultraviolet light.
There is evidence that this pathogen is seedborne.
Disease cycle
Little is known about the specifics of disease develop-
ment. The bacterium is splash dispersed by rain and
overhead sprinkler irrigation. Leaf symptoms always
begin on the lower, protected leaves where shading

keeps the conditions humid and cool. As disease
develops, the symptoms gradually move up the broccoli
raab stem and eventually reach the top shoots.
Seedborne inoculum would account for the occurrence
of this disease in broccoli raab fields that never were
planted to this crop before. 155 Tan lesions of bacterial blight of broccoli.
Pseudomonas syringae pv. maculicola

156
BACTERIAL LEAF SPOT

This disease is occasionally important during wet
summers in Europe and other production areas, but is
usually of minor significance. Cabbage is reported to be
the most commonly affected crop, but bacterial leaf
spot also occurs on cauliflower, collards, Brussels
sprout, radish, and turnip. In the USA, this disease is
often most important as a seedling disease that reduces
quality and vigor of greenhouse produced transplants.
156 Leaf spots of bacterial leaf spot of cauliflower.
Infections start as dark, water-soaked specks on leaves 157
that can be seen from both leaf surfaces (156). Leaf
spots typically remain small and measure 3–4 mm in
diameter, but enlarging and merging of spots occurs if
conditions are favorable. Older leaf spots turn tan and
may sometimes have a purple border surrounding
them. Severe infection can cause blotching, leaf distor-
tion and premature leaf fall. Infected cauliflower heads
may be discolored. On transplants (157), bacterial leaf
spot may resemble early downy mildew infections that
are not sporulating. The small, dark leaf spot symptoms
are the reason for the older disease name of pepper leaf
spot.
157 Cauliflower transplants infected with bacterial leaf
Causal agent spot.
The cause of bacterial leaf spot is Pseudomonas
syringae pv. maculicola. The pathogen is an aerobic,
Gram-negative bacterium that can be isolated on Control
standard microbiological media. Colonies are cream to Reduce or eliminate the use of overhead sprinkler irri-
light yellow in color and smooth. When cultured on gation. Do not plant a subsequent crucifer crop in fields
King's medium B, this organism produces a diffusible having undecomposed, infested crop residues. Copper
pigment that fluoresces blue under ultraviolet light. applications provide only minimal protection against
Strains of this pathogen are host specific to crucifers. this pathogen. In greenhouses, schedule irrigations to
The pathogen is seedborne. allow for maximum drying of foliage. Remove trans-
plant trays that show symptoms of the disease. Copper
Disease cycle applications in the controlled setting of greenhouses are
The pathogen appears to survive between crops on probably more effective than in field use. Sanitize old
infested debris. In the field the bacterium is splash transplant trays and bench tops so the pathogen is not
dispersed by rain and overhead sprinkler irrigation. spread to new plantings. Mowing of transplants greatly
Disease development can be particularly severe on increases the risk of spreading the disease. Use seed that
greenhouse produced transplants due to the use of does not have significant levels of the pathogen.
overhead sprinklers, humid protected conditions, and Appropriate seed treatments can also contribute to the
the practice of clipping and mowing transplants to management of seedborne inoculum. Treat infested
strengthen transplant stems. seed with hot water.
B RASSICACEAE 159
References Xanthomonas campestris pv. campestris

Cintas, N. A., Bull, C. T., Koike, S. T., and Bouzar, H. 2001. BLACK ROT
A new bacterial leaf spot disease of broccolini, caused by
Pseudomonas syringae pv. maculicola, in California. Plant
Disease 85:1207. Introduction and significance
Koike, S. T., Smith, R. F., Van Buren, A. M., and Maddox, D. A. Black rot is one of the most important diseases of
1996. A new bacterial disease of arugula in California. Plant crucifers. It is most damaging in tropical, subtropical,
Disease 80:464.
and other areas with warm, humid climates. For
Lewis-Ivey, M. L., Wright, S., and Miller, S. A. 2002. Report of
bacterial leaf spot on collards and turnip leaves in Ohio. Plant example, significant black rot occurs on cabbage grown
Disease 86:186. in Africa. In cooler regions, losses are less severe, but the
Peters, B. J., Asha, G. J., Cotherb, E. J., Hailstones, D. L., disease has become more prevalent in recent years,
Nobleb, D. H., and Urwin, N. A. R. 2004. Pseudomonas
syringae pv. maculicola in Australia: pathogenic, phenotypic
possibly because spread is favored by modern propaga-
and genetic diversity. Plant Pathology 53:73–79. tion systems. The seedborne nature of the pathogen has
Shackleton, D. A. 1996. A bacterial leaf spot of cauliflower in resulted in its distribution throughout the world.
New Zealand caused by Pseudomonas syringae pv.
maculicola. New Zealand Journal of Science 9:872–877.
Wiebe, W. L. and Campbell, R. N. 1993. Characterization of
Pseudomonas syringae pv. maculicola and comparison with Black rot symptoms can vary greatly depending on the
Pseudomonas syringae pv. tomato. Plant Disease particular brassica host, age of host when infected, par-
77:414–419.
ticular strain of the pathogen, and environmental con-
Zhao, Y. F., Damicone, J. P., and Bender, C. L. 2002. Detection,
survival, and sources of inoculum for bacterial diseases of ditions. Initial symptoms consist of small, water-soaked
leafy crucifers in Oklahoma. Plant Disease 86:883–888. leaf spots. These then become brown specks with a
Zhao, Y. F., Damicone, J. P., Demezas, D. H., Rangaswamy, V., chlorotic margin and can mimic other bacterial diseases
and Bender, C. L. 2000. Bacterial leaf spot of leafy crucifers in
Oklahoma caused by Pseudomonas syringae pv. maculicola.
(158). Other early symptoms are angular or V-shaped
Plant Disease 84:1015–1020. yellow lesions that often develop along the leaf edges.
158
156 Early infection of black rot of cauliflower.

159
Causal agent
The cause of black rot is the aerobic, Gram-negative
bacterium Xanthomonas campestris pv. campestris.
The pathogen can be isolated on standard microbio-
logical media and produces yellow, mucoid, slow
growing colonies typical of most xanthomonads.
Various starch-based media aid in the isolation and
identification of this organism. Strains of this pathogen
are host specific to crucifers and infect Brassica species,
radish, crucifer weeds, and ornamental crucifers such as
stock (Matthiola spp.) and wallflower (Cheiranthus
cheiri). This pathogen is seedborne, and different races
have been documented. Also, the highly virulent
159 Advanced infection of black rot of cauliflower. variants that cause the blight and plant collapse
symptoms can be differentiated from leaf spot causing
strains via monoclonal antibody and molecular tests.
160
160 Vascular Strains infecting horseradish are X. campestris pv.
blackening of black amoraciae; this organism is only a weak pathogen on
rot of cauliflower. cabbage and cauliflower.
Disease cycle
Initial inoculum comes from infested seed, diseased
weeds and volunteer crucifers, and infested but un-
decomposed crop residues. Bacteria are dispersed by
splashing rain or sprinkler irrigation from inoculum
sources to susceptible plants. Cotyledons and leaves are
infected through leaf openings called hydathodes,
which are located where veins end at the leaf margin.
Infection can also occur through wounds or roots.
Symptoms only occur when sufficient inoculum builds
up on the leaf and if weather conditions are conducive
for infection and symptom expression. If conditions are
humid and warm, and there is splashing water, disease
can progress rapidly and cause extensive damage. In
seed crops, infected plants may be symptomless, though
the pathogen is present in the vascular system and is
These lesions later dry up and turn tan or brown (159). able to spread to pods and seed.
Black veins are sometimes seen within these tan lesions.
Severely infected leaves may wither and drop off the Control
plant. If systemic infection occurs, the vascular tissues Use seed that does not have significant levels of the
in petioles and main stems turn black (160). Some pathogen. Treat seed with sodium hypochlorite or hot
strains produce symptoms known as ‘blight,’ which are water. Produce seed in areas having a dry climate, and
characterized by a sudden collapse of interveinal tissues have such seed inspected and certified. Rotate crops
and a lack of veinal necrosis. Systemic lesions may with non-hosts for 2 to 3 years to avoid problems from
develop in the center of the leaf when temperatures are infected crop residues. However, once crop residues are
high (20-28º C), but most marginal lesions occur at 16º gone, the bacterium does not survive in the soil. Do not
C. However, if temperatures are cool, black rot place seedbed or transplant areas adjacent to field pro-
symptoms may not be expressed. duction crops. Remove symptomatic transplants and
B RASSICACEAE 161
surrounding plants and trays. Mowing of transplants Shaw, J. J. and Kado, C. I. 1988. Whole plant wound inoculation
for consistent reproduction of black rot of crucifers.
greatly increases the risk of spreading the pathogen. Use Phytopathology 78:981–986.
resistant cultivars if available. The application of Shigaki, T., Nelson, S. C., and Alavarez, A. M. 2000.
chemicals to foliage is not very effective for black rot Symptomless spread of blight inducing strains of
Xanthomonas campestris pv. campestris on cabbage seedlings
control. in misted seedbeds. European Journal of Plant Pathology
106: 339–346.
References Tamura, K., Takikawa, Y., Tsuyumu, S., and Goto, M. 1994.
Bacterial spot of crucifers caused by Xanthomonas campestris
Alvarez, A. M., Benedict, A. A., Mizumoto, C. Y., Hunter, J. E.,
pv. raphani. Annals of the Phytopathological Society of Japan
and Gabriel, D. W. 1994. Serological, pathological, and
60:281–287.
genetic diversity among strains of Xanthomonas campestris
infecting crucifers. Phytopathology 84:1449–1457. Vauterin, L., Rademaker, J., and Swings, J. 2000. Synopsis on the
taxonomy of the genus Xanthomonas. Plant Disease
Alvarez, A. M. and Lou, K. 1985. Rapid identification of
90:677–682.
Xanthomonas campestris pv. campestris by ELISA. Plant
Disease 69:1082–1086. Vicente, J. G., Conway, J., Roberts, S. J., and Taylor, J. D. 2001.
Identification and origin of Xanthomonas campestris pv.
Babadoost, M., Derie, M. L., and Gabrielson, R. L. 1996.
campetris races and related pathovars. Phytopathology
Efficacy of sodium hypochlorite treatments for control of
91:492–499.
Xanthomonas campestris pv. campestris in brassica seeds.
Seed Science and Technology 24:7–15. Williams, P. H. 1980. Black rot: a continuing threat to world
crucifers. Plant Disease 64:736–742.
Chun, W. W. C., and Alvarez, A.M. 1983. A starch-methionine
medium for isolation of Xanthomonas campestris pv. Zhao, Y., Damicone, J. P., Demezas, D. H., and Bender, C. L.
campestris from plant debris in soil. Plant Disease 2000. Bacterial leaf spot diseases of leafy crucifers in
67:632–635. Oklahoma caused by pathovars of Xanthomonas campestris.
Claflin, L. E., Vidaver, A. K., and Sasser, M. 1987. MXP, a semi-
selective medium for Xanthomonas campestris pv. phaseoli.
Franken, A. A. J. M. 1992 . Comparison of immunofluorescence
microscopy and dilution-plating for the detection of
Xanthomonas campestris pv. campestris in crucifer seeds.
Kocks, C. G., Ruissen, M. A., Zadoks, J. C., and Duijkers, M. G.
1998. Survival and extinction of Xanthomonas campestris pv.
campestris in soil. European Journal of Plant Pathology
104:911–923.
Kocks, C .G., Zadoks, J. C., and Ruissen, M. A. 1999. Spatio-
temporal development of black rot (X. campestris pv.
campestris) in cabbage in relation to initial inoculum levels in
field plots in The Netherlands. Plant Pathology 48:176–188.
Massomo, S. M. S., Nielsen, H., Mabagala, R. B., Mansfeld-
Giese, K., Hockenhull, J., and Mortensen, C. N. 2003.
Identification and characterisation of Xanthomonas
campestris pv. campestris strains from Tanzania by
pathogenicity tests, Biolog, rep-PCR and fatty acid methyl
ester analysis. European Journal of Plant Pathology
109:775–789.
Poplawsky, A. R. and Chun, W. 1995. Strains of Xanthomonas
campestris pv. campestris with atypical pigmentation isolated
from commercial crucifer seed. Plant Disease 79:1021–1024.
Randhawa, P. S. and Schaad, N. W. 1984. Selective isolation of
Xanthomonas campestris pv. campestris from crucifer seeds.
Sahin, F. and Miller, S. A. 1997. A new pathotype of
Xanthomonas campestris pv. amoraciae that causes bacterial

leaf spot of radish. Plant Disease 81:1334.
Schaad, N. W. and Dianese, J. C. 1981. Crucifer weeds as sources
of inoculum of Xanthomonas campestris in black rot of
crucifers. Phytopathology 71:1215–1220.
Schultz, T. and Gabrielson, R. L. 1986. Xanthomonas campestris
pv. campestris in western Washington crucifer seed fields:
occurrence and survival. Phytopathology 76:1306–1309.
Albugo candida
162
WHITE RUST, WHITE BLISTER

This is a common disease of crucifer crops and related
weeds and ornamentals. Affected vegetables include
broccoli, Brussels sprouts, cauliflower, radish, horse-
radish, mustard, Chinese cabbage, rappini, and turnip.
Yield reductions are rare, and the main impact of the
disease is reduced quality due to the prominent signs of
the pathogen.

Early signs are small, raised, white or cream-colored
blisters (sori) that measure 2–3 mm in diameter and
form underneath the plant epidermis on leaves, stems,
and flower stalks (161). The epidermis covering the
pustule will later rupture, releasing powdery white
sporangia. Later, larger blisters (2–3 cm diameter) may
develop. The pathogen also causes distortion of leaf
tissue, which may have a yellow or red discoloration.
Severely infected leaves wither and die. Older pustules
can become brown and rotten, making them difficult to
recognize later in the season. Infection can develop sys-
temically and cause twisted, deformed growth of the
stem, leaves, or flowers. On flowering shoots, this
condition is known as ‘stagheads’ because of the
extensive twisting of infected tissue (162). Clubroot-like
swellings may be produced on roots. 162 Cauliflower seed stalk infection with white rust.
161 163
F UNGAL D ISEASES
161 Leaf pustules of white rust of bok choy. 163 Pustules of white rust of radish.
B RASSICACEAE 163
On radish, white rust signs include the characteristic Control

raised white pustules on the leaves that break open to Bury crop residues after harvest to reduce spread of
release white powdery spores (163). White rust also airborne spores to nearby crops. Use resistant cultivars
causes severe infection of flower shoots and swellings when available and rotate with non-hosts where the
on the root. However, note that root galls on radish disease occurs regularly. Some disease control effects
may also be caused by clubroot disease. Radish isolates have been reported for applications of P and K fertiliz-
are unlikely to affect other crucifers such as cabbage, ers (70–100 kg/ha). Apply protectant fungicides such as
cauliflower, and turnip. chlorothalonil, phenylamide, and strobilurin products.

White rust is caused by the oomycete Albugo candida. Goyal, B. K., Verma, P. R., Spurr, D. T., and Reddy, M. S. 1996.
In infected tissues this organism produces globose, Albugo candida staghead formation in Brassica juncea in
relation to plant age, inoculation sites, and incubation
chocolate-brown oospores that measure 30–55 μm in conditions. Plant Pathology 45:787–794.
diameter and have a thick ornamented spore wall. Liu, J. Q. and Rimmer, S. R. 1993. Production and germination
Within the raised pustules, club-shaped sporangio- of oospores of Albugo candida. Canadian Journal of Plant
Pathology15:265–271.
phores produce sporangia that are borne in basipetal
Koike, S. T. 1996. Outbreak of white rust, caused by Albugo
chains. Sporangia are globose to oval, hyaline, with thin candida, on Japanese mustard and tah tsai in California. Plant
walls, and measure 12–18 μm in diameter. Downy Disease 80:1302.
mildew (Peronospora parasitica) sometimes grows on Petrie, G. A. 1988. Races of Albugo candida (white rust and
staghead) on cultivated Cruciferae in Saskatchewan.
white rust pustules. There are many races of this Canadian Journal of Plant Pathology 10:142–150.
pathogen, some of which have restricted host ranges Petrie, G. A. and Verma, P. R. 1974. A simple method for
and cannot infect all crucifers. germinating oospores of Albugo candida. Canadian Journal
of Plant Science 54:595–596.
Pidskalny, R. S. and Rimmer, S. R. 1985. Virulence of Albugo
Disease cycle candida from turnip rape (Brassica campestris) and mustard
This pathogen survives in debris and soil as resilient (Brassica juncea) on various crucifers. Canadian Journal of
oospores. Oospores are therefore the main primary Plant Pathology 7:283–286.
inoculum, which germinate to produce five to seven Scheck, H. J. and Koike, S. T. 1999. First occurrence of white rust
of arugula, caused by Albugo candida. Plant Disease 83:877.
swimming zoospores. Zoospores swim to or are Verma, P. R. and Petrie, G. A. 1975. Germination of oospores of
splashed onto susceptible hosts, resulting in infection Albugo candida. Canadian Journal of Botany 53:836–842.
and formation of the raised pustules. Airborne Williams, P. H. and Pound, G.S. 1963. Nature and inheritance of
sporangia from the pustules result in pathogen spread resistance to Albugo candida in radish. Phytopathology
53:1150–1154.
within the crop. After a period of drying, sporangia also
release zoospores on the surface of the host plant; these
zoopsores encyst and penetrate the host directly. Leaf
surface moisture from dew, fog, or rain is required for
infection. Infection can occur in 4 to 6 hours under
optimal temperatures. Germination occurs over the
range of 0–18º C, but infection requires warmer tem-
peratures of 15–25º C, with an optimum of 20º C.
Greater disease severity occurs with increasing leaf-
wetness duration. Symptoms appear about 10–14 days
after infection.
F UNGAL D ISEASES
Alternaria brassicae,A. brassicicola Susceptible crops such as turnip and Chinese

ALTERNARIA LEAF SPOT/ cabbage can be almost defoliated by Alternaria leaf
HEAD ROT, DARK LEAF SPOT spot. In the UK, Alternaria leaf spot can significantly
reduce Brussels sprout yields because of the low
Introduction and significance tolerance for spots and blemishes (167). Alternaria leaf
Alternaria pathogens are important on crucifer crops spot is also important on stored white cabbage, turnip,
worldwide, causing foliar, pod, seed, and broccoli-head and swede roots because disease development continues
diseases. All the major brassica types (B. campestris, at low temperatures.
B. oleracea, B. napus, B. rapa) are susceptible. In many Alternaria brassicicola causes a disease of cauliflower
cases, these pathogens do not reduce the weight and size and broccoli heads (168) when spores are splashed or
of the harvested commodity, but cause losses because of blown onto the immature flower heads. Symptoms
reduced quality and appearance. However, Chinese consist of a water-soaked decay of the crucifer head that
cabbage, bok choy, and leafy brassicas can be seriously later turns dark brown to black. The tissue becomes soft
damaged and rendered unmarketable. and mushy and the pathogen sporulates on the head.
Secondary molds and bacteria cause further decay.
Symptoms and diagnostic features Alternaria head rot can be severe during wet and cold
The main symptom of this disease is leaf spot. On weather in California. Alternaria head rot and bacterial
leaves, small, dark specks measuring 1–2 mm in head rot symptoms on broccoli are similar, so diagnosis
diameter first develop and later enlarge into circular, tan needs to be done carefully. In seed crops, Alternaria
to brown spots that are visible from both sides of the species cause black or brown spots on the stems and
leaf. These can enlarge to 5–25 mm in diameter and pods, which results in premature ripening and splitting
usually contain concentric rings, giving the spots a of the pods.
target-like appearance (164, 165). Spots sometimes
have yellow halos caused by a fungal toxin. If condi- Causal agents
tions are favorable, dark green conidia will be visible on Alternaria leaf spot and related diseases are caused by
the spots. Old leaf spots become papery in texture and A. brassicae and A. brassicicola. These pathogens can
may tear. Spots are most apparent on the oldest leaves. be isolated on standard microbiological media. Both
Leaf spots caused by A. brassicicola tend to be darker species sporulate well in culture if incubated under 12-
and may have a more irregular margin than those hour light/12-hour dark conditions. The two species are
caused by A. brassicae. Spots on petioles tend to be readily distinguished by spore size and morphology.
brown and oval or elliptical in shape (166). Alternaria brassicae conidia from leaves are obclavate
164 165
F UNGAL D ISEASES
164 Symptoms of Alternaria leaf spot of Chinese 165 Close-up of Alternaria leaf spot of cauliflower.
cabbage.
B RASSICACEAE 165
166 Petiole lesions 166 in shape with one slender, unbranched beak that
of Alternaria leaf measures 55–75 μm long; beaks extend from the apical
spot of bok choy. end of the spore body. The total conidial length,
including the narrow beak, for A. brassicae is 75–350
μm. The width of the main spore body is 10–35 μm.
Conidia have six to 19 transverse septa and one to eight
longitudinal or oblique septa and are borne in short
chains of up to four spores. Alternaria brassicicola
conidia are borne in longer chains of 20 or more and are
smaller, measuring 18–130 x 8–20 μm. Conidia are
cylindrical and tapering near the apex. This species
lacks the long beak, and has 1 to 10 transverse and few
longitudinal septa.
The pathogen on radish (169) is yet another species,
A. raphani. Alternaria raphani conidia are obclavate in
shape with one short, unbranched beak. The total
conidial length is 50–130 μm. The width of the main
167
spore body is 14–30 μm. Conidia have three to seven
transverse septa and several longitudinal or oblique
septa and are borne in short chains of two to three
spores.
Disease cycle
Seedborne inoculum can be both on the seed surface or
internal in seed tissue. A. brassicae may survive for only
a few months when seed storage temperatures are
greater than 20º C, while A. brassicicola may survive
for 12 years when there is internal seed infection.
167 Alternaria leaf spot on Brussels sprouts caused by Seedlings produced from infected seed may have tiny
A. brassicae. Larger lesions are caused by the ring spot necrotic spots or show stunting or death of cotyledons.
pathogen. Infected seed can be reduced in vigor and have lower
168 169
F UNGAL D ISEASES
168 Broccoli infected with Alternaria head rot. 169 Leaf infections of Alternaria leaf spot of radish.
germination rates. At least 12 hours of 90% relative References

humidity are required for sporulation on plant tissues. Babadoost, M. and Gabrielson, R. L. 1979. Pathogens causing
Spore production is optimal at 18–24º C for Alternaria diseases of Brassica seed crops in Western
Washington. Plant Disease Reporter 63:815–820.
A. brassicae and 20–30º C for A. brassicicola.
Bains, P. S. and Tewari, J. P. 1987. Purification, chemical
Sporulation of these pathogens is favored by alternat- characterization and host-specificity of the toxin produced by
ing light and dark periods. Conidia are released during Alternaria brassicae. Physiological and Molecular Plant
periods of falling humidity and spore trap records
Bassey, E. O. and Gabrielson, R. L. 1983. The effect of humidity,
reveal peaks in the afternoon when humidity is low. seed infection level, temperature, and nutrient stress on
Spores are dispersed by splashing water and by wind. cabbage seedling disease caused by Alternaria brassicicola.
Both Alternaria species require free water for infection. Seed Science and Technology 11:403–410.
Bassey, E. O. and Gabrielson, R. L. 1983. Factors affecting
A minimum of 6–8 hours leaf wetness is required for accuracy of 2,4-D assays of crucifer seed for Alternaria
infection, and severe disease is associated with brassicicola and relation of assays to seedling disease
prolonged warm, wet weather. Older leaves and pods potential. Seed Science and Technology 11:411–420.
are more susceptible to infection and show increased Cerkauskas, R. F., Stobbs, L. W., Lowery, D. T., Van Driel, L.,
Liu, W., and VanSchagen, J. 1998. Diseases, pests, and abiotic
disease as they senesce. These pathogens are able to problems associated with oriental cruciferous vegetables in
survive on crop residues, and microsclerotia and southern Ontario in 1993-1994. Canadian Journal of Plant
chlamydospores enable A. brassicae to survive for Pathology 20:87–94.
Chen, L. Y., Price, T. V., and Park-Ng, Z. 2003. Conidial
longer periods. When oilseed rape or other crucifer seed dispersal by Alternaria brassicicola on Chinese cabbage
crops are harvested, airborne inoculum can be (Brassica pekinensis) in the field and under simulated
dislodged and carry over to vegetable plantings. These conditions. Plant Pathology 52:536–545.
two pathogens also affect many crucifer weeds and Dillard, H. R., Cobb, A. C., and Lamboy, J. S. 1998.
Transmission of Alternaria brassicicola to cabbage by flea
native Brassica species. Insect transmission has been beetles. Plant Disease 82:153–157.
reported for A. brassicicola. Guillemette, T., Iacomi-Vasilescu, B., and Simoneau, P. 2004.
Conventional and real-time PCR-based assay for detecting
pathogenic Alternaria brassicae in cruciferous seed. Plant
Control Disease 88:490–496.
Use seed that does not have significant levels of the Hong, C. X. and Fitt, B. D. L. 1996. Factors affecting the
pathogen. Apply seed treatments if seed is infected. Seed incubation period of dark leaf and pod spot (Alternaria
brassicae) on oilseed rape (Brassica napus). European Journal
treatments include fungicides such as thiram and
of Plant Pathology 102:545–553.
iprodione, and hot water soaks at 50º C for 20 minutes. Huang, R. and Levy, Y. 1995. Characterization of iprodione-
Destroy diseased crop residues after harvest to reduce resistant isolates of Alternaria brassicicola. Plant Disease
inoculum sources. Do not plant vegetable brassicas 79:828–833.
Humpherson-Jones, F.M. and Maude, R.B. 1982. Studies on the
close to field brassicas such as oilseed rape. Foliar fungi-
epidemiology of Alternaria brassicicola in Brassica oleracea
cides can provide effective control. Such protectants seed production crops. Annals of Applied Biology 100:61-71.
include iprodione, triazoles such as difenoconazole and Koike, S. T. 1996. Japanese mustard, tah tsai, and red mustard as
tebuconazole, and strobilurin products. Forecasting hosts of Alternaria brassicae. Plant Disease 80:822.
Koike, S. T. 1997. Broccoli raab as a host of Alternaria brassicae.
systems to predict infection are still being developed.
Some differences in cultivar susceptibility may exist. For Koike, S. T. and Molinar, R. H. 1997. Daikon (Raphanus sativus
broccoli head rot, avoid using overhead sprinkler irri- L. cv. longipinnatus) as a host of Alternaria brassicae in
gation. Broccoli cultivars that are resistant to the head- California. Plant Disease 81:1094.
Tsuneda, A. and Skoropad, W. P. 1977. Formation of
rot phase of this disease have not been identified;
microsclerotia and chlamydospores from conidia of
however, those cultivars that form a more rounded, Alternaria brassicae. Canadian Journal of Botany
dome-shaped head generally have less severe head rot. 56:1333–1334.
F UNGAL D ISEASES
Seed crops should be produced in arid climates and

without the use of overhead sprinklers.
B RASSICACEAE 167
Botrytis cinerea (teleomorph = Botryotinia fuckeliana)

170
GRAY MOLD

Disease caused by Botrytis usually has a minor impact
on crucifers because infected, older leaves are removed
during harvest. More severe problems can occur if
crops are affected by other problems, such as chemical
burn, nutrient deficiency, or weather damage, and are
subsequently colonized by gray mold. Gray mold is an
important problem in stored produce, particularly on
white cabbage. 170 Gray mold on cauliflower head.
Symptoms and diagnostic features 171

Symptoms are brown blotches on leaves or stems that
extend in size from 1–2 cm in diameter to very large
sections of diseased tissue. Gray mold results in a soft,
mushy rot in which tissues disintegrate if handled. Gray
fungal growth is usually present in tufts near the center
of foliar lesions or generally over cauliflower heads
(170) or other organs. On stored cabbage (171) the
outer wrapper leaves may bear extensive sporulation.
Gray mold symptoms are almost always associated
with senescence or physical damage to host tissues.
Causal agent 171 Gray mold on stored white cabbage.

Gray mold is caused by the ascomycete fungus
Botryotinia fuckeliana. However, this stage is rarely
observed on crucifers and the disease is associated with moisture is available and rapidly colonize this food
the anamorph Botrytis cinerea. Conidiophores are base. Once established in the senescent tissue, the
long, can measure up to 1–2 mm, become gray-brown pathogen will progress into adjacent healthy stems and
with maturity, and branch irregularly near the apex. leaves, resulting in disease symptoms and the produc-
Conidia are clustered at the branch tips and are single- tion of additional conidia. Cool temperatures, free
celled, pale brown, ellipsoid to obovoid, and measure moisture, and high humidity favor disease develop-
6–18 x 4–11 μm. If formed, sclerotia are black, oval or ment. Factors that predispose crucifer crops to gray
irregular in shape, and measure 4–15 mm. On host mold are physical damage due to passing farm
tissue the fungus produces characteristically profuse equipment, burn from fertilizers and pesticides, pest
mycelial growth that is initially fluffy, white or pale infestations (especially from boring insects such as root
gray, later becoming darker gray- brown when it maggots), drought stress, frost damage, overmaturity of
sporulates. the crop, and tipburn due to nutritional imbalances.
Disease cycle Control

F UNGAL D ISEASES
Botrytis cinerea survives in and around fields as a sapro- Prevent or minimize injury to the crop. Provide suffi-
phyte on crop debris, as a pathogen on numerous crop cient fertilizers for the crop, and harvest the crop before
and weed plants, and as sclerotia in the soil. Conidia the commodity becomes overmature. For cabbage,
develop from these sources and become windborne. handle and harvest the crop under dry conditions and
When conidia land on senescent or damaged crucifer before the occurrence of frost. Postharvest fungicide
tissue, they will germinate within a few hours if free dips are used on cabbage in some countries.
References cause chlorosis, early defoliation, and necrosis of the

Davies, R. M. and Heale, J. B. 1985. Botrytis cinerea in stored tips of young leaves of cauliflower and cabbage.
cabbage: the use of germ tube growth on leaf discs as an indi- Powdery mildew colonies may be gray and restricted in
cation of potential head rot. Plant Pathology 34:408–414.
size on resistant cultivars as the host reaction produces
Yoder, O. C. and Whalen, M. L. 1975. Factors affecting post-
harvest infection of stored cabbage tissue by Botrytis cinerea. black speckling beneath the colony. Conspicuous gray
Canadian Journal of Botany 53:691–699. or purple symptoms occur on the stems of Brussels
sprout, while on sprouts there may be white colonies or
fine black speckling in radiating lines.
Erysiphe cruciferarum Causal agent

POWDERY MILDEW Powdery mildew is caused by the ascomycete fungus
Erysiphe cruciferarum. The asexual conidia measure
Introduction and significance 30–52 x 11–17 μm and are borne singly or in chains of
Crucifer crops are frequently affected by powdery only two spores. There appears to be physiological spe-
mildew, which occurs in all production areas. There are cialization within the pathogen; for example, isolates
large differences in susceptibility between different from turnip will not infect Brussels sprout, and vice
species and cultivars. Severe epidemics commonly occur versa. The sexual stage has only been reported occa-
in swede and turnip that result in reduced yield and sionally and consists of spherical cleistothecia that are
quality. More commonly, the foliage and stems of brown or black. Like all powdery mildews, E. crucifer-
brassicas may exhibit disease, though these infections arum is an obligate pathogen.
have limited effects on quality and yield.
Disease cycle
Symptoms and diagnostic features The pathogen survives on overwintering crops and vol-
Powdery mildew is initiated from airborne conidia and unteers. The main period of powdery mildew activity in
appears as small, radiating, diffuse colonies of superfi- northern Europe is usually from July until October, but
cial white mycelium that can measure from 5–15 mm in there is great seasonal variation for the disease. Conidia
diameter. These ectophytic colonies are readily removed readily spread via winds and can travel significant
by rubbing the plant surface. Severe, advanced infec- distances. Powdery mildew conidia do not require
tions produce a dense white powdery covering of leaves water for germination, which can take place at low
(172, 173), stems, and seed crop pods. Severe attacks relative humidity. Rain or free water can actually inhibit
172 173
F UNGAL D ISEASES
172 Severe powdery mildew of swede. 173 Close-up of powdery mildew on underside of
Brussels sprout leaf.
B RASSICACEAE 169
powdery development on the upper leaf surface. Germ- Fusarium oxysporum f. sp. conglutinans,
tube growth occurs mainly at 98–100% relative F. oxysporum f. sp. raphani
humidity. In some areas of California, powdery mildew FUSARIUM WILT,
is most severe on greenhouse-grown vegetable crucifers. FUSARIUM YELLOWS
The exact role of cleistothecia in the disease cycle is not
known, but this spore stage could provide ascospores as Introduction and significance
primary inoculum. This is sometimes a destructive disease of crucifers in
temperate and tropical regions. In California, this
Control disease affects primarily cabbage and radish.
Apply fungicides such as sulfur, triazole, and morpho-
line products. Less susceptible crops such as cauliflower Symptoms and diagnostic features
and cabbage may not require fungicide treatment. For Initial symptoms consist of yellowing of the lower
swede and turnip, delay planting dates as this can leaves, often on one side of the plant (174). These leaves
reduce disease severity. Plant resistant cultivars, partic- later turn brown and drop off. A tan to brown discol-
ularly for Brussels sprout, cabbage, and swede. Two oration of the xylem in the main stem, larger petioles,
forms of resistance have been recognized: suppression and larger roots is characteristic of this disease (175).
of fungal development beyond the appressorial stage, With time, the entire plant may yellow, wilt, and
and delayed spore production. collapse. This disease causes more severe symptoms on
summer crops due to warmer soil temperatures;
References Fusarium develops most rapidly at temperatures
Dixon, G. R. 1974. Field studies of powdery mildew (Erysiphe ranging from 24–29º C, and little symptom develop-
cruciferarum) on Brussels sprouts. Plant Pathology ment occurs below 16º C. Verticillium wilt (caused by
23:105–109.
Verticillium species) has similar vascular discoloration,
Koike, S. T. and Saenz, G. S. 1997. First report of powdery
mildew, caused by Erysiphe cruciferarum, on broccoli raab in but such coloration tends to be black and not brown.
California. Plant Disease 81:1093. Black rot (caused by Xanthomonas campestris) also
Rudyard, S. A. and Wheeler, B. E. J. 1985. The development of causes vascular discoloration, but the blackened xylem
Erysiphe cruciferarum on field-grown Brussels sprouts and
associated changes in soluble amino-acids in foliage leaves. tends to be in the upper, less woody parts of the plant.
Plant Pathology 34:616–625 Fusarium yellows is also a damaging disease of
Vakalounakis, D. J. 1993. First record of Erysiphe cruciferarum radish and is particularly important in the USA. Initial
on Lunaria biennis in Greece. Plant Pathology 43:424–425.
symptoms consist of a dull, yellow-green chlorosis of
174 One-sided 174 175 175 Vascular

chlorosis and discoloration of
necrosis on Fusarium wilt
cabbage caused by of cabbage.
Fusarium wilt.
F UNGAL D ISEASES
176
leaves that is followed by more general yellowing of the
whole plant (176). Leaves may die prematurely and
drop off the plant. Growth is stunted (177) and some
plants die rapidly. Most characteristic is a brown to
black vascular discoloration in the central core of the
radish root (178). Symptom development is tempe-
rature dependent and is most severe at 17–35º C. At
lower temperatures, plants may be infected, but remain
symptomless.
Causal agents
Fusarium yellows on brassica hosts is caused by the
fungus Fusarium oxysporum f. sp. conglutinans. The
176 Stunted plants of Fusarium wilt of radish seedlings. pathogen can be isolated on standard microbiological
media. Semi-selective media such as Komada or FS can
be useful for some samples or to purify isolates. The
177
pathogen morphology and colony characteristics are
similar to other F. oxysporum fungi. Microconidia are
one- or two-celled and measure 6–15 x 2.5–4 μm.
Macroconidia are two to four septate and measure
25–33 x 3.5–5.5 μm. This pathogen is host specific to
crucifers, and can be further divided into various vege-
tative compatibility groups (VCG). Several races have
been identified. Race 1 infects a wide range of crucifers,
including radish. Race 2 is able to infect radish and
some other brassicas, but is not able to cause disease on
B. oleracea crops such as cabbage, cauliflower, and
Brussels sprout. Some researchers suggest that this race
2 be designated as F. oxysporum f. sp. raphani.
177 Stunted plants of Fusarium wilt of radish. Healthy Disease cycle

plant on left. This pathogen is soilborne and produces chlamy-
dospores that enable it to survive for many years in soil.
It may also be seedborne. Infection occurs through the
178
root system and the pathogen subsequently penetrates
the vascular tissues, where growth and sporulation take
place.
Control
Prevent the movement of infested soil to clean fields.
Provide adequate fertilizers to the plants; in particular,
it appears that potassium deficiency may increase
F UNGAL D ISEASES
disease severity. Plant resistant cultivars. Type A resist-

ance is monogenic and prevents pathogen penetration
of the vascular system except at high temperatures
(>30º C). Type B resistance is polygenic and allows only
178 Vascular discoloration of Fusarium wilt of radish. limited vascular colonization at low temperatures, but
loses this resistance as temperatures rise.
B RASSICACEAE 171
References Leptosphaeria maculans (anamorph = Phoma lingam),

L. biglobosa (anamorph = P. lingam)
Beckman, C. H. 1967. Respiratory response of radish varieties
resistant and susceptible to vascular infection by Fusarium BLACK LEG,
oxysporum f. sp. conglutinans. Phytopathology 57:699–702.
Bosland, P. W. and Williams, P. H. 1987. An evaluation of
PHOMA LEAF SPOT & CANKER
Fusarium oxysporum from crucifers based on pathogenicity,
isozyme polymorphism, vegetative compatibility, and geo- Introduction and significance
graphic origin. Canadian Journal of Botany 65:2067–2073.
Black leg is probably one of the most important diseases
Bosland, P. W., Williams, P. H., and Morrison, R. H. 1988.
Influence of soil temperature on expression of yellows and of crucifer vegetables as well as forage and arable
wilt of crucifers by Fusarium oxysporum. Plant Disease crucifers, particularly oilseed rape. Many regions,
72:777–780. including North America, Australia, and Europe, expe-
Farnham, M. W., Keinath, A. P., and Smith, J. P. 2001.
Characterization of Fusarium yellows resistance in collard.
rience significant crop loss from this problem. Black leg
Plant Disease 85:890–894. may be less important in China because the pathogen
Komada, H. 1975. Development of a selective medium for quan- there is the less aggressive B-type. Black leg is the
titative isolation of Fusarium oxysporum from natural soil. accepted and most common name for this disease,
Review of Plant Protection Research 8:114–124.
Momol, E. A. and Kistler, H. C. 1992. Mitochondrial plasmids
though Phoma leaf spot and canker is also used. On
do not determine host range of crucifer-infecting strains of root crops, the disease is called dry rot.
Fusarium oxysporum. Plant Pathology 41:103–112.
Ramirez-Villapadua, J., Endo, R. M., Bosland, P., and Williams, Symptoms and diagnostic features
P. H. 1985. A new race of Fusarium oxysporum f. sp.
conglutinans that attacks cabbage with type A resistance. Foliar symptoms are leaf spots that can be green-
Plant Disease 69: 612–613. brown, pale brown, tan, or almost white. Spots contain
numerous dark, tiny fruiting bodies or pycnidia (179,
180). Spots tend to be circular or oval in shape and
range in size from 0.5-3.0 cm in diameter. There may be
a chlorotic halo around the lesion, and leaf veins within
and extending out of the lesion may be black. These
symptoms are believed to be caused by A-type isolates.
Symptoms caused by the B-type are usually smaller
(1–3 mm) and darker spots, similar to those caused by
Alternaria pathogens. These leaf spots have only a few
pycnidia that are difficult to see without a dissecting
microscope. Radish appears unaffected by B-type, but
179 180
F UNGAL D ISEASES
179 Leaf lesion with pycnidia of black leg of 180 Microscopic view of black leg pycnidia.
cauliflower.
develops leaf lesions after infection by A-type isolates. standard microbiological media. However, it probably
From leaf spots, the pathogen spreads via leaf veins to is easiest to identify this pathogen by directly examining
the petiole and eventually the main stem. diseased tissue for the fruiting bodies of the Phoma
The main stem may then develop the black leg lingam asexual stage. Look for globose, dark brown to
symptom where large, sunken, elongated, brown to black, ostiolate pycnidia that exude small (3–5 x
black cankers form (181, 182, 183). These cankers 1–2 μm), single-celled, cylindrical conidia. The conidial
have uneven borders and, as the tissue deteriorates, the exudate is deep pink, which is a useful diagnostic
stems may become girdled, resulting in stunting, feature to distinguish P. lingam from other Phoma
wilting, and general poor growth. If cankers enlarge, species such as P. exigua or P. herbarum. After a brief
the stem may rot and break, causing the plant to fall incubation in humid conditions, white mycelial growth
over. Cankers usually contain pycnidia. The woody usually forms around the edge of lesions or cankers,
tissues of the stem become black, which is why the which is a useful diagnostic feature. The ascospores of
disease is called black leg. Seedlings with cankers may L. maculans are large, yellow-brown, multicellular
fail to mature or die. Though cankers may come from spores measuring 35–70 x 5–8 μm. They are produced
the spread of the pathogen from leaves, cankers also in black, globose pseudothecia measuring 300–350 μm
form directly from inoculum making contact with the in diameter and forming on infected woody residues of
hyocotyl or stem, usually at the soil level. crucifer hosts.
On root crops such as swede and turnip, a dry rot of This pathogen is now considered to be a species
the bulb, or hypocotyl, develops. The upper neck and complex. Many, but not all, isolates can be placed into
shoulder areas have large brown lesions with black one of two virulence groups (A and B). Each group can
margins. Pycnidia form in large numbers in the lesions. be further divided into phylogenetically distinct
Sectioning the bulb usually reveals a large dry rot subgroups (A: PG2, PG3, PG4; B: NA1, NA2, NA3).
extending deep into the fleshy tissues (184, 185). When The A-group is slow-growing in culture and does not
lesions dry, severely affected bulbs become shrivelled produce brown pigment in culture though it does make
and unmarketable. Secondary fungal and bacterial sirodesmin toxins (isolates are designated as Tox+). The
decay organisms often invade this dry rot tissue. B-group grows more rapidly in culture and produces a
brown pigment on potato dextrose agar, but it does not
Causal agents have sirodesmin toxins (Tox0). Molecular diagnostic
Black leg is caused by the ascomycete fungus Lepto- tests are now available to distinguish these species. The
sphaeria maculans. The pathogen can be isolated on aggressive or A-types are currently named L. maculans
181 181 Stem 182 Internal

182
infection discoloration
of black leg of of black leg of
cauliflower. Brussels sprout.
F UNGAL D ISEASES
B RASSICACEAE 173
and these cause the most severe black leg symptoms. 184 184 Dry rot of
The less aggressive B-type has recently been named L. swede caused by
biglobosa, which is differentiated by morphological and black leg.
cultural characteristics. Interestingly, both Lepto-
sphaeria species have a P. lingam asexual stage.
Research and discussion are still ongoing regarding the
taxonomy of this pathogen.
Disease cycle
The pathogen is commonly seedborne and low levels of
infection (<0.1%) may initiate significant disease
outbreaks. In some areas, however, low levels of
seedborne inoculum are less important than airborne
ascospores. High numbers of ascospores can be
released from infected winter oilseed rape debris for
several months each year. Spores can travel more than
a kilometer to infect vegetable crucifers. Once the
Phoma leaf spot stage is established, secondary spread Control
takes place by water-dispersed conidia. The importance Use seed that does not have significant levels of the
of conidia in the disease cycle appears to vary between pathogen. Test seed using established seed-assay
different crops and geographic regions. Optimum tem- protocols. If seed are possibly infested, treat them with
peratures for ascospore infection are 15–20º C. fungicides or hot water. Effective fungicides include
A minimum of 4 hours leaf wetness is required for thiram, iprodione, and fenpropimorph. Resistant
infection, but maximum infection requires up to 48 cultivars have not been developed, though some
hours. Symptoms appear in 3 to 4 days at 20º C or 14 Brassica oleracea crops show considerable tolerance to
days at 5º C. B-group ascospores produce long straight the leaf-infection phase of blackl eg. Apply foliar fungi-
hyphae, which penetrate the leaf through stomata or cides to protect susceptible cultivars. Avoid placing
wounds, while A-type ascospores produce shorter, vegetable crucifers close to oilseed rape fields; close
curled hyphae that penetrate through the cuticle as well proximity is likely to increase disease pressure from
as through stomata and wounds. airborne ascospores.
183 Close-up of 185 Section of

183 185
Brussels sprout swede bulb
stem infection and showing internal
pycnidia of black rotting due to
leg. black leg.
F UNGAL D ISEASES
References
Bonman, J. M., Gabrielson, R. L., Williams, P. H., and Delwiche, West, J. S., Kharbanda, P. D., Barbetti, M.J., and Fitt, B. D. L.
P. A. 1981. Virulence of Phoma lingam to cabbage. Plant 2001. Epidemiology and management of Leptosphaeria
Disease 65:865–867. maculans (Phoma stem canker) on oilseed rape in Australia,
Gabrielson, R. L. 1983. Blackleg disease of crucifers caused by Canada and Europe. Plant Pathology 50:10–27.
Leptosphaeria maculans (Phoma lingam) and its control. Williams, P. H. 1992. Biology of Leptosphaeria maculans.
Seed Science and Technology 11:749–780. Canadian Journal of Plant Pathology. 14:30–35.
Gabrielson, L. 1988. Inoculum thresholds for seed-borne Williams, R. H. and Fitt, B. D. L. 1999. Differentiating A and B
pathogens. Phytopathology 78:868–872. groups of Leptosphaeria maculans, causal agent of stem
Huang, H. J., Toscano-Underwood, C., Fitt, B. D. L., Hiu, X. J., canker (blackleg) of oilseed rape. Plant Pathology
and Hall, A. M. 2003. Effects of temperature on ascospore 48:161–175.
germination and penetration of oilseed rape (Brassica napus)
leaves by A- or B-group Leptosphaeria maculans (Phoma
stem canker). Plant Pathology 52:245–255.
Johnson, R. D. and Lewis, B. G. 1994. Variation in host range,
systemic infection and epidemiology of Leptosphaeria
maculans. Plant Pathology 43:417–424.
Maguire, J. D., Gabrielson, R. L., Mulanax, M. W., and Russell,
T. S. 1978. Factors affecting sensitivity of 2,4-D assays of
crucifer seed for Phoma lingam. Seed Science and Technology
6:915–924. Mycosphaerella brassicicola
Maude, R. B., Humpherson Jones, F. M., and Shuring, C. G. (anamorph = Asteromella brassicae)
1984. Treatments to control Phoma and Alternaria infections
of brassica seeds. Plant Pathology 33:525–535. RING SPOT
Mengistu, A., Rimmer, S. R., Koch, E., and Williams, P. H. 1991.
Pathogenicity grouping of isolates of Leptosphaeria maculans Introduction and significance
on Brassica napus cultivars and their disease reaction profiles
on rapid-cycling Brassicas. Plant Disease 75:1279–1282.
This disease is common in cool moist areas, particular-
Pongam, P., Osborn, T. C., and Williams, P. H. 1999. Assessment ly coastal regions of north-west Europe, California,
of genetic variation among Leptosphaeria maculans isolates New Zealand, and Australia. Severe problems are
using pathogenicity data and AFLP analysis. Plant Disease usually associated with intensive cropping and over-
83:149–154.
Purwantara, A., Barrins, J. M., Cozijnsen, A. J., Ades, P. K., and
lapping production of brassicas. It is important in
Howlett, B. J. 2000. Genetic diversity of isolates of the winter cauliflower, Brussels sprout and cabbage in the
Leptosphaeria maculans species complex from Australia, UK, where it is the most important foliar disease on
Europe, and North America using amplified fragment length
polymorphism analysis. Mycological Research 104:772–781. these crops. In California this disease is mostly found on
Shoemaker, R. A. and Brun, H. 2001. The teleomorph of the Brussels sprouts.
weakly aggressive segregate of Leptosphaeria maculans.
Canadian Journal of Botany 79:412–419.
Thurwachter, F., Garbe, V., and Hoppe, H. H. 1999. Ascospore
discharge, leaf infestation and variations in pathogenicity as Symptoms occur on foliage and on the pods of seed
criteria to predict impact of Leptosphaeria maculans on crops. Initially spots are dark, measure 3–5 mm in
oilseed rape. Journal of Phytopathology 147:215–222. diameter, and are green-brown or gray-black (186,
Toscano-Underwood, C., West, J. S., Fitt, B. D. L., Todd, A. D.,
187). Spots enlarge to 2–3 cm in diameter, appear gray
and Jedryczka, M. 2001. Development of Phoma lesions on
oilseed rape leaves inoculated with ascospores of A- and B- when dry, but turn black when the foliage is wet. Leaf
group Leptosphaeria maculans (stem canker) at different spots are visible on both sides of the leaf. Leaf spots are
temperatures and wetness durations. Plant Pathology
50:28–41.
restricted by veins so that they often have an angular
Vanniasingham, V. M. and Gilligan, C. A. 1989. Effects of host, appearance; this is one feature that distinguishes
pathogen, and environmental factors on latent period and ringspot from Alternaria leaf spot. Ring spot spots are
production of pycnidia of Leptosphaeria maculans on oilseed often surrounded by a yellow halo, and when spotting
rape leaves in controlled environments. Mycological
F UNGAL D ISEASES
Research 93:167–174. is severe, there is extensive leaf yellowing (188) and

West, J. S., Balesdent, M.-H., Rouxel, T., Narcy, J. P., Huang, early defoliation. Severe ring spot can result in signifi-
Y-J., Roux, J., Steed, J. M., Fitt, B. D. L., and Schmit, J. 2002. cant yield loss. The larger leaf spots have concentric
Colonization of winter oilseed rape tissues by A/Tox+ and
B/Tox0 Leptosphaeria maculans (Phoma stem canker) in
zones of tiny black fruiting bodies, hence the name ring
France and England. Plant Pathology 51:311–321. spot, that form 3 to 4 weeks after infection.
B RASSICACEAE 175
The small size and high density of these fruiting 186

bodies differs from those of Phoma leaf spot (black leg)
which has widely-spaced, brown pycnidia. Symptoms
are usually first found on the oldest leaves, but under
high disease pressure new symptoms can occur on any
leaf. Symptoms on sprouts of Brussels sprout are
initially black spots that measure 3–5 mm in diameter.
Lesions develop first on the lower sprouts. Mature
lesions on sprouts reach 1–2 cm in diameter and are
gray when dry but black when wet. Pod symptoms are
similar to those on leaves and may be confused with
those of Alternaria or white leaf spot diseases. Ring spot
can also develop on stored cabbage heads and may
penetrate through several leaf layers during storage. 186 Ring spot lesions on Brussels sprout.
Causal agent
Ring spot is caused by the ascomycete fungus 187
Mycosphaerella brassicicola. The pseudothecia of the
sexual stage are usually present in older leaf lesions and
appear as very small, black specks and structures
arranged in concentric rings. Pseudothecia release
ascospores that are hyaline, two-celled, with rounded
ends, and measure 30–45 x 12–18 μm. The pathogen
has an asexual stage named Asteromella brassicae.
Asteromella brassicae also forms in the leaf spots, but
spores are considered non-infective. Conidia are
hyaline, cylindrical, measure 3–5 x 1 μm, and are
produced in globular brown pycnidia. There is evidence
that some isolates have restricted host ranges and infect
only cabbage. The pathogen may be seedborne. 187 Ring spot on Brussels sprout.
Disease cycle
Ring spot is initiated by airborne ascospores, which 188
enables the pathogen to spread from nearby crops and
infected residues to new plantings. Survival on plant
residues is thought to be limited. Once ring spot is estab-
lished in a crop, secondary spread occurs by new
ascospores produced in leaf lesions. Seedborne
inoculum may be another source of the pathogen. The
fungus requires briefer periods of leaf wetness than
Alternaria, and conditions in the UK are rarely limiting
for infection in crops like Brussels sprout. The optimum
F UNGAL D ISEASES
temperatures for infection are 16–20º C, and symptoms

appear 10 to 14 days after infection. Mature pseudo-
thecia appear after 4 consecutive days with 100%
relative humidity, perhaps as soon as 3 weeks after
initial infection. Severe disease is usually associated with
prolonged periods (7 to 14 days) of wet weather. 188 Ring spot on cabbage.
Control Mycosphaerella capsellae

Rotate with non-hosts and bury infected crop residues (anamorph = Pseudocercosporella capsellae)
to reduce inoculum sources. Do not plant vegetable WHITE LEAF SPOT
brassicas adjacent to field-grown brassicas, such as
oilseed rape, or kale used for game cover in the UK. Introduction and significance
Plant resistant Brussels sprout and cauliflower cultivars. White leaf spot is a minor foliar disease of brassicas that
Apply fungicides such as chlorothalonil, triazole, and may occasionally cause economic losses in parts of
strobilurin products. Treat infected seed with hot water northern Europe, North America, and the southern
or a thiram soak. Disease forecasting and inoculum hemisphere. Swede, turnip, various mustards, and
detection systems are being evaluated in the UK. Chinese cabbage are among the affected hosts, with
fewer reports from Brassica oleracea vegetables. In the
References UK, this disease is most often reported on turnip and
Davies, J. M. L., Ann, D. M., Dobson, S. C., Jones, O. W., swede.
Gladders, P., Melville, S. C., McPherson, G.M., Popham, M.
D., Price, R. I., and Wafford, J.D. 1986. Fungicide spray
timing on Brussels sprouts. Aspects of Applied Biology Symptoms and diagnostic features
12: 21–28. The primary symptoms are leaf spots that first are small
Dring, D. M. 1961. Studies on Mycosphaerella brassicicola. (2–3 mm in diameter), gray to gray-green, and circular.
Later in disease development, lesions remain circular,
Hartill, W. F. T. and Sutton, P. G. 1980. Inhibition of germination
of Mycosphaerella brassicicola ascospores on young cabbage become light tan to white, and can grow up to
and cauliflower leaves. Annals of Applied Biology 10–12 mm in diameter (189). Dark streaks and
96:153–161. speckling are sometimes apparent within these leaf
Kennedy, R., Wakeham, A. J., and Cullington, J. E. 1999.
Production and immunodetection of ascospores of
spots. White conidial growth may be observed on the
Mycosphaerella brassicicola ringspot of vegetable crucifers. leaf spots, often on the leaf undersides (190). On seed
Plant Pathology 48:297–307. crops, the most severe symptom is known as ‘gray stem’
Van den Ende, J. E. and Frinking, H. D. 1993. Comparison of from the color of the infected upper stems. Pods develop
inoculation methods with Mycosphaerella brassicicola on
Brassica oleracea var. capitata: ascospores versus mycelial elongated to oval lesions that may resemble Alternaria
fragments. Netherlands Journal of Plant Pathology 99, infections but often have the diagnostic light tan color
Supplement 3:69–81. and dark reticulation.
Wafford, J. D., Gladders, P., and McPherson, G. M. 1986. The
incidence and severity of Brussels sprout diseases and the
influence of oilseed rape. Aspects of Applied Biology Causal agent
12:1–12. White leaf spot is caused by the ascomycete fungus
Wakeham, A. J. and Kennedy, R. 2002. Quantification of Mycosphaerella capsellae. The fungus forms perithecia
airborne inoculum using antibody based systems. The BCPC
Conference – Pests & Diseases 1:409–416. and ascospores that are slightly curved, hyaline, two-
Wicks, T. J. and Vogelzang. B. 1988. Effect of fungicides applied celled, and measure 15–23 x 3–3.5 μm. However, the
after infection on the control of Mycosphaerella brassicicola pathogen is mostly present on plants as its anamorph
on Brussels sprouts. Australian Journal of Experimental
Agriculture 28:411–416. stage Pseudocercosporella capsellae. Pseudocerco-
sporella capsellae can be isolated on standard microbi-
ological media, though the fungus is very slow-growing
and difficult to obtain in pure culture. After many days
on potato dextrose agar (PDA), isolations can result in
slow-growing, raised, black, stromatic colonies that
produce few conidia. On 2% water agar, colony mor-
F UNGAL D ISEASES
phology is similar to that on PDA, but colonies also

release a purple-pink pigment into the media. Confirm-
ation of white leaf spot might better be accomplished by
microscopic examination of leaf-spot tissue that has
been just collected from the field or incubated under
moist conditions. From plant tissue, conidiophores are
B RASSICACEAE 177
solitary or grouped in fascicles. Conidia are hyaline, References

cylindrical, one to three septate, and measure 30–70 x Campbell, R. and Greathead, A. S. 1978. Pseudocercosporella
2–3 μm. Yet another spore stage, called spermatia, is white spot of crucifers in California. Plant Disease Reporter
62:1066–1068.
produced in black spermogonia on leaves and pods and
Cerkauskas, R. F., Stobbs, L. W., Lowery, D. T., Van Driel, L.,
consists of very small spores that measure 3–4 x 1 μm; Liu, W., and VanSchagen, J. 1998. Diseases, pests, and abiotic
spermatia appear to be non-infective. problems associated with oriental cruciferous vegetables in
southern Ontario in 1993-1994. Canadian Journal of Plant
Disease cycle Inman, A. J., Fitt, B. D. L., and Evans, R. L. 1992. Epidemiology
Under UK conditions, disease development in winter in relation to control of white leaf spot (Mycosphaerella
oilseed rape suggests that ascospores are produced capsellae) on oilseed rape. Proceedings of the Brighton Crop
Protection Conference – Pests and Diseases 2:681–686.
mainly in autumn (October to January) and spread via Inman, A. J., Fitt, B. D. L., Todd, A. D., and Evans, R. L. 1999.
air to new spring crops. The sexual stage therefore Ascospores as primary inoculum for epidemics of white leaf
enables the pathogen to survive between crops. spot (Mycosphaerella capsellae) in winter oilseed rape in the
UK. Plant Pathology 48:308–319.
Ascospore discharge is associated with wet conditions,
Inman, A. J., Sivanesan, A., Fitt, B. D. L., and Evans, R. L. 1991.
and wet periods are required for infection. Symptoms The biology of Mycosphaerella capsellae, the teleomorph of
appear in 6 to 8 days under optimum temperatures of Pseudocercosporella capsellae, cause of white leaf spot of
15–20º C, but may take 24 days to appear at 5º C. oilseed rape. Mycological Research 95:1334–1342.
Koike, S. T. 1996. Red mustard, tah tsai, and Japanese mustard
Conidia that grow on leaf spots are splash or wind as hosts of Pseudocercosporella capsellae in California. Plant
dispersed only short distances to other leaves and Disease 80:960.
plants. The pathogen does not persist in soil, but Petrie, G. A. and Vanterpool, T. C. 1978. Pseudocercosporella
survives on weed hosts and volunteer brassicas. capsellae, the cause of white leaf spot and grey stem of
Cruciferae in western Canada. Canadian Plant Disease
Survey 58:69–72.
Control
Control measures are rarely needed. Plow in infected
crop residues after harvest. Do not plant vegetable
brassicas adjacent to oilseed rape in regions where
white leaf spot is common.
189 190
F UNGAL D ISEASES
189 Symptoms of white leaf spot of bok choy. 190 Sporulation of white leaf spot of Chinese cabbage.
Peronospora parasitica fungal conidiophores bearing spores on ‘tree-like’

DOWNY MILDEW branches. This growth is distinct from the white
radiating mycelium of powdery mildew. In established
Introduction and significance downy mildew lesions, there is usually irregular dark
This common disease occurs worldwide and affects speckling and eventually the center of the lesion
most vegetable, ornamental, and weed crucifers. It is becomes bleached and papery. Downy mildew is often
particularly important at the seedling stage, but it can most severe on the cotyledons and first true leaves (191)
also cause problems on crops close to maturity. Severe and this can result in the death of seedlings, particular-
attacks result in loss of seedlings. In California, downy ly if frost conditions occur.
mildew is rarely a concern on established, older plants. On older plants, downy mildew causes variously
sized yellow blotches that have an angular appearance
Symptoms and diagnostic features because of the major leaf veins. If disease development
The first symptoms are irregular yellow patches on the is extensive, leaves may take on a blighted effect due to
cotyledons or young leaves with white fungal growth the numerous infection sites (192). On Brussels sprout,
on the underside of the lesions. Under cool, humid con- downy mildew causes either irregular shaped, yellow
ditions, sporulation can also occur on the upper lesion lesions with irregular dark speckling, or black lesions.
surface. With a hand lens, it is possible to see the erect Systemic infection results in a gray or black flecking and
193 Systemic 193

191
infection of downy
mildew in broccoli
stems.
191 Cotyledon infection of downy mildew of cauli-

flower.
192 194
F UNGAL D ISEASES
192 Leaf infections of downy mildew of cauliflower. 194 Black discoloration and white sporulation of
downy mildew on cauliflower florets.
B RASSICACEAE 179
streaking of internal tissues, notably in cauliflower and 197

broccoli flower stalks, sprouts of Brussels sprout, and
cabbage heads (193, 194). Pod infection occurs in seed
crops and in some species there is infection and distor-
tion of the flower stem.
Downy mildew is an important problem on radish
because the pathogen can infect the fleshy root and
cause external black patches and lesions on the root
shoulder and internal grey or black flecking and
streaking in the hypocotyl and root (195, 196, 197 ).
Either symptom renders the radish unmarketable. The
surface of the root can show scarring and is prone to
cracking or splitting. On radish leaves, downy mildew
produces irregularly shaped, angular, yellow lesions
that contain dark speckling (198, 199). White spo-
rulation of the pathogen occurs on the undersurface of
the leaf. 197 Black lesions of downy mildew of white radish.
195 198
195 Black lesions of downy mildew of red radish. 198 Leaf infections of downy mildew of radish.
196 199
F UNGAL D ISEASES
196 Internal root discoloration of downy mildew of 199 Leaf infections of downy mildew of radish.
radish.

Downy mildew is caused by the oomycete Peronospora Cerkauskas, R. F., Stobbs, L. W., Lowery, D. T., Van Driel, L.,
parasitica. Due to recent taxonomic work, some Liu, W., and VanSchagen, J. 1998. Diseases, pests, and abiotic
problems associated with oriental cruciferous vegetables in
researchers have renamed this organism Hyalo- southern Ontario in 1993-1994. Canadian Journal of Plant
peronospora parasitica. This obligate pathogen forms Pathology 20:87–94.
mycelium and haustoria inside host tissues. The spo- Constantinescu, O. and Fatehi, J. 2002. Peronospora-like fungi
(Chromista, Peronosporales) parasitic on Brassicaceae and
rangiophores emerge through the stomata, are dichoto- related hosts. Nova Hedwigia 74:291–338.
mously branched, and terminate with slender tips. The Dickinson, C. H. and Greenhalgh, J. R. 1977. Host range and
sporangia are hyaline, elliptical, and measure 10–20 x taxonomy of Peronospora on crucifers. Transactions of the
20–22 μm. Sexual oospores are globular, thick walled, British Mycological Society 69:111–116.
Dickson, M. H. and Petzoldt, R. 1993. Plant age and isolate
and measure 26–43 μm. Some P. parasitica isolates and source affect expression of downy mildew resistance in
races form few or no oospores. There is some evidence broccoli. Horticultural Science 28:730–731.
that the pathogen may be seedborne. There is consider- Jensen, B. D., Hockenhull, J., and Munk, L. 1999. Seedling and
able host specialization within P. parasitica and strains adult plant resistance to downy mildew (Peronospora para-
sitica) in cauliflower (Brassica oleracea convar. botrytis var.
affecting radish may be only weakly pathogenic on botrytis). Plant Pathology 48:604–612.
other brassicas. Kluczewski, S. M. and Lucas, J. A. 1982. Development and
physiology of infection by the downy mildew fungus
Peronospora parasitica (Pers. ex Fr.) Fr. in susceptible and
Disease cycle resistant Brassica species. Plant Pathology 31:373–379.
Cool (10–15º C), moist conditions favor downy mildew Kluczewski, S. M. and Lucas, J. A. 1983. Host infection and
sporulation, germination of sporangia, and infection. oospore formation by Peronospora parasitica in agricultural
Lesion expansion is most rapid at 20º C, and at this and horticultural Brassica species. Transactions of the British
Mycological Society 81:591–596.
temperature the asexual cycle can be completed in only Koike, S .T. 1998. Downy mildew of arugula, caused by
3 or 4 days. Sporangia are dispersed via winds and Peronospora parasitica, in California. Plant Disease 82:1063.
splashing water and penetrate through the leaf cuticle McKay, A. G., Floyd, R. M., and Boyd, C. J. 1992. Phosphonic
or stomata. If oospores are produced, these may persist acid controls downy mildew (Peronospora parasitica) in
cauliflower curds. Australian Journal of Experimental
in crop residues and in soil and act as sources of initial Agriculture 32:127–129.
inoculum. Ramsey, G. B., Smith, M. A., and Wright, W. R. 1954.
Peronospora on radish roots. Phytopathology 44:384–385.
Control Sherriff, C. and Lucas, J. A. 1989. Heterothallism and homothal-
lism in Peronospora parasitica. Mycological Research
Manage downy mildew on transplants by improving 92:311–316.
air movement around the plants, irrigating early in the Sherriff, C. and Lucas, J .A. 1990. The host range of isolates of
day so foliage can readily dry, and applying fungicides. downy mildew, Peronospora parasitica, from Brassica crop
Fungicides such as metalaxyl can be used as seed treat-
Silue, D., Nashaat, N. I., and Tirilly, Y. 1996. Differential
ments for controlling early downy mildew on trans- responses of Brassica oleracea and B. rapa accessions to seven
plants, though metalaxyl resistance occurs in the UK isolates of Peronospora parasitica at the cotyledon stage.
and other regions. For field control, fungicides may also
Thomas, C. E. and Jourdain, E. L. 1990. Evaluation of broccoli
be necessary. Plant resistant or tolerant cultivars. and cauliflower germplasm for resistance to Race 2 of
Peronospora parasitica. Horticultural Science 25:1429–1431.
Wang, M., Farnham, M. W., and Thomas, C. E. 2001.
Inheritance of true leaf stage downy mildew resistance in
broccoli. Journal of the American Society for Horticultural
Science 126:727–729.
F UNGAL D ISEASES
B RASSICACEAE 181
Plasmodiophora brassicae
201
CLUBROOT

Clubroot is one of the most readily recognized diseases
of crucifers. The disease may be increasing in impor-
tance as growers intensify rotations of brassicas and
simultaneously try to reduce production costs by using
less lime in the fields. Clubroot occurs wherever
crucifers are grown and is believed to have originated in
the Mediterranean region. Severely infested fields are
often taken out of brassica production.

Above-ground symptoms are severe stunting,
yellowing, wilting, and other signs of a dysfunctional
root system (200). Plant roots show extensive galling,
swelling, and distortion (201, 202). Large galls on the
hypocotyl and main taproot are more damaging than
galls on the smaller lateral roots. Fresh galls are firm in
texture and retain the off-white color of root tissue. 201 Bok choy infected with clubroot disease.
However, as disease progresses, the galls and swellings
darken, become infested with secondary decay
organisms, and are soft and rotted. Decay of roots Causal agent
releases inoculum into the soil. Disease tends to be more Clubroot is caused by the pathogen Plasmodiophora
severe on summer crops because of warmer growing brassicae. This organism, previously considered a
conditions, earlier infection of plants, and weather con- fungus, is currently considered more closely related to
ditions that stress plants. Root galls caused by the turnip ciliate protozoans because of its reproductive structures
gall weevil (Ceutorhynchus pleurostigma) or small gall- and lack of a cell wall. The pathogen is placed in its own
like structures known as hybridization nodules may phylum, the Plasmodiophoromycota. The presence of
superficially resemble clubroot. clubbed roots containing resting spores (4 μm diameter)
200 202
F UNGAL D ISEASES
200 Stunted, declining cauliflower infected with 202 Cauliflower transplants infected with clubroot
clubroot disease. disease.
is diagnostic for this disease. The organism cannot be hairs of various non-crucifer plants including grasses
truly grown in vitro, though the amoebal stage has and some weeds, but the clubroot stage only occurs in
recently been cultured. Plasmodiophora brassicae has a crucifers. On watercress, clubroot produces swellings
complex life cycle that is still not fully understood. The on the shoot. Weed hosts, such as shepherd’s purse
pathogen can survive in soil for long periods, 20 years (Capsella bursa-pastoris), may aid pathogen survival.
or longer, as thick-walled resting spores.
Many races of P. brassicae have been identified by Control
using sets of cultivars with different genetic resistances. Rotate crucifer crops with non-hosts on a 5 to 6 year
Depending on how an isolate infects one or more of the cycle; this management step will not eliminate the
cultivars in the set, the isolate can be categorized as to a pathogen from soil, but will prevent inoculum from
race or subset of the P. brassicae group. Several differ- continuing to increase. Maintain records of infested
ential sets are used around the world: differential hosts fields so that susceptible crops can be planted elsewhere.
by Williams; European clubroot differentials (ECD); It is important to note that in California and other
CR F1 cultivars in Japan. regions, mustard cover crops are planted in the fall and
winter to add organic matter to the soil, increase soil
Disease cycle microbial diversity, and possibly suppress some soil-
The life cycle of clubroot is complex. Uninucleate thick- borne pathogens due to the glucosinolates released
walled resting spores formed in the root galls are from decaying mustard plant residues. However, such
liberated into soil when the galls decay. Resting spores mustards are susceptible to the clubroot pathogen and
germinate in the presence of plant roots when tempera- could sustain or increase P. brassicae inoculum levels.
tures are at least 16º C. Host infection is favored by For many fields, clubroot is successfully managed by
temperatures above 18º C and disease severity increases applying lime and keeping soil pH above 7.2 to 7.3.
with rising temperatures up to 26º C. Light intensity Such soils are called responsive soils; the lime does not
also influences clubroot development, with 600 Wh kill the pathogen, but creates conditions that prevent
m-2 day-1 producing maximum clubroot severity on the formation of the root clubs. However, for other
cabbage seedlings. nonresponsive soils the liming treatment is much less
The resting spore germinates by releasing a single effective. Calcium oxide acts rapidly and is generally
biflagellate zoospore that swims in soil water, finds a considered more effective than calcium carbonate for
host root by chemotaxis, and attaches itself to a root clubroot control. A finely graded product is preferable
hair. The attached zoospore forms a bullet-shaped to coarse material. There is evidence that the benefits of
structure (stachel) that allows it to forcibly inject calcium salt applications are not solely due to effects on
zoospore contents into the root hair. Within the root soil pH. The greatest reduction of symptoms has been
hair, the pathogen becomes enclosed by the host cell obtained with calcium salts that raised both soil calcium
plasmalemma and starts the second stage of its life cycle concentration and soil pH.
by forming a multi-nucleate plasmodium. The plas- Prevent the movement of infested soil and contami-
modium produces 10 to 20 haploid secondary zoo- nated equipment to uninfested fields. Ensure that trans-
spores that are capable of infecting other root hairs or plants and other materials do not harbor the pathogen.
fuse in pairs to form larger binucleate cells, which infect It is possible for transplants grown in soilless rooting
cells of the root cortex. As the organism grows and medium to have clubroot due to contamination from
divides, large multinucleate plasmodia form within the infested dust and dirt. The resting spores can survive
root. Infection leads to multiplication and enlargement passage through the digestive system of cattle, so use
of root cells due to changes in plant hormone caution in using manures as soil amendments. Resistant
F UNGAL D ISEASES
(cytokinins and auxins) levels. The root cells accumu- cultivars are available for various crucifer crops, but
late starch when sugars are diverted to the affected these do not generally provide complete control.
roots. Galls develop within 3 to 4 weeks of infection. Recently, resistance has broken down for clubroot
Infection occurs over a wide range of both acid and resistant Chinese cabbage cultivars grown in Japan.
alkaline soils, though acid soils favor the development Clubroot populations are highly variable and cultivar
of root symptoms. The pathogen can infect the root resistance will not be effective at all sites.
B RASSICACEAE 183
In the UK, soils are tested before planting to identify Manzanares-Dauleux, M. J., Divaret, I., Baron, F., and Thomas,
G. 2001. Assessment of biological and molecular variability
potential risks from clubroot. Such tests involve between and within field isolates of Plasmodiophora
growing brassica seedlings in soil samples and take brassicae. Plant Pathology 50:165–173.
about 6 weeks to complete. Tests are available through Murakami, H., Tsushima, S., Akimoto, T., Murakami, K., Goto,
I., and Shishido, Y. 2000. Effects of growing leafy daikon
the Advisory services. Soil fumigants have not proven (Rhaphanus sativus) on populations of Plasmodiophora
to be economically viable for crucifer production. brasicae (clubroot). Plant Pathology 49:584–589.
Myers, D. F. and Campbell, R. N. 1985. Lime and the control of
clubroot of crucifers: effects of pH, calcium, magnesium, and
References
their interactions. Phytopathology 75:670–673.
Ann, D., Channon, A., Melville, S., and Antill, D. 1987. Robak, J. 1996. The effect of some crop rotations on decrease of
Clubroot control in cabbage and cauliflower by adding clubroot, Plasmodiophora brassicae, in soils. Proceedings of
fungicide to the compost used for raising transplants in loose- Brighton Crop Protection Conference – Pests & Diseases
filled cells. 1987. BCPC Monograph No. 39 Application to 2:647–651.
Seeds and Soil: 395–402.
Voorrips, R. E. 1996. Production, characterization and
Arnold, D. L., Blakesley, D., and Clarkson, J. M. 1996. Evidence interaction of single-spore isolates of Plasmodiophora
for growth of Plasmodiophora brassicae in vitro. Mycological brassicae. European Journal of Plant Pathology
Research 100:535–540. 102:377–383.
Buczacki, S.T., Ockendon, J. G., and Freeman, G. H. 1978. An Wallenhammar, A. C. and Arwidsson, O. 2001. Detection of
analysis of some effects of light and soil temperature on Plasmodiophora brassicae by PCR in naturally infested soils.
clubroot disease. Annals of Applied Biology 88:229–238. European Journal of Plant Pathology 107:313–321.
Campbell, R .N., Greathead, A. S., Myers, D. F., and deBoer, G. J. Webster, M. A. and Dixon, G. R. 1991. Calcium, pH, and
1985. Factors related to control of clubroot of crucifers in the inoculum concentration influencing colonization by
Salinas Valley, California. Phytopathology 75:665–670. Plasmodiophora brassicae. Mycological Research 95:64–73.
Castlebury, L. A., Maddox, J. V., and Glawe, D. A. 1994. Webster, M. A. and Dixon, G. R. 1991. Boron, pH, and
A technique for the extraction and purification of viable inoculum concentration influencing colonization by
Plasmodiophora brassicae resting spores from host root Plasmodiophora brassicae. Mycological Research 95:74–79.
tissue. Mycologia 86:458–460.
Colhoun, J. 1958. Clubroot Disease of Crucifers Caused by
Plasmodiophora brassicae: A Monograph. Phytopathological
Paper No. 3. Commonwealth Mycological Institute.
Dixon, G. R .1996. Repression of the morphogenesis of
Plasmodiophora brassicae Wor. by boron – A review. Acta
Dixon, G. R. and Webster, M. A. 1988. Antagonistic effects of
boron, calcium and pH on pathogenesis caused by
Plasmodiophora brassicae Woronin (clubroot) – a review of
recent work. Crop Research 28:83–95.
Dobson, R. L., Robak, J., and Gabrielson, R. L. 1983.
Pathotypes of Plasmodiophora brassicae in Washington,
Oregon, and California. Plant Disease 67:269–271.
Donald, E. C., Lawrence J. M., and Porter, I. J. 2004. Influence of
particle size and application method on the efficacy of
calcium cyanamide for control of clubroot of vegetable
brassicas. Crop Protection 23:297–303.
Donald, E. C., Porter, I. J., and Lancaster, R. A. 2001. Band
incorporation of fluazinam (Shirlan) into soil to control
clubroot of vegetable brassica crops. Australian Journal of
Experimental Agriculture 41:1223–1226.
Faggian, R., Bulman, S. R., Lawrie, A. C., and Porter, I. J. 1999.
Specific polymerase chain reaction primers for the detection
of Plasmodiophora brassicae in soil and water.
F UNGAL D ISEASES
Kuginuki, Y., Yoshikawa, H., and Hirai, M. 1999. Variation in

virulence of Plasmodiophora brassicae in Japan tested with
clubroot-resistant cultivars of Chinese cabbage (Brassica rapa
L. ssp. pekinensis). European European Journal of Plant
Jones, D. R., Ingram, D. S., and Dixon, G. R. 1982. Factors
affecting tests for differential pathogenicity in populations of
Plasmodiophora brassicae. Plant Pathology 31:229–238.
Phytophthora brassicae affects Chinese cabbage heads after short storage

PHYTOPHTHORA STORAGE ROT periods (204).
Introduction and significance Causal agent

This disease is mainly important as a storage rot of Phytophthora storage rot is caused by the oomycete
white cabbage in Europe, where losses can reach 50%. Phytophthora brassicae. On solid media the pathogen
Its prevalence as a foliar pathogen is probably under- produces abundant sporangia that have indistinct
estimated. papilla and measure 40–74 x 25–48 μm. Few oogonia
of the sexual stage are formed; oospores measure
Symptoms and diagnostic features 30–65 μm in diameter. Though previously designated
Symptoms consist of leaf spots that are grey or black, as P. porri, P. brassicae only infects brassica plants and
water-soaked, and measure 5–20 mm in diameter. is genetically and morphologically distinct from the
These spots may resemble symptoms of gray mold or allium pathogen.
bacterial soft rot. Savoy cabbage (203) is especially sus-
ceptible because of the furrowed leaves that retain Disease cycle
water for longer periods than smooth-leaved cabbage. The precise epidemiology of this disease is not known.
For stored white cabbage, a firm brown rot extends Oospores, sporangia, or zoospores in soil are probably
from the stem base into the leaves. This disease also splashed up onto cabbage heads and infect host tissues.
Infection might also take place through handling and
wounds that occur during harvest. Problems are often
203
associated with particularly wet and muddy harvest
conditions. Storage rot symptoms appear within
2 weeks at 20° C, but may take several weeks to appear
at 0–2° C. There is usually little spread within storage
bins. Leaf spot symptoms often occur in the field after
heavy rain, again suggesting that soilborne inoculum is
spread to plants by splashing water.
Control
Harvest cabbage under dry field conditions. Handle
cabbage heads carefully and keep them free of soil and
mud. Disinfect the cutting knives used for harvesting
203 Storage rot symptoms on savoy cabbage. if they become dirty. Pre-storage dips with fungicides
containing metalaxyl have given good control of
204
storage rot.
References
Geeson, J. D. 1976. Storage rot of white cabbage caused by
Phytophthora porri. Plant Pathology 25:115–116.
Hamm, P. B. and Koepsell, P. A. 1984. Phytophthora root rot of
cabbage and cauliflower in Oregon. Plant Disease
68:533–535.
Man in t’Veld, W. A., de Cock, A .W. A. M., Ilieva, E., and
F UNGAL D ISEASES
Lévesque, C. A. 2002. Gene flow analysis of Phytophthora

porri reveals a new species: Phytophthora brassicae sp. nov.
European Journal of Plant Pathology 108:51–62.
Thompson, A. H., and Phillips, A. J. L. 1988. Root rot of
cabbage caused by Phytophthora drechsleri. Plant Pathology
37:297–299.
204 Chinese cabbage in storage affected by
Phytophthora brassicae.
B RASSICACEAE 185
Phytophthora megasperma Later, the entire plant wilts and is unmarketable. At the
PHYTOPHTHORA ROOT ROT soil line, the stem may develop dark, discrete lesions or
turn black in general and become soft (205). Plants tend
Introduction and significance to fall over or be easily dislodged because the lateral
This disease can damage vegetable brassicas, although roots have decayed (206, 207, 208). In the UK, P.
it is usually of minor importance. Phytophthora megasperma is thought to have caused severe rotting of
megasperma is the most important and common swede after several weeks of cold storage.
species that causes root rot. In South Africa,
P. drechsleri appears to be most prominent on cabbage. Causal agents
Some damping-off problems may be due to Phythophthora root rot is caused by the oomycete
P. cactorum. Swede may occasionally develop a storage organism P. megasperma. The pathogen can be isolated
rot from Phytophthora infections. on standard microbiological media. Semi-selective
media such as PARP or PARPH can be useful for some
Symptoms and diagnostic features samples or to clean up isolates. However, the
The external surfaces and internal tissues of infected hymexazol in PARPH may inhibit the growth of some
roots are pale brown to black in color, rotted, and Phytophthora species. The pathogen produces spor-
usually have a strong, unpleasant smell. Leaves, espe- angia that are non-papillate and measure 35–50 x
cially older ones, turn purple-red or yellow, and wilt. 25–35 μm. Examination of rotted root tissues will often
205 207
205 Necrotic cauliflower stem with Phytophthora 207 Collapsed cabbage with Phytophthora root rot.
root rot.
206 208 F UNGAL D ISEASES
206 Cabbage field with Phytophthora root rot. 208 Collapsed cauliflower with Phytophthora root rot.
reveal the sexual oospores of this organism, which are Pyrenopeziza brassicae
circular and thick walled. Floating pieces of sympto- (anamorph = Cylindrosporium concentricum)
matic roots in water may readily induce sporangia to LIGHT LEAF SPOT
form. Other species, such as P. drechsleri and P.
cactorum, also cause root rot diseases on crucifers. Introduction and significance
Light leaf spot occurs widely in northern Europe, the
Disease cycle UK, Poland, and also in New Zealand and other areas
The pathogen survives in and relies on wet soil condi- with a cool, moist climate. This is the most important
tions. Plants become infected when soils are overly wet, disease of winter oilseed rape in northern England and
over irrigated, or drain poorly. Hence, root rot is most Scotland, and oilseed rape can be an important source
often found at low spots in the field or at the end of irri- of inoculum for vegetable brassicas. The main damage
gation runs. Phytophthora megasperma is a soil inhab- results from disease on leaves and petioles.
itant and is able to affect a wide range of crop and weed
species. This pathogen is therefore able to survive in the Symptoms and diagnostic features
absence of susceptible brassica crops. In the soil, This disease can be difficult to identify because
oospores germinate to produce sporangia, or sporangia symptoms vary and are influenced by weather condi-
are already present on organic matter or in the soil. tions and host susceptibility. On very susceptible
Sporangia release zoospores that swim to roots and cultivars, leaves exhibit large white blotches that
infect the host. Disease development is favored by soil contain small green flecks. The pathogen grows under
temperatures in the range between 15-25° C. the leaf cuticle and disrupts the waxy surface as it sporu-
lates, resulting in lifting of the leaf cuticle and appear-
Control ance of bleached areas; this feature gives the disease the
Prepare soils so that they are levelled, drain well, and name light leaf spot. Blotches are usually surrounded by
are not compacted. Manage irrigation so that crops are numerous dark fruiting bodies and associated white
not over watered. Avoid fields with a history of drops of spores that form in concentric rings (209, 210).
Phytophthora problems. Rotate crops so that crucifers In some cases the spore droplets do not appear until
are not planted back-to-back; however, crop rotations leaves are incubated under moist conditions for 1 or 2
have limited effectiveness because P. megasperma is days at 10–15º C. Sporulation can also occur on appar-
a soil inhabitant. Some cultivars of cauliflower may ently healthy, green leaf tissue. Lesions can occur on
be tolerant to the disease. Fungicides are not usually
effective.
References 209
Geeson, J. D., Browne, K. M., and McKeown, B. 1990. Storage
rot of swede caused by Phytophthora sp. Plant Pathology
39:629–631.
Hamm, P. B. and Koepsell, P. A. 1984. Phytophthora root rot of
cabbage and cauliflower in Oregon. Plant Disease
68:533–585.
Hansen, E .M., Brasier, C. M., Shaw, D. S., and Hamm, P. B.
1986. The taxonomic structure of Phytophthora
megasperma: evidence for emerging biological species groups.
Kontaxis, D. G. and Rubatsky, V. E. 1983. Managing
F UNGAL D ISEASES
Phytophthora root rot in cauliflower. California Agriculture

37:12.
Thompson, A. H. and Phillips, A. J .L. 1988. Root rot of cabbage
caused by Phytophthora drechsleri. Plant Pathology
37:297–299.
209 Severe light leaf spot on cauliflower with abundant

white sporulation around lesions.
B RASSICACEAE 187
both upper and lower leaf surfaces, which causes the 211
opposite leaf side to become yellow or red. Early
infection of immature leaves or the growing point
causes considerable leaf distortion and stunting. Leaf
infection may also result in localized bubbling of the
lamina, which is caused by the abnormal production of
plant hormones.
On Brussels sprout, small groups of black spots
occur in a ‘thumb print’ pattern, measuring 1–2 cm in
diameter, on the leaf undersides and on the sprouts
(211). This black spotting may appear similar to
spotting caused by other pathogens such as Alternaria
species, Mycosphaerella brassicicola, and Peronospora 211 Light leaf spot on Brussels sprout buds.
parastica. Severe light leaf spot infection of sprouts can
cause early senescence and rotting of the outer leaves.
Other symptoms include circular, red spots that 212
measure 0.5–1.5 cm in diameter and occur singly on
older leaves that are starting to turn yellow (212). These
spots may not produce conidia after incubation.
Senescing leaves may also have small ‘green islands’
which are associated with groups of black spots. On
cauliflower, light leaf spot may cause pink-brown or
black discoloration of petioles (213). When this occurs
at the base of leaves attached to the cauliflower head, it
adversely affects the appearance of the head. Similar
symptoms are prevalent on the stems and pods of
flowering brassica crops. Diseased pods can lead to
seedborne infection, though the importance of this has 212 Close-up of light leaf spot watermark symptom on
not been established. senescent Brussels sprout leaf.
210 213
F UNGAL D ISEASES
210 Light leaf spot lesion on cabbage head. 213 Blackening of cauliflower petioles infected with
light leaf spot.

The cause of light leaf spot is the ascomycete fungus Avoid planting susceptible vegetable brassicas in close
Pyrenopeziza brassicae. On affected hosts, the asexual proximity to oilseed rape. Note, however, that airborne
stage Cylindrosporium concentricum is more usually ascospores can travel long distances in wind and still
encountered. This form of the pathogen makes a make contact with vegetable crops. Destroy infected
cushion-shaped mass of conidiophores called an crop residues after harvest to reduce airborne
acervulus. Acervuli break through the leaf epidermis ascospores. Cultivars vary in their susceptibility to light
and release white spore droplets. Conidia are hyaline, leaf spot, so choose and plant more tolerant selections.
smooth, cylindrical, one-celled, and measure 10–16 x Apply protectant fungicides if such are available.
3–4 μm. The fungus has two mating types that must Disease forecasting systems have been developed for
both be present for the P. brassicae sexual stage to be winter oilseed rape in the UK, and these and other
formed. This stage produces small black fruiting struc- programs may assist vegetable growers in timing
tures called apothecia that are cup-shaped, sessile fungicide applications.
(without stalks), and measure 1–2 mm in diameter.
Apothecia usually develop on the infected petioles of References
senescing or dead leaves and other plant residues. Bradburne, R., Majer, D., Magrath, R., Werner, C. P., Lewis, B.,
Airborne ascospores are released for a relatively short and Mithen, R. 1999. Winter oilseed rape with high levels of
resistance to Pyrenopeziza brassicae derived from wild
period, perhaps for only a few weeks. Ascospores are Brassica species. Plant Pathology 48:550–558.
hyaline, cylindrical, measure 8–14 x 2.5–3.5 μm, and Cheah, L-H. and Hartill, W. F. T. 1985. Disease cycle in New
are zero to one septate. Zealand of light leaf spot of brassicas, induced by
Pyrenopeziza brassicae. New Zealand Journal of Agricultural
Research 28:567–573.
Disease cycle Gilles, T., Fitt, B. D. L., and Jeger, M. J. 2000. Epidemiology in
Ascospores become airborne and can either initiate new relation to methods for forecasting light leaf spot
infections within the same crop or be dispersed to (Pyrenopeziza brassicae) severity on winter oilseed rape
(Brassica napus) in the UK. European Journal of Plant
nearby crops. The formation of apothecia is tempera- Pathology 106:593–605.
ture sensitive and is inhibited above 20º C. Ascospores Gilles, T., Fitt, B. D. L., Welham ,S .J., Evans, N., Steed, J.M., and
and conidia have similar infection requirements, as Jeger, M. J. 2001. Modelling the effects of temperature and
wetness duration on development of light leaf spot on oilseed
studied on oilseed rape. On oilseed rape, 6 hours of leaf rape leaves inoculated with Pyrenopeziza brassicae conidia.
wetness are required for infection at 12–20º C. Much Plant Pathology 50:42–52.
longer periods of leaf wetness are required for infection Gilles, T., Fitt, B. D. L., Kennedy, R., Welham, S. J., and Jeger, M.
at lower temperatures. Following infection, symptoms J. 2000. Effects of temperature and wetness duration on
conidia infection, latent period and asexual sporulation of
appear after 14 days at 15º C and 28 days at 5º C. Pyrenopeziza brassicae on leaves of oilseed rape. Plant
Disease severity is higher with longer periods of leaf Pathology 49:498–508.
wetness and cool temperatures. Optimum temperature Karolewskia, Z., Evans, N., Fitta, B. D. L., Baierl, A., Todd, A.
D., and Foster, S. J. 2004. Comparative epidemiology of
for disease development is 15–16º C, but there is limited Pyrenopeziza brassicae (light leaf spot) ascospores and
activity above 20º C. Once foliar symptoms develop, conidia from Polish and UK populations. Plant Pathology
secondary inocula (conidia) appear and are dispersed to 53:29–37.
Mattock, S. E., Ingram, D. S., and Gilligan, C. A. 1981.
other leaves and plants by splashing water.
Resistance of cultivated brassicas to Pyrenopeziza brassicae.
McCartney, H. A. and Lacey, M. 1990. The production and
release of ascospores of Pyrenopeziza brassicae in oilseed rape
crops. Plant Pathology 39:17–32.
Rawlinson, C. J., Sutton, B. C., and Muthyalu, G. 1978.
F UNGAL D ISEASES
Taxonomy and biology of Pyrenopeziza brassicae sp. nov.

(Cylindrosporium concentricum), a pathogen of winter
oilseed rape (Brassica napus ssp. oleifera). Transactions of the
British Mycological Society 71:425–439.
B RASSICACEAE 189
Sclerotinia minor, S. sclerotiorum Symptoms and diagnostic features

WHITE MOLD, Two species of Sclerotinia cause disease on brassicas.
SCLEROTINIA STEM ROT, Sclerotinia minor (214) only infects stems or leaves in
WATERY SOFT ROT contact with the soil. Once infected, tissues become
water-soaked, brown, and soft. Plants wilt and collapse
Introduction and significance when the stem is girdled by the lesion. White mycelium
Sclerotinia diseases are usually of minor importance in and numerous small (up to 3–5 mm), black sclerotia
brassica crops. The pathogens have wide host ranges form on the outside and sometimes on the inside of
and will cause problems if inoculum pressure is high or stems.
conditions favor their development. There can be sig- Sclerotinia sclerotiorum can also infect lower leaves
nificant losses in seed crops because flower petals are and stems, resulting in symptoms similar to those
very susceptible and facilitate stem infections. caused by S. minor. In addition, S. sclerotiorum
produces ascospores that infect the upper parts of
plants, resulting in a pale brown, watery, soft rot of
these tissues (215, 216, 217). In the field, the apothecia
that produce ascospores are often difficult to find.
214 216
214 Broccoli seedling infected with Sclerotinia minor. 216 Diseased cauliflower infected with Sclerotinia
sclerotiorum.
215 217
F UNGAL D ISEASES
215 Cauliflower seedlings, in a transplant tray, infected 217 Diseased cabbage infected with Sclerotinia
by Sclerotinia sclerotiorum sclerotiorum.
218
Control
Management steps for controlling white mold in
vegetable brassicas is not usually required. For an inte-
grated approach to Sclerotinia control, see the bean
white mold section in the chapter on legume diseases.
References
Dillard, H. R. and Cobb, A. C. 1995. Relationship between leaf
injury and colonization of cabbage by Sclerotinia
sclerotiorum. Crop Protection 14:677–682.
Dillard, H. R. and Hunter, J. E. 1986. Association of common
ragweed with Sclerotinia rot of cabbage in New York State.
Plant Disease 70: 26–28.
Disease 87:159–166.
Hims, M. J. 1979. Wild plants as a source of Sclerotinia
sclerotiorum infecting oilseed rape. Plant Pathology 28:
197–198.
Hudyncia, J., Shew, H. D., Cody, B. R., and Cubeta, M. A. 2000.
Evaluation of wounds as a factor to infection of cabbage by
ascospores of Sclerotinia sclerotiorum. Plant Disease
84: 316–320.
Koike, S. T., Gonzales, T. G., Vidauri, M., and Subbarao, K. V.
1994. First report of Sclerotinia minor as a pathogen of
cauliflower in California. Plant Disease 78:1216.
Turkington, T. K. and Morrall, R. A. A. 1993. Use of petal
infestation to forecast Sclerotinia stem rot of canola: the
influence of inoculum variation over the flowering period and
canopy density. Phytopathology 83: 682–689.
218 Broccoli seed plant infected with Sclerotinia

sclerotiorum and showing sclerotia inside seed stalks.
Along with the characteristic white mycelium, S. scle-

rotiorum forms sclerotia (218) that are significantly
larger (5–10 mm long) than those of S. minor.
Causal agents and disease cycle

White mold is caused by two pathogens, Sclerotinia
sclerotiorum and S. minor. These pathogens are
ascomycete fungi and can be isolated on standard
microbiological media. The two species are differenti-
ated on the basis of sclerotia size, with S. minor
F UNGAL D ISEASES
producing smaller, more numerous sclerotia than S.

sclerotiorum. Also, only S. sclerotiorum normally
produces the sexual apothecia fruiting body and
ascospores. For detailed descriptions of these pathogens
and the disease cycle, see the bean white mold section in
the chapter on legume diseases.
B RASSICACEAE 191
Thanatephorus cucumeris seedlings consist of browning and cracking of the

(anamorph = Rhizoctonia solani) epidermis, lesion formation, and outer stem tissue
RHIZOCTONIA DISEASES: decay. When the outer stem deteriorates, only the
DAMPING-OFF, WIRESTEM, fibrous inner xylem is intact and remains as a wiry
BOTTOM/ROOT ROT tissue, hence the name wirestem (220). Affected plants
wilt, turn purple (or blue in the case of cabbage), and
Introduction and significance remain stunted. Seedlings may break off at the soil line.
On Brassicas, there are several Rhizoctonia diseases: Transplanted crucifers are subject only to this wirestem
damping-off, wirestem, bottom rot, root rot, and foliar phase of seedling diseases. The pathogen can be identi-
blight. Rhizoctonia can be very damaging to seedlings fied in the field by its coarse mycelium that sometimes
just after planting, while black spot on swede can result causes soil particles to adhere to and dangle from
in rejection of crops for market. In fields heavily diseased stems (221). Cauliflower is more susceptible
cropped to susceptible plants, Rhizoctonia can cause than cabbage or Brussels sprout .
significant stand reduction due to seedling (damping-
off, wirestem) diseases. This pathogen is an important
cause of root rot on radish. 220

Damping-off and wirestem occur on newly emerged or
young seedlings (219). For direct seeded crops, the
fungus can attack seed or newly emerged seedlings and
kill them prior to emergence (pre-emergence damping-
off), or can attack roots and lower stem tissue
(hypocotyl) shortly after the plant has emerged above
ground (post-emergence damping-off). For recently
emerged plants, the stem in contact with soil develops a
dark, water-soaked to brown discoloration; these stems
are often girdled and the plants fall over. Seedlings
become progressively less susceptible as they get older
and later infection is confined to the outer tissues of the 220 Close-up of wirestem caused by Rhizoctonia solani
hypocotyl and roots. Hypocotyl infections of older on cauliflower. Healthy plant is on the right.
219 221
F UNGAL D ISEASES
219 Wirestem caused by Rhizoctonia solani on cauli- 221 Wirestem caused by Rhizoctonia solani on cauli-
flower in the field. flower. Mycelial strands dangle with soil particles.
222 223
222 Bottom rot caused by Rhizoctonia solani on 223 Rhizoctonia causing yellowing of foliage on radish
Chinese cabbage. plants.
Bottom rot is a problem on cabbage, Chinese Causal agent

cabbage, and other head-forming brassicas (222). Rhizoctonia diseases are caused by R. solani. The
Once head formation begins, the petioles of lower pathogen is isolated on standard microbiological
leaves in contact with the soil become infected and media, and low nutrient media (water agar or acidified
develop dark brown, oval lesions. Secondary decay corn meal agar) are often useful because the character-
organisms may follow and make these lesions soft and istic hyphal structures are more readily seen. Look for
watery. Rhizoctonia solani often produces a web of brown hyphae that are up to 12 μm in diameter, have
mycelial growth and sclerotia over the surface of the dolipore septa, approximately right angle branching,
lesions. On root brassicas, root rot is a common and a crosswall in the adjacent branch. Loose aggrega-
problem, especially in the UK. Small (0.5–1.0 cm), tions of hyphae form sclerotia in some isolates. This
sunken, black or brown lesions develop on roots and fungus does not produce asexual spores. If environ-
result in disfigured taproots. Sometimes roots show mental conditions are suitable, the perfect stage
large brown lesions with concentric rings of fungal (Thanatephorus cucumeris) of this basidiomycete
growth. pathogen may be observed as a white, thin, flat
Rhizoctonia root rot reduces radish stands because hymenial layer present on plant surfaces near the soil.
seed or germinated seedlings are killed before emerging This layer bears basidia and hyaline basidiospores that
from the soil (pre-emergence damping-off) or seedlings measure 6–14 x 4–8 μm. Specific molecular tests or
die shortly after emerging above ground (post- reactions with reference isolates are required to identify
emergence damping-off) (223). Plants that are attacked the anastomosis groups (AG); because only compatible
at later stages show grey or black streaking and lesions isolates fuse or mate with each other, mating studies
on the root surface (224). This external scarring reveal distinct AGs within R. solani. Rhizoctonia solani
contrasts with black root rot caused by Aphanomyces is not host specific to crucifers and will infect a wide
raphani in which there is blackening of internal tissues. range of other crops.
Radishes have an uneven appearance when only one
F UNGAL D ISEASES
side of the root is affected. Disease cycle

Bok choy plants in Asia and cabbage in the USA have Rhizoctonia solani survives saprophytically in soil as
suffered from a foliar blight caused by R. solani. mycelium or sclerotia; these fungal structures are the
Circular to irregularly shaped spots measuring 1–3 mm inocula for infecting seedlings and older plants.
in diameter occur on leaves. Spots become necrotic and Airborne basidiospores are produced by the Thanate-
sometimes have irregular borders. phorus stage, but their importance in disease develop-
B RASSICACEAE 193
224 References
Abawi, G. S. and Martin, S. B. 1985. Rhizoctonia foliar blight of
cabbage in New York State. Plant Disease 69:158–161.
Chet, I. and Baker, R. 1980. Induction of suppressiveness to
Rhizoctonia solani in soil. Phytopathology 70:994–998.
Henis, Y., Ghaffar, A., and Baker, R.1978. Integrated control of
Rhizoctonia solani damping-off of radish: Effect of successive
plantings, PCNB, and Trichoderma harzianum on pathogen
and disease. Phytopathology 68:900–907.
Humayden, H. S., Williams, P. H., Jacobsen, B. J., and
Bissonnette, H. L. 1974. Resistance in radish to
Aphanomyces raphani and Rhizoctonia solani. Plant Disease
Kataria, H. R., Verma, P. R., and Rakow, G. 1993. Fungicidal
control of damping-off and seedling root-rot in Brassica sp.
caused by Rhizoctonia solani in the growth chamber. Annals
224 Root lesions of Rhizoctonia solani on radish root. of Applied Biology 123:247–256.
Keijer, J., Korsman, M. G., Dullemans, A. M., Houterman, P. M.,
de Bree, J., and van Silfhout, C.H. 1997. In vitro analysis of
host plant specificity in Rhizoctonia solani. Plant Pathology
46:659–669.
Keinath, A. P. 1995. Relationships between inoculum density of
Rhizoctonia solani, wirestem incidence and severity, and
ment is not determined. Rhizoctonia is favored by growth of cabbage. Phytopathology 85:1487–1492.
warm soil conditions (25–30º C), but is capable of Keinath, A. P. and Farnham, M. W. 1997. Differential cultivars
causing problems at much lower temperatures when and criteria for evaluating resistance to Rhizoctonia solani in
seedling Brassica oleracea. Plant Disease 81:946–952.
seedling growth is slow. On brassicas, AG2-1 appears
Keinath, A. P. and Farnham, M. W. 2001. Effect of wirestem
to be most important on young plants and at lower tem- severity on survival and head production of transplanted
peratures, while AG4 is associated with mature plant broccoli and cabbage. Plant Disease 85:639–643.
infection and warmer conditions. Both these AGs are Keinath, A. P., Harrison, H. F., Marino, P. C., Jackson, D. M.,
and Pullaro, T. C. 2003. Increase in populations of
also reported on radish. Fungal growth occurs at Rhizoctonia solani and wirestem of collard with velvet bean
osmotic water potentials as low as -4 MPa (= -40 bars), cover crop mulch. Plant Disease 87:719–725.
but the optimum is -500 kPa (= -5 bars). Populations of Roy, S. K., Das, B. C., and Bora, L. C. 1998. Non-pesticidal
R. solani in soil fluctuate in response to host substrates management of damping-off of cabbage caused by
Rhizoctonia solani. Journal of the Agricultural Science
and activity of the soil microflora. Society of North East India 11:127–130.
Thornton, C. R., O’Neill, T. M., Hilton, G., and Gilligan, C. A.
Control 1999. Detection and recovery of Rhizoctonia solani in
naturally infested glasshouse soils using a combined baiting,
Practice thorough sanitation at transplant nurseries to double monoclonal antibody ELISA. Plant Pathology
prevent contamination by R. solani. Clean and sanitize 48:627–634.
transplant trays and benches. Ensure that rooting media Yang, G. H., Chen, X. Q., Chen, H. R., Naito, S., Ogoshi, A., and
Zhao, J. F. 2004. First report of foliar blight in Brassica rapa
are not contaminated by infested soil or diseased plant
ssp. chinensis caused by Rhizoctonia solani AG-4. Plant
residues. Successful sanitation steps at the transplant Pathology 53:260.
nursery eliminate the need to apply fungicides to the
transplants during their production. When direct
seeding in the field, use seed that has been treated with
a fungicide. When placing transplants in the field, avoid
planting them too deeply in the soil as the hypocotyl
F UNGAL D ISEASES
stem tissue is the most susceptible part of the plant.

Practice crop rotation so that non-hosts are included in
the rotation. Do not plant susceptible crucifers in fields
having undecomposed crop residues. Fungicide treat-
ments in the field have had limited effectiveness.
Verticillium dahliae,V. longisporum Symptoms and diagnostic features

VERTICILLIUM WILT Symptoms can appear 3 to 4 weeks after transplanting
for cauliflower in California. The older, lower leaves
Introduction and significance turn yellow and wilt (225), with one side of the leaf
Verticillium wilt is an important problem in various more severely affected than the other. These leaves later
crucifer vegetables in California. In France, Germany, turn brown and drop off the stem, often when plants
and Sweden, Verticillium wilt is a significant problem approach maturity and form flower buds. The xylem of
on oilseed rape, which could pose a threat to vegetable stems and roots becomes black and microsclerotia can
brassicas. In the UK, the last report of Verticillium wilt be detected in vascular tissues (226, 227). Overall
in brassicas was on Brussels sprout in 1961. Verticillium growth of the plant is stunted (228). Verticillium wilt
wilt is a problem on horseradish. can be a significant problem for cabbage, cauliflower,
Brussels sprouts, Chinese cabbage, and bok choy.
Horseradish has also been reported as a host. It is inter-
225
esting that broccoli, a close relative of cauliflower, is not
susceptible to this pathogen. In California, the disease
is most prevalent in summer and autumn crops
Causal agents
Verticillium wilt is caused by imperfect fungus
Verticillium. The pathogen can be isolated on standard
microbiological media. Semi-selective media such as
NP-10 can be useful for some samples or to purify
isolates. On general media, the pathogen forms the
expected verticillate conidiophores, hyaline single-celled
conidia, and black microsclerotia. However, the species
involved in causing Verticillium wilt of brassica is not
225 Collapsed and dying foliage of cauliflower infected clear. Verticillium dahliae is a key pathogen of
with Verticillium wilt. worldwide importance on many crops, and has been
listed as the cause of Verticillium wilt of crucifers.
226 However, in 1997 a second species, V. longisporum,
was proposed as the distinct pathogen that causes
Verticillium wilt of crucifers. Verticillium longisporum
has been distinguished from V. dahliae by its elongated
rather than spherical microsclerotia, longer spores
(7.1–8.8 μm compared with 3.5–5.5 μm for
V. dahliae) and fewer phialides per node on conidio-
phores (3 v. 4 to 5). There is uncertainty about the
validity of the name V. longisporum because not all
Verticillium isolates from crucifers have these features,
V. dahliae isolates from other crops can infect brassicas,
and molecular data indicates the existence of at least
three distinct types of Verticillium isolates from crucifer.
F UNGAL D ISEASES
Therefore this new species name has yet to be generally

accepted. The pathogen may be seedborne.
226 Discolored vascular tissue of Chinese cabbage

infected with Verticillium wilt.
B RASSICACEAE 195
227 228
227 Discolored vascular ring of cauliflower infected 228 Stunted Brussels sprouts infected with
with Verticillium wilt. Verticillium wilt.

The pathogen is a true soilborne organism and forms Barbara, D. J. and Clewes, E. 2003. Plant pathogenic Verticillium
microsclerotia that enable it to survive in soil for a species: how many of them are there? Molecular Plant
decade or longer. Plants can be infected within a few
Bhat, R. G. and Subbarao, K. V. 2001. Reaction of broccoli to
weeks after planting. Microsclerotia germinate, enter isolates of Verticillium dahliae from various hosts. Plant
plants via roots, and grow systemically within the host. Disease 85:141–146.
Disease symptoms often are expressed when plants Collins, A., Okoli, C. A. N., Morton, A., Parry, D., Edwards, S.
G., and Barbara, D. J. 2003. Isolates of Verticillium dahliae
mature and form reproductive structures such as flower pathogenic to crucifers are of at least three distinct molecular
buds. Soil populations of only one microsclerotia per types. Phytopathology 93:364–376.
gram of soil can result in 5% infection. This pathogen Karapapa, V. K., Bainbridge, B. W., and Heale, J. B. 1997.
Morphological and molecular characterization of
is becoming more widespread in Europe and may be Verticillium longisporum comb. nov. pathogenic to oilseed
introduced or distributed via contaminated soil moved rape. Mycological Research 101:1281–1294.
by machinery, footwear, plant material (such as potato Koike, S .T., Subbarao, K. V., Davis, R. M., Gordon, T. R., and
tubers), or by wind-blown soil particles. Hubbard, J. C. 1994. Verticillium wilt of cauliflower in
Sorensen, L. H., Schneider, A. T., and Davis, J. R. 1991. Influence
Control of sodium polygalacturonate sources and improved recovery
Maintain records so that infested fields are not used for of Verticillium species from soil. (Abstract). Phytopathology
81:1347.
susceptible crucifers. Avoid moving infested soil and
Subbarao, K. V., Chassot, A., Gordon, T. R., Hubbard, J. C.,
equipment to clean fields. Plant non-susceptible Bonello, P., Mullin, R., Okamoto, D., Davis, R. M. and
crucifers such as broccoli. Resistant cultivars are not Koike, S. T. 1995. Genetic relationships and cross
available, though for cauliflower there are vigorous pathogenicities of Verticillium dahliae isolates from
cauliflower and other crops. Phytopathology 85:1105–1112.
hybrids that show some tolerance to the disease. If it is Subbarao, K. V., Hubbard, J. C., and Koike, S. T. 1999.
necessary to use infested fields, schedule plantings of Evaluation of broccoli residue incorporation into field soil for
susceptible crops like cauliflower for winter periods; Verticillium wilt control in cauliflower. Plant Disease
83:124–129.
cold soil temperatures inhibit the activity of the
Xiao, C. L. and Subbarao, K. V. 1998. Relationships between
F UNGAL D ISEASES
pathogen and can suppress development of disease. Verticillium dahliae inoculum density and wilt incidence,
Interestingly, researchers find that incorporating the severity, and growth on cauliflower. Phytopathology
88:1108–1115.
biomass from brassica cover crops or crops such as
Xiao, C ., Subbarao, K. V., Schulbach, K. F., and Koike, S. T.
broccoli can also reduce soil inoculum of V. dahliae and 1998. Effects of crop rotation and irrigation on Verticillium
subsequent disease on cauliflower. dahliae microsclerotia in soil and wilt on cauliflower.

229

Beet western yellows virus (BWYV) is widespread in
winter oilseed rape in Europe. Yield reductions of
10–30% have been reported in oilseed rape and growth
may be reduced in vegetable brassicas. In other areas
such as coastal California, BWYV is rarely found in
brassicas but is occasionally detected in lettuce, spinach,
and endive.

Symptoms include reddening of the foliage, though this
is very similar to nutrient or stress factors and therefore
is not diagnostic. Infected plants of B. napus and other 229 Yellowing of cauliflower foliage caused by Beet
vegetable brassicas can remain symptomless. Occasion- western yellows virus.
ally, distinctive red or yellow coloration may develop in
cauliflower (229). In the UK, tipburn symptoms in
stored white cabbage have been attributed to BWYV, References
though not all infected heads developed symptoms. Hardwick, N .V., Davies, J. M.L., and Wright, D. M. 1994. The
incidence of three virus diseases of winter oilseed rape in
England and Wales in the 1991/92 and 1992/3 growing
Causal agent and disease cycle season. Plant Pathology 43:1045–1049.
BWYV is a polerovirus and infects many hosts, Hunter, P. J., Jones, J. E., and Walsh, J. A. 2002. Involvement of
including crucifers, beet, lettuce, and other crop and beet western yellows virus, cauliflower mosaic virus, and
turnip mosaic virus in internal disorders of stored white
weed plants. BWYV has isometric particles with cabbage. Phytopathology 92:816–826.
diameters of 25 nm and single-stranded, linear RNA Pallett, D. W., Thurston, M. I., Cortina-Borja, M., Edwards,
genomes. Some isolates or strains of this virus have M-L., Alexander, M., Mitchell, E., Raybould, A. F., and
different abilities to infect certain plants; thus, not all Cooper, J. I. 2002. The incidence of viruses in wild Brassica
rapa ssp. sylvestris in southern England. Annals of Applied
strains of BWYV may be able to infect all known hosts, Biology 141:163–170.
greatly complicating the etiology of this disease for Smith, H. G. and Hinckes, J. A. 1985. Studies on beet western
crucifers. BWYV is transmitted by aphids in a persist- yellows virus in oilseed rape (Brassica napus ssp. oleifera) and
sugar beet (Beta vulgaris). Annals of Applied Biology
ent manner (for up to 50 days). Myzus persicae is likely 107:473–484.
to be the main vector on brassicas.
Control
(see Part 1).
V IRAL D ISEASES
B RASSICACEAE 197
Cauliflower mosaic virus

230
CAULIFLOWER MOSAIC

Cauliflower mosaic virus (CaMV) is common in
temperate regions worldwide. It is often found causing
only mild symptoms in crucifers, but yield losses of
20–50% can occasionally occur.

Symptoms consist of leaf mosaics or mottles that are
similar to those caused by other viruses. Infection of
young plants can result in some stunting and leaf vein
clearing, often near the base of the leaf. Leaf enations
are sometimes produced. On mature cauliflower there
can be vein banding with dark green areas near the 230 Mild symptoms on Brussels sprouts caused by
veins and chlorotic patches in the interveinal leaf tissue. Cauliflower mosaic virus.
The mosaic of light and dark green regions continues to
develop and waxy bloom is lost in interveinal areas. On
cabbage, the virus causes a diffuse mottle with distinct References
vein clearing at high temperatures (28º C) or chlorotic Hunter, P. J., Jones, J. E., and Walsh, J. A. 2002. Involvement of
vein banding at lower temperatures (20º C). Brussels beet western yellows virus, cauliflower mosaic virus, and
turnip mosaic virus in internal disorders of stored white
sprouts show fairly mild symptoms and plants can be cabbage. Phytopathology 92:816–826.
distinguished by their paler green color (230). In Shepherd, R. J., Wakeman, R. J., and Romanko, R. R. 1968.
Chinese cabbage, vein clearing occurs over the whole DNA in cauliflower mosaic virus. Virology 36:150–152.
leaf, which can senesce prematurely. Inner leaves show
obvious light and dark green mottling between the
veins. CaMV is not implicated directly in storage
disorders of cabbage, but it can exacerbate problems
caused by other viruses. In seed crops, the flowering
shoots of infected plants may be stunted, twisted, and
develop black spotting on stems and pods.

CaMV is the type member of the caulimovirus group
and has isometric particles that measure 50 nm, and
double stranded DNA. CaMV is transmitted in a semi-
persistent manner by many aphid species, particularly
Brevicoryne brassicae and Myzus persicae, which both
breed on crucifers. Aphids can acquire the virus in
only1–2 minutes and transmit it immediately.
Control
V IRAL D ISEASES

(see Part 1).
Turnip mosaic virus

231
TURNIP MOSAIC

Turnip mosaic virus (TuMV) is the most severe of the
common viruses of crucifers and occurs worldwide. It
affects most cultivated brassicas, horseradish, and
watercress. Other vegetables, such as lettuce, and orna-
mentals are hosts. Rhubarb is also affected in Europe.

TuMV causes chlorotic or necrotic spots and rings, or a
general mosaic. Some cultivars develop systemic
necrosis and mosaics. Early infection causes severe 231 Bok choy infected with Turnip mosaic virus.
crinkling and stunting of leaves (231) and, in some Healthy plant is on the right.
cases, necrosis and death of plants. On cabbage, some
sectors of the leaves may be more severely affected by 232
black spotting than others (232). In stored cabbage,
inner leaves of heads affected by TuMV may develop
large (5-10 mm) black lesions (sometimes referred to as
cigar burn) that can result in crop rejection.

TuMV is a member of the potyvirus group and has fila-
mentous particles measuring 750 x 12 nm. There are
several strains of the virus and these differ in host range
and symptomatology. TuMV is transmitted by many
aphid species in a nonpersistent manner. Brevicoryne
brassicae and Myzus persicae are important vectors.
232 Necrotic spotting on cabbage caused by Turnip
Control mosaic virus.
(see Part 1). Watercress should be raised annually from
seed. Dig out and remove old, possibly infected rhubarb
plants, and replant with new, virus-free stocks.
References
Edwardson, J. R. and Purcifull, D. E. 1970. Turnip mosaic virus-
induced inclusions. Phytopathology 60: 85–88.
Hughes, S. L., Green, S. K., Lydiate, D. J., and Walsh, J. A. 2002.
Resistance to Turnip mosaic virus in Brassica rapa and
B. napus and the analysis of genetic inheritance in selected
lines. Plant Pathology 51: 567–573.
Jenner, C. E. and Walsh, J. A. 1996. Pathotype variation in turnip
V IRAL D ISEASES
mosaic virus with special reference to European isolates. Plant

Pathology 45: 848–856.
199
Capsicum Pepper
PEPPER (Capsicum annuum, C. frutescens, and other species) is an important Solanaceae

(nightshade family) crop that is grown for its flavorful, pungent fruit. This group of plants most
likely originated in the tropical and subtropical regions of the Americas. Pepper fruit are used in
different ways as fresh fruit that are raw or cooked, dehydrated whole fruit, or ground into
spices and used in diverse processed products. Peppers are used in medicines, cosmetics, and
grown as ornamental plants. Peppers are categorized by their degree of sweetness or hotness.
Differing levels of capsaicin, a phenolic amide, give pepper its hotness.
Xanthomonas campestris pv. vesicatoria 233 Leaf spots of

233
BACTERIAL SPOT bacterial spot on
pepper trans-
Introduction and significance plants.
Bacterial spot occurs throughout the world but is most
serious in tropical and subtropical pepper–growing
areas where it is favored by high humidity and rainfall.

Initial foliar symptoms consist of irregularly shaped,
water-soaked spots on leaves (233). These spots later
turn dark brown to black-brown and usually remain 234 Leaf spots of
234
smaller than 5 mm in diameter (234). As disease pro- bacterial spot of
gresses, the spots may coalesce and result in leaves pepper.
having large necrotic areas. Severely diseased foliage,
especially lower leaves, can defoliate from the plant.
While infected leaves may show some chlorosis, the
individual spots usually are not surrounded by yellow
halos. Dark streaks and patches may develop on
petioles and stems. Infections on fruit appear as irregu-
larly shaped, brown, raised rough scabs that measure 2
to 5 mm in diameter (235). Fruit spots are often
clustered near the stem end of the fruit where water and 235 Fruit lesions
235
water-splashed inoculum collect. of bacterial spot of
pepper.
Causal agent
Bacterial spot is caused by the aerobic, Gram-negative

bacterium Xanthomonas campestris pv. vesicatoria.
logical media and produces yellow, mucoid, slow
growing colonies typical of most xanthomonads.
However, X. campestris pv. vesicatoria only weakly
hydrolyzes starch, so starch-based semi-selective media
such as SX or MXP media are not diagnostic for identi- and certification programs help regulate the availabil-
fying this pathogen. Tween medium is helpful because ity and cleanliness of such seed. Seed tests usually
this bacterium forms characteristic white calcium salt involve the washing of a 10,000 seed sample and sub-
crystals when growing on it. sequent plating of the liquid onto semi-selective
Xanthomonad pathogens from pepper and tomato medium. Discard heavily infested seed.
hosts are a complex group of organisms. At least eight Inspect transplants and remove suspect plants and
pepper strains of this pathogen are host specific to surrounding transplant trays. Sanitize benches that hold
pepper and are designated as P1, P2, P3, etc. Other transplants, transplant trays, and equipment that comes
strains are host specific to tomato. Finally, other strains in contact with plants. Consider applying preventative
are pathogenic on both of these hosts; these pepper- copper sprays for protecting transplants. Avoid using
tomato strains are designated as PT strains. Researchers overhead sprinkler irrigation in the field. With an
further find that xanthomonad pathogens from pepper appropriate disinfectant, periodically and regularly
and tomato can be divided into various groups (A, B, C, sanitize tools such as clippers and pruning shears. Do
and D) based on genetic and biochemical parameters. not allow equipment or workers to pass through fields
The assignment of these groups to various species and when foliage is wet. In the field, copper and copper-
pathovars is still being debated. maneb sprays may be helpful depending on weather
This pathogen is seedborne. Another bacterial conditions and disease pressure. Once the pepper crop
disease is caused by Pseudomonas syringae pv. syringae is finished, incorporate the residues to enhance plant
and causes symptoms that closely resemble those of decomposition and the dissipation of bacteria. Rotate
bacterial spot. to a non-host crop before returning to pepper and do
not allow volunteer peppers or weed hosts to survive.
Disease cycle
Primary inoculum can come from infested seed, plant References
debris in soil, or reservoir plant hosts. Infested seed is a Abbasi, P. A., Soltani, N., Cuppels, D. A., and Lazarovits, G.
particularly important inoculum source because if such 2002. Reduction of bacterial spot disease severity on tomato
and pepper plants with foliar applications of ammonium
seed are used to produce transplants, these plant lignosulfonate and potassium phosphate. Plant Disease
materials are often grown under conditions that can 86:1232–1236.
encourage disease development and spread. The Bashan, Y., Diab, S., and Okon, Y. 1982. Survival of
Xanthomonas campestris pv. vesicatoria in pepper seeds and
practice of using overhead sprinkler irrigation in green- roots in symptomless and dry leaves in non-host plants and in
houses can significantly spread the pathogen. Once the soil. Plant and Soil 68:161–170.
diseased transplants are in the field, the pathogen can be Bashan, Y., Okon, Y., and Henis, Y. 1982. Long-term survival of
spread plant-to-plant via splashing water, contaminat- Pseudomonas syringae pv. tomato and Xanthomonas
campestris pv. vesicatoria in tomato and pepper seeds.
ed tools and implements, and workers’ hands. Disease Phytopathology 72:1143–1144.
development is favored by high humidity and warm Bouzar, H., Jones, J. B., Stall, R. E., Hodge, N. C., Minsavage, G.
temperatures in the 24–30° C range. The pathogen is V., Benedict, A. A., and Alvarez, A. M. 1994. Physiological,
chemical, serological, and pathogenic analyses of a
not a true soilborne organism, but it can survive in the worldwide collection of Xanthomonas campestris pv.
soil on infested plant residues. The pathogen can also vesicatoria strains. Phytopathology 84:663–671.
overwinter on volunteer pepper plants and on weeds Buonaurio, R., Stravato, V. M., and Scortichini, M. 1994.
such as black nightshade (Solanum nigrum) and ground Characterization of Xanthomonas campestris pv. vesicatoria
from Capsicum annuum in Italy. Plant Disease 78:296–299.
cherry (Physalis minima). Conover, R. A. and Gerhold, N. R. 1981. Mixtures of copper and
Control maneb or mancozeb for control of bacterial spot of tomato
Carefully monitor pepper seed fields so that bacterial and their compatibility for control of fungus diseases.
Proceedings Florida State Horticultural Society 94:154–156.
spot problems can be identified and managed from an
Gitaitis, R. D., Chang, C. J., Sijam, K., and Dowler, C. C. 1991.
early stage. Use seed that does not have significant levels A differential medium for semiselective isolation of
of the pathogen. Appropriate seed treatments can also Xanthomonas campestris pv. vesicatoria and other
cellulolytic Xanthomonads from various natural sources.
contribute to the management of seedborne inoculum.
Treat seed with hydrochloric acid, calcium hypochlo-
rite, hot water, or other materials. Seed health testing
C APSICUM 201
Jones, J. B., Stall, R. E., and Bouzar, H. 1998. Diversity among Athelia rolfsii (anamorph = Sclerotium rolfsii)
Xanthomonads pathogenic on pepper and tomato. Annual
Review of Phytopathology 36:41–58. SOUTHERN BLIGHT
Kousik, C. S. and Ritchie, D. F. 1995. Isolation of pepper races 4
and 5 of Xanthomonas campestris pv. vesicatoria from Introduction and significance
diseased peppers in southeastern U. S. fields. Plant Disease
79:540. Southern blight, or Sclerotium stem rot, occurs on a
Kousik, C. S. and Ritchie, D. F. 1998. Response of bell pepper large number of vegetable and ornamental plants.
cultivars to bacterial spot pathogen races that individually
overcome major resistance genes. Plant Disease 82:181–186.
Martin, H. L., Hamilton, V. A., and Kopittke, R. A. 2004.
Copper tolerance in Australian populations of Xanthomonas On pepper, the early symptoms consist of a water-
campestris pv. vesicatoria contributes to poor field control of soaked lesion on crown and lower stem tissue that is in
bacterial spot of pepper. Plant Disease 88:921–924. contact with the soil. These infection sites turn light to
McGuire, R. G., Jones, J. B., and Sasser, M. 1986. Tween media
dark brown and can rapidly girdle the entire crown.
for semiselective isolation of Xanthomonas campestris pv.
vesicatoria from soil and plant material. Plant Disease Above-ground symptoms consist of wilting and a quick
70:887–891. collapse of all foliage (236). If soil moisture conditions
Obradovic, A., Mavridis, A., Rudolph, K., Janse, J. D., are suitable, the pathogen will form a thick, white
Arsenijevic, M., Jones, J. B., Minsavage, G. V., Wang, J.-F.
2004. Characterization and PCR-based typing of mycelial mat or layer on crown, lower stem, and even
Xanthomonas campestris pv. vesicatoria from peppers and
tomatoes in Serbia. European Journal of Plant
Pathology110:285–292.
Rowell, B., Jones, R. T., Nesmith, W., Satanek, A., and Snyder, J.
C. 2001. Bacterial spot resistance, yield, and quality of bell
236
and specialty peppers. HortTechnology 11:648–657.
Sijam, K., Chang, C. J., and Gitaitis, R. D. 1992. A medium for
differentiating tomato and pepper strains of Xanthomonas
campestris pv. vesicatoria. Canadian Journal of Plant
Stahl, R. E., Beaulieu, C., Egel, D., Hodge, N. C., Leite, R. P.,
Minsavage, G. V., Bouzar, H., Jones, J. B., Alvarez, A. M., and
Benedict, A. A. 1994. Two genetically diverse groups of
strains are included in Xanthomonas campestris pv.
vesicatoria. International Journal of Systematic Bacteriology
44:47–53.
Tegegn, T. 1985. A review of bacterial leaf spot of peppers
(Capsicum annuum) caused by Xanthomonas campestris pv.
vesicatoria and some methods of its control. Acta
F UNGAL D ISEASES
236 Collapsed pepper plant affected by southern

blight.
237
Control
Rotate with non-host plants so that soil inoculum levels
are reduced; however, because of the ability of S. rolfsii
to survive in soil, crop rotations will not eliminate the
disease. Deep plowing of fields prior to planting, which
inverts the soil profile, may help reduce inoculum levels.
Pre-plant treatment of soil with effective fumigants will
provide some control but will not eradicate the
pathogen and are expensive to use.
References
Brown, J. E., Stevens, C., Osborn, M. C., and Bryce, H. M. 1989.
Black plastic mulch and spunbonded polyester row cover as
method of southern blight control in bell pepper. Plant
Disease 73:931–932.
Jenkins, S. F. and Averre, C. W. 1986. Problems and progress in
integrated control of southern blight of vegetables. Plant
Disease 70:614–619.
Punja, Z. K. 1985. The biology, ecology, and control of
Sclerotium rolfsii. Annual Review of Phytopathology
23:97–127.
Ristaino, J. B., Perry, K. B., and Lumsden, R. D. 1996. Soil
solarization and Gliocladium virens reduced the incidence of
southern blight (Sclerotium rolfsii) in bell pepper in the field.
Biocontrol Science & Technology 6:583–593.
237 Pepper stem exhibiting white mycelial growth

from Sclerotium rolfsii.
on the soil surrounding the crown (237). Small (1–2 Botrytis cinerea (teleomorph = Botryotinia fuckeliana)
mm in diameter), spherical, tan to brown sclerotia form GRAY MOLD
profusely on and in this white growth. Sclerotia are
characterized by having an outer differentiated, Introduction and significance
pigmented rind. Gray mold of pepper is found in all pepper producing
regions of the world. The disease can occasionally be
Causal agent damaging, especially if humid conditions prevail. The
Southern blight is caused by Sclerotium rolfsii, which is disease can often be more prevalent in greenhouse
an imperfect fungus in the Mycelia Sterilia category and settings.
produces no asexual spores. Sclerotium rolfsii has a
broad host range and forms a basidiomycete perfect Symptoms and diagnostic features
stage (Athelia rolfsii), though it is unknown whether Petioles and stems become infected and develop tan to
this stage is involved in the disease. light brown lesions (238). The developing lesion can
eventually girdle the entire petiole or stem and show
F UNGAL D ISEASES
Disease cycle concentric rings due to the sporulation of the pathogen

Because of its resilient sclerotia, the pathogen can and coloration of the lesion. Leaves may also have
survive in the soil and in crop debris for many years. brown lesions and sporulation. The gray mold
When susceptible crops are planted into infested soil, pathogen often infects petioles, stems, and leaves that
the sclerotia germinate and infect the plant. The fungus are damaged or senescing. Flower petals are also subject
is favored by high temperatures above 30° C. to gray mold infections. Infections on green or ripe fruit
C APSICUM 203
result in a soft, decayed, brown to gray rot that can 238

eventually envelop the entire fruit (239). The fungus
usually sporulates on the fruit calyx or in the center of
the fruit lesion where the epidermis has split. Pepper
transplants that are damaged during the planting
process can develop stem infections and die. Gray mold
can be particularly damaging in greenhouses due to the
elevated humidity in such environments.
Causal agent
Gray mold is caused by Botrytis cinerea. The sexual
stage, Botryotinia fuckeliana, is rarely found on the
crop. Conidiophores of B. cinerea are long (1–2 mm),
become gray-brown with maturity, and branch irregu-
larly near the apex. Conidia are clustered at the branch
tips and are single-celled, pale brown, ellipsoid to
obovoid, and measure 6–18 x 4–11 μm. The pathogen
can be isolated on standard microbiological media.
Some isolates sporulate poorly in culture unless
incubated under lights (12 h light/12 h dark). The
pathogen forms survival structures (sclerotia) that are
black, oblong or dome-shaped, and measure 4–10 mm.
The fungus grows best at 18–23° C but is inhibited at
warm temperatures above 32° C. On host tissue the 238 Stem lesion of gray mold of pepper.
fungus produces characteristically profuse sporulation
that is dense, velvety, and grayish brown in color. 239
Disease cycle
Botrytis cinerea survives in and around fields as a sapro-
phyte on crop debris, as a pathogen on numerous crops
and weed plants, and as sclerotia in the soil. Conidia
develop from these sources and become windborne.
When conidia land on senescent or damaged pepper
tissue, they will germinate if free moisture is available
and rapidly colonize this food base. Once established,
the pathogen will grow into adjacent healthy stems and
leaves, resulting in disease symptoms and the produc-
tion of additional conidia. Cool temperatures, free 239 Fruit lesion of gray mold of pepper.
moisture, and high humidity favor the development of
the disease. Pepper tissues that are damaged from other
diseases can also become colonized by B. cinerea acting References
as a secondary decay organism. Elad, Y., Yunis, H., and Volpin, H. 1993. Effect of nutrition on
F UNGAL D ISEASES
susceptibility of cucumber, eggplant, and pepper crops to

Botrytis cinerea. Canadian Journal of Botany 71:602–608.
Control
Park, S. E., Lee, J. T., Chung, S.O., Kim, H. E., Park, S. H., Lee, J.
Reduce plant wetness by avoiding or reducing sprinkler T., Chung, S. O., and Kim, H. K. 1999. Forecasting the
irrigation. To reduce overall humidity, adequately pepper grey mould rot to predict the initial infection by
Botrytis cinerea in greenhouse conditions. Plant Pathology
ventilate or heat greenhouses. Fungicides may be useful Journal 15:158–161.
in protecting fruit from gray mold.
Colletotrichum capsici, C. coccodes,

240
C. gloeosporioides
ANTHRACNOSE

Pepper anthracnose occurs throughout many of the
pepper growing regions of the world. The disease has
greatest impact on the fruit. Both immature and ripe
fruit are subject to infection, though ripe fruit are more
susceptible.
240 Fruit lesions on Jalapeno pepper caused by
Symptoms and diagnostic features anthracnose.
Initial symptoms on pepper fruit consist of round to
oval, tan lesions. As disease develops, the fruit lesions 241
expand, remain circular in shape, and show concentric
rings of black, orange, and tan colors (240, 241). The
black color comes from the fungal structures (micro-
sclerotia and acervuli) that form in the rings. If humid,
wet weather occurs, the fruiting bodies in the lesions
will release orange to pink-colored spore masses.
Lesions can enlarge and become quite large (30 mm or
more in diameter) and sunken. Leaves and stems are
also susceptible to anthracnose and develop irregularly
shaped, tan to brown lesions that often have darker
brown borders.
Causal agents 241 Fruit lesions on bell pepper caused by anthracnose.

Anthracnose is caused by several species of the fungus
Colletotrichum: C. capsici, C. coccodes, C. gloeospori-
oides. All species form minute (approximately 0.3 mm
in diameter), cup-shaped acervuli fruiting bodies that
are usually present in fruit lesions. Acervuli release
single-celled, cyndrical hyaline conidia. These measure development are 20–24° C. With wet, humid condi-
19–28 x 2.7–5 μm (C. capsici), 16–24 x 2–5 μm (C. tions, conidia are produced in a gelatinous material in
coccodes), or 11–19 x 2.7–5 μm (C. gloeosporioides). acervuli. Dispersal of conidia requires splashing water
Some species produce long, brown, septate setae that from rain or sprinklers. The pathogen can be seedborne
are present in the acervuli. C. coccodes and C. gloeo- in pepper.
sporioides form small (0.2–0.4 mm in diameter), irreg-
ularly shaped survival structures called microsclerotia. Control
Rotate crops so that non-hosts are grown every other
Disease cycle year. Many weeds can support the pathogen, so practise
The fungus survives in soil in the form of microsclero- good weed control. Use seed that does not have signifi-
F UNGAL D ISEASES
tia or as acervuli and microsclerotia in dried plant cant levels of the pathogen. Appropriate seed treat-
residue. The pathogen can be splashed up onto pepper ments can also contribute to the management of
foliage and fruit and initiate infections. In addition, fruit seedborne inoculum. Because infested seed can result in
that are in contact with the soil become infected by diseased transplants, inspect transplants and discard
soilborne inoculum. Ripe fruit are particularly suscep- diseased plants. Avoid sprinkler irrigation, as splashing
tible to infection. Optimum temperatures for disease water spreads conidia. Apply fungicides as necessary.
C APSICUM 205
References 242
Farley, J. D. 1976. Survival of Colletotrichum coccodes in soil.
Freeman, S., Katan, T., and Shabi, E. 1998. Characterization of
Colleototrichum species responsible for anthracnose diseases
of various fruits. Plant Disease 82:596–605.
Lewis Ivey, M. L., Nava-Diaz, C., and Miller, S. A. 2004.
Identification and management of Colletotrichum acutatum
on immature bell peppers. Plant Disease 88:1198–1204.
Manandhar, J. B., Hartman, G. L., and Wang, T. C. 1995.
Conidial germination and appressorial formation of
Colleotrichum capsici and C. gloeosporioides isolates from
pepper. Plant Disease 79:361–366.
Manandhar, J. B., Hartman, G. L., and Wang, T. C. 1995.
Anthracnose development on pepper fruits inoculated with
Colleotrichum gloeosporioides. Plant Disease 79:380–383.
Raid, R. N. and Pennypacker, S. P. 1987. Weeds as hosts for 242 Powdery mildew sporulation on underside of
Colletotrichum coccodes. Plant Disease 71:643–646.
pepper leaf.
Leveillula taurica (anamorph = Oidiopsis taurica)

243
POWDERY MILDEW

Powdery mildew is widespread on peppers throughout
the world and sometimes can cause severe damage and
crop loss.

The disease initially causes light green, irregularly
shaped patches on leaves. These patches can later turn
chlorotic and have brown, necrotic centers. Careful
examination of the undersides of these leaves reveals the
white powdery growth of this pathogen (242). The
edges of severely infected leaves will curl upward. Such
leaves will fall off the plant and result in defoliation of
older foliage. Significant leaf drop will cause the fruit to
be exposed and become sunburned (243). Fruit damage
can therefore indirectly result from powdery mildew.
This pathogen only infects the older leaves, with the
younger leaves escaping infection until they mature.
Causal agent
Powdery mildew is caused by Leveillula taurica
(anamorph = Oidiopsis taurica). This mildew species
F UNGAL D ISEASES
does not form epiphytic mycelium and all conidio-

phores develop from endophytic mycelium and emerge 243 Defoliation and resulting sunburned fruit caused
through stomata in the lower leaf epidermis. Conidio- by powdery mildew of pepper.
phores can be branched and carry one or sometimes
two conidia. Conidia are hyaline, single-celled, and
dimorphic. Primary (terminal) conidia are lanceolate
with distinct apical points. Secondary conidia are Phytophthora capsici,

ellipsoid–cylindric and lack the apical point. Conidial P. nicotianae var. parasitica
dimensions for both types vary according to the host PHYTOPHTHORA BLIGHT/
plant but generally are 50–70 x 16–24 μm. For both ROOT AND CROWN ROTS
conidial types, length-to-width ratios are greater than
three. Though not reported to occur on pepper, this Introduction and significance
fungus can form a sexual stage consisting of globose There are two important soilborne Phytophthora
cleistothecia having numerous hypha-like appendages species that cause several diseases on pepper. Phyto-
and containing up to 20 asci. Leveillula taurica appears phthora diseases take the forms of seed decays, seedling
to have a broad host range of numerous crops and damping-off, transplant stem rots, root and crown rots,
weeds. However, research indicates that there may be foliar blights and fruit rots. This section will focus on
distinct subpopulations that have more restricted host root and crown rots and foliar blights. In recent years
ranges. this pathogen has increased in importance on various
vegetable crops in the USA.
Disease cycle
Leveillula taurica is an obligate pathogen and survives
on overwintering peppers, alternate hosts, or possibly 244
as cleistothecia on other crops. Conidia are dispersed by
winds. Powdery mildew development is favored by
mild temperatures below 30°C.
Control
Apply fungicides, such as sulfur, if the disease becomes
severe. Some pepper types (nonpungent cultivars) are
tolerant to powdery mildew, and researchers are devel-
oping resistant lines for other pepper types.
References
Correll, J. C., Gordon, T. R., and Elliott, V. J. 1987. Host range,
specificity, and biometrical measurements of Leveillula
taurica in California. Plant Disease 71:248–251.
244 Root rot of Phytophthora root rot of pepper.
de Souza, V. L. and Café-Filho, A. C. 2003. Resistance to
Leveillula taurica in the genus Capsicum. Plant Pathology Healthy plant is on the left.
52:613–619.
Palti, J. 1971. Biological characteristics, distribution, and control
of Leveillula taurica. Phytopathologia Mediterranea 245
10:139–153.
Reuveni, R. and Rotem, J. 1973. Epidemics of Leveillula taurica
on tomatoes and peppers as affected by conditions of
humidity. Phytopathologische Zeitschrift 76:153–157.
Shifress, C., Pilowsky, M., and Zacks, J. M. 1992. Resistance to
Leveillula taurica mildew in Capsicum annuum.
Phytoparasitica 20:279–283.
F UNGAL D ISEASES
245 Wilting of plant affected by Phytophthora root rot

(on left). Healthy plant is on right.
C APSICUM 207
246
246 Pepper field affected by Phytophthora root rot.
Symptoms and diagnostic features Phytophthora blight is caused by P. capsici. Both species
Symptoms of Phytophthora root rot initially consist of are oomycete organisms, soil inhabitants, and can
water-soaked root lesions that later turn dark gray to persist in soils for extended periods of time. Phyto-
chocolate-brown (244). The discoloration can occur on phthora capsici forms irregularly shaped sporangia that
both the fine feeder and larger taproots. As lesions can be spherical, ovoid, elongated, or have more than
expand, individual roots become girdled or entirely one apex. Sporangia are papillate, deciduous, have
rotted. The discoloration will affect both vascular and pedicels that are 10 or more μm in length, and measure
stele tissues of the root and can move up the main 30–60 x 25–35 μm. Phytophthora parasitica sporangia
taproot and into the plant crown and lower main stem. vary greatly and can be ellipsoidal, ovoid, pyriform, or
In advanced stages, the roots will be soft and decayed. spherical with distinct papilla. Sporangia are not
The plant crown can show both surface and internal deciduous and measure 11–60 x 20–45 μm.
discoloration. Above ground symptoms consist of
foliage that first turns dull gray-green, then later wilts Disease cycle
(245). The entire plant canopy can rapidly collapse and The root and crown diseases require the presence of wet
die (246). soils and free water. Compacted, finely textured, and
Phytophthora blight of pepper results in above- poorly draining soils create conditions favorable for
ground infections. Irregularly shaped, black lesions root rot. In addition to pepper, these Phytophthora
develop on stems and in axils of branches. Leaves can species can infect tomato, cucurbits, and other hosts.
have gray to brown, circular to oval, water-soaked The blight disease occurs if inoculum is splashed from
spots that can enlarge and cover large portions of the the soil and onto lower foliage and stems. Later in
leaf. This disease can also cause fruit infections that disease development, P. capsici forms sporangia on
F UNGAL D ISEASES
result in rotted fruit tissues that support white sporula- infected leaves, stems, or fruit. These sporangia are
tion of the pathogen. carried by winds or splashing water onto other plants,
resulting in spread of the disease. Infection conditions
Causal agents are optimum if free moisture is present and tempera-
Phytophthora root and crown rots are caused by P. tures are 24–33° C.
capsici and P. parasitica (= P. nicotianae var. parasitica).
Control Phytophthora spp., Pythium spp.,

Plant peppers in soils that are prepared properly and Rhizoctonia solani (teleomorph = Thanatephorus
cucumis)
drain well. Carefully manage irrigation so that excess
soil water is avoided. Keep bed tops dry by using sub- DAMPING-OFF,
surface drip irrigation. Fungicides may help manage PYTHIUM ROOT ROT
both root and fruit infections. Some new pepper
cultivars have some resistance to these pathogens. Introduction and significance
Several soilborne pathogens cause seed, seedling, and
References transplant diseases of pepper. Pathogens include species
Cafe-Filho, A. C. and Duniway, J. M. 1996. Effect of location of of Phytophthora, Pythium, and Rhizoctonia. If soil
drip irrigation emitters and position of Phytophthora capsici conditions favor the pathogen, plant stands can be sig-
infections in roots on Phytophthora root rot of pepper.
Phytopathology 86:1364–1369. nificantly reduced.
Cafe-Filho, A. C. and Duniway, J. M. 1995. Dispersal of
Phytophthora capsici and Phytophthora parasitica in furrow- Symptoms and diagnostic features
irrigated rows of bell pepper, tomato, and squash. Plant
Pathology 44:1025–1032.
These diseases have various phases. Pepper seeds can be
Cafe-Filho, A. C. and Duniway, J. M. 1995. Effects of furrow infected prior to germination and result in seed death.
irrigation schedules and host genotype on Phytophthora root Newly germinated seedlings can be infected to such a
rot of pepper. Plant Disease 79:39–43. degree that plants do not emerge above the soil (pre-
Hausbeck, M. K. and Lamour, K. H. 2004. Phytophthora capsici
on vegetable crops: research progress and management
emergence damping-off). Pepper seedlings might
challenges. Plant Disease 88:1292–1303. emerge from the ground but become diseased after
Hwang, B.-K. and Kim, C.-H. 1995. Phytophthora blight of emergence (post-emergence damping-off). Finally,
pepper and its control in Korea. Plant Disease 79:221–227. transplants placed in the ground can develop root rots
Lamour, K. H. and Hausbeck, M. K. 2003. Effect of crop
rotation on the survival of Phytophthora capsici in Michigan.
or stem lesions from these same pathogens. Initial
Plant Disease 87:841–845. symptoms of post-emergence damping-off occur on
Larkin, R. P., Ristaino, J. B., and Campbell, C. L. 1995. seedling stems in contact with the soil. These symptoms
Detection and quantification of Phytophthora capsici in soil. consist of shriveled stems that have discolored, tan to
Oelke, L. M., Bosland, P. W., and Steiner, R. 2003.
dark brown lesions. With time the lower stem collapses,
Differentiation of race specific resistance to Phytophthora roots decay, and the cotyledons and leaves will wilt.
root rot and foliar blight in Capsicum annuum. Journal of the Such plants sometimes fall over. Damping-off diseases
often result in death of the seedling and subsequent
Parra, G. and Ristaino, J. B. 2001. Resistance to mefenoxam and
metalaxyl among field isolates of Phytophthora capsici reduction of plant stands. However, even if plants do
causing Phytophthora blight of bell pepper. Plant Disease not succumb to these pathogens, the surviving plant
85:1069–1075. may be stunted, delayed in development, and less pro-
Ristaino, J. B. 1991. Influence of rainfall, drip irrigation, and
inoculum density on the development of Phytopthora root
ductive (247).
and crown rot epidemics and yield in bell pepper. These three pathogens can also infect roots and
Phytopathology 81:922–929. crowns of older plants. Such infections are usually
Ristaino, J. B. and Gumpertz, M. L. 2000. New frontiers in the restricted to the small feeder roots which turn brown
study of dispersal and spatial analysis of epidemics caused by
species in the genus Phytophthora. Annual Review of and become rotted. Affected plants have reduced vigor
Phytopathology 38:541–576. and foliage may turn chlorotic.
Ristaino, J. B. and Johnston, S. A. 1999. Ecologically based
approaches to management of Phytophthora blight of bell
pepper. Plant Disease 83:1080–1089. Causal agents
Sujkowski, L. S., Parra, G. R., Gumpertz, M. L., and Ristaino, J. Several species of Phytophthora and Pythium can cause
F UNGAL D ISEASES
B. 2000. Temporal dynamics of Phytophthora blight on bell damping-off in pepper. These pathogens are in the
pepper in relation to the mechanisms of dispersal of primary
oomycete group of organisms. These organisms survive
inoculum of Phytophthora capsici in soil. Phytopathology
90:148–156. in the soil as saprophytes and are favored by wet soil
conditions. With the exception of P. ultimum, these
pathogens usually produce zoospores that swim to and
infect susceptible tissues. Sexual structures (antheridia,
C APSICUM 209
oogonia, and oospores) are produced by all species. In 247

addition to pepper, these pathogens can infect
numerous other plants.
Rhizoctonia solani is a soilborne fungus with a very
broad host range. R. solani has no asexual fruiting
structures or spores, but produces characteristically
coarse, brown, approximately right-angled branching
hyphae. The hyphae are distinctly constricted at branch
points, and cross walls with dolipore septa are
deposited just after the branching. Hyphal cells are
multi-nucleate. Small, tan to brown loosely aggregated
clumps of mycelia function as sclerotia. This fungus can
survive by infecting and thriving on a great number of
plant hosts, besides pepper, and can also persist in the
soil as a saprophyte. The teleomorph stage, Thanate-
phorus cucumis, is not commonly observed.
247 Poor growth of pepper plants infected by Pythium
Disease cycle (plant on the right). Healthy plant is on the left.
Most of these soilborne pathogens survive in fields for
indefinite amounts of time. Wet soil conditions and cool
temperatures (15–20° C) generally favor these organ- References
isms and their ability to grow and infect hosts. Chellemi, D. O., Mitchell, D. J., Kannwischer-Mitchell, M. E.,
However, for pathogens such as P. aphanidermatum Rayside, P. A., and Rosskopf, E. N. 2000. Pythium spp.
associated with bell pepper production in Florida. Plant
and P. myriotylum, warmer soil conditions (32–37° C) Disease 84:1271–1274.
are favorable. Rhizoctonia solani can also be favored by Mao, W., Lewis, J. A., Lumsden, R. D., and Hebbar, K. P. 1998.
warmer soils. Seedlings are most susceptible to Biocontrol of selected soilborne diseases of tomato and
pepper plants. Crop Protection 17:535–542.
infection, though these pathogens can infect the feeder
roots of mature plants.
Control
Damping-off is primarily controlled by creating condi-
tions unfavorable for the pathogens. Plant on raised
beds and in soils that drain well so that overly wet soil
conditions are avoided. Carefully manage irrigation so
that excess water is not applied. Plant seed that has been
treated with fungicides, and avoid planting seed too
deeply, which delays seedling emergence and increases
the chance of infection. Post-plant fungicides may
provide control for some of these pathogens. Avoid
planting too soon into fields that still have extensive
crop residue in the soil. Rotate crops because consecu-
tive pepper plantings will increase the populations of
the soilborne pathogens. For transplants, prepare good
F UNGAL D ISEASES
quality beds and do not place transplants too deep into

the beds.
Sclerotinia minor, S. sclerotiorum 249 Upper canopy 249

WHITE MOLD, infections of
SCLEROTINIA ROT Sclerotinia
sclerotiorum of
Introduction and significance pepper.
White mold, or Sclerotinia rot, is an occasional problem
on peppers. The types of symptoms seen on pepper
depend on which species of Sclerotinia is involved and
which stage of the pathogen is present. White mold
caused by S. sclerotiorum is generally the more
important disease.

Sclerotinia minor only infects the pepper stem tissue
that is in contact with the soil (248). Sclerotinia minor
causes a water-soaked lesion to develop at the crown
and lower stem. The lesion enlarges and can girdle the
plant, resulting in the collapse of the canopy and foliage.
With time the crown and stem lesions turn light tan to White mycelium can be observed on infected lesions if
off-white in color. White mycelium and small conditions are favorable. The large, black sclerotia can
(3–5 mm), black, irregularly shaped sclerotia form grow on the outer surface or in the central cavity of
around and within the decayed crown. stems (250). Sclerotinia sclerotiorum can also infect
Sclerotinia sclerotiorum is the other species that can pepper crowns and lower stems (251). Though not
attack pepper. Airborne ascospores can cause infections always observed, fruit can become infected and develop
throughout the pepper canopy (249). These above- a water-soaked, dull green lesion that later turns into a
ground infections usually occur on damaged stems or soft, watery rot. This pathogen produces white
petioles, or where a nutrient source, such as a senescent mycelium and black, oblong or dome-shaped sclerotia
flower petal, falls onto stems or petioles. These infec- that are 5–10 mm long.
tions are water-soaked lesions that gradually enlarge
and encircle the stems. Older infections turn off-white, Causal agents and disease cycle
white-gray, or tan in color and show zonate rings. White mold is caused by two species of Sclerotinia,
S. minor and S. sclerotiorum. The two pathogens are
distinguished primarily by the size of sclerotia.
Sclerotinia minor sclerotia are significantly smaller than
248
those of S. sclerotiorum. In addition, S. sclerotiorum
produces apothecia, while S. minor does not generally
do so in the field. For detailed descriptions of these
pathogens and the disease cycles, see the bean white
mold section in the chapter on legume diseases.
Control
For an integrated approach to Sclerotinia control, see
F UNGAL D ISEASES
the bean white mold section in the chapter on legume

diseases. Against S. sclerotiorum, fungicides may only
be partially effective due to the sporadic release of
infective ascospores during the course of a pepper crop.
If peppers are grown in the greenhouse, reduce
248 Pepper crowns infected by Sclerotinia minor. humidity levels by ventilating the structures.
C APSICUM 211
250 Mycelium
Stemphylium solani, S. lycopersici
250
and sclerotia of GRAY LEAF SPOT
Sclerotinia
sclerotiorum inside Introduction and significance
a pepper stem. Gray leaf spot disease is found in many pepper-
producing areas and can commonly be found on both
pepper and tomato.

The main symptoms occur on leaves and initially
consist of small (1–2 mm in diameter) reddish-brown
spots. These spots enlarge into circular to oval spots
that measure 3–5 mm in diameter and consist of white
centers with red to brown margins. In severe cases,
leaves having many spots can turn chlorotic and drop
off the plant. Young pepper plants at the seedling stage
are most sensitive to infection. Spots can also occur on
petioles and stems but are not found on pepper fruit.
251 Pepper stems 251
Stem lesions are irregular in shape, white in color, and
exhibiting have red to brown margins. Stem lesions can weaken
mycelium of the plant and result in broken stems.
Sclerotinia
sclerotiorum. Causal agents
Gray leaf spot is caused by two species of the fungus
Stemphylium. On V–8 juice agar incubated under
lights, these pathogens produce dark green-brown
mycelium and abundant conidia after approximately
10 days. For S. solani, conidiophores are mostly
unbranched and 4–7 μm wide with distinctly swollen
apical cells (8–11 μm wide) having darkly pigmented
bands. Conidia dimensions are mostly 33–55 x 18–28
μm. Conidia are multicelled, pale to golden brown,
smooth to finely verruculose, having three to six trans-
verse and several longitudinal septa. The spore has a
pointed apex and is usually constricted at the middle
transverse septum.
References For S. lycopersici, conidiophores are mostly
Abawi, G. S. and Grogan, R. G. 1979. Epidemiology of diseases unbranched and 6–7 μm wide with distinctly swollen
caused by Sclerotinia species. Phytopathology 69:899–904. apical cells (8–10 μm wide) having darkly pigmented
Gonzalez, T. G., Henderson, D. M., and Koike, S. T. 1998. First
bands. Conidia dimensions are mostly 50–74 x 16–23
report of bell pepper (Capsicum annuum) as a host of
Sclerotinia minor. Plant Disease 82:832. μm. Conidia are multicelled, pale to medium brown,
Kohn, L. M. 1979. Delimitation of the economically important smooth to finely verruculose, having one to eight trans-
F UNGAL D ISEASES
plant pathogenic Sclerotinia species. Phytopathology verse and several longitudinal septa. The spore has a
69:881–886.
conical apex and is usually constricted at three trans-
Purdy, L. H. 1979. Sclerotinia sclerotiorum: history, diseases and
symptomatology, host range, geographic distribution, and verse septa. The taxonomy of these species is still in
impact. Phytopathology 69:875–880. need of clarification. Stemphylium botryosum f. sp.
Yanar, Y. and Miller, S. A. 2003. Resistance of pepper cultivars lycopersici and S. floridanum are other Stemphylium
and accessions of Capsicum spp. to Sclerotinia sclerotiorum.
Plant Disease 87:303–307. fungi or pathogen synonyms that are pathogenic on
Solanaceous hosts. The perfect stages of these 252

pathogens, which are various species of Pleospora, are
rarely found on this crop.
Disease cycle
These two Stemphylium pathogens survive as sapro-
phytes on crop residues, or as pathogens on volunteer
or wild Solanaceae plants. Winds and splashing water
spread conidia to pepper hosts. Free moisture is
required for infection to take place. The disease is most
severe if conditions are humid and overcast, and if
foliage is wet with dew or rain. These pathogens can be
seedborne.
Control 252 Chlorosis of pepper caused by Verticillium wilt.

pathogen. Appropriate seed treatments can also con-
tribute to the management of seedborne inoculum. light brown discoloration (253). This coloring is most
Inspect transplants and remove symptomatic plants. evident in the main stems closer to the crown; such dis-
Rotate crops so that infected crop residues and coloration may not be evident in the upper, smaller
volunteer plants are not present. Use fungicides if stems. Disease symptoms can be accentuated if the
necessary. infected plant is bearing a heavy load of fruit or is
stressed by some other factor. Even if infected plants do
References not die completely, plant growth and yields can be
Blazquez, C. H. 1969. Occurrence of gray leaf spot on peppers in significantly reduced (254).
Florida. Plant Disease Reporter 53:756.
Braverman, S. W. 1968. A new leaf spot of pepper incited by
Causal agent
Stemphylium botryosum f. sp. capsicum. Phytopathology
58:1164–1167. Verticillium wilt is caused by the fungus Verticillium
dahliae. The pathogen can be isolated on standard
microbiological media, though semi-selective media
such as NP–10 can be useful for isolation. On general
Verticillium dahliae purpose media, the pathogen forms the characteristic
VERTICILLIUM WILT hyaline, verticillate conidiophores bearing 3–4 phialides
at each node, and hyaline, single-celled, ellipsoidal
Introduction and significance conidia that measure 2–8 x 1–3 μm. Older cultures
Verticillium wilt is a well-known disease that affects form dark brown to black torulose microsclerotia that
hundreds of different plant species and is an important consist of groups of swollen cells formed by repeated
problem on pepper throughout the world. The closely budding. Microsclerotia size varies greatly and is in the
related tomato and aubergine (eggplant) are also subject range of 15 to 100 μm in diameter. Microsclerotia
to this disease. enable the pathogen to survive in the soil for extended
periods of time (up to 8 to 10 years). Verticillium
Symptoms and diagnostic features dahliae is listed as having an extensive host range of
F UNGAL D ISEASES
On pepper, early symptoms consist of the slight crops and weeds. However, research has indicated that
chlorosis of lower leaves. The chlorosis can progress the V. dahliae isolates from various crops have distinct
until leaves are bright yellow (252); such leaves will wilt host ranges and may therefore exist as different strains.
and eventually fall off the plant. Plant shoots and the For example, isolates from bell pepper can infect many
overall foliage will wilt, especially during the warmer other non-pepper hosts; however, isolates from chile
times of the day. Internal vascular tissue has a tan to pepper infect only pepper and aubergine (eggplant).
C APSICUM 213
When V. dahliae isolates from tomato are inoculated 253 Vascular 253
onto pepper, some will infect pepper while others discoloration of
cannot cause disease. Therefore, the precise etiology of pepper caused by
the various Verticillium wilt diseases from different Verticillium wilt.
crops appears to be quite complex.
Disease cycle
The pathogen survives in the soil as dormant microscle-
rotia or as epiphytes on non-host roots. Cool to
moderate weather conditions favor the pathogen, and
disease is enhanced at temperatures between 20–24° C.
The microsclerotia germinate and infective hyphae
enter host roots through wounds.
Control
In general, Verticillium wilt is best controlled by
planting resistant or tolerant cultivars. However,
presently there are no commercially available pepper
cultivars with sufficient resistance. Pre-plant treatment
of soil with effective fumigants will give some control
but will not eradicate the pathogen. For greenhouse
production, steaming of soil can also provide some
control. Rotate crops so that pepper is not planted in
fields having a history of the problem. Rotation with 254
non-host crops, such as small grains and corn, can
lower inoculum levels but will not eradicate the patho-
gen. Minimize spread of infested soil to uninfested
areas.
References
Bhat, R. G. and Subbarao, K. V. 1999. Host range specificity in
Verticillium dahliae. Phytopathology 89:1218–1225.
Bhat, R. G., Smith, R. F., Koike, S. T., Wu, B. M., and Subbarao,
K. V. 2003. Characterization of Verticillium dahliae isolates
and wilt epidemics of pepper. Plant Disease 87:789–797.
Bletsos, F. A., Thanassoulopoulos, C. C., and Roupakias, D. G.
1999. Water stress and Verticillium wilt severity on eggplant
(Solanum melongena L.). Journal of Phytopathology
147:243–248.
Evans, G. and McKeen, C. D. 1975. A strain of Verticillium
dahliae pathogenic to sweet pepper in southwestern Ontario.
Canadian Journal of Plant Science 55:857–859.
Nagao, H., Arai, H., Oshima, S., Koike, M., and Iijima, T. 1998.
Vegetative compatibility of an isolate of Verticillium dahliae
pathogenic to both tomato and pepper. Mycoscience
F UNGAL D ISEASES
39:37–42.
Riley, M. K. and Bosland, P. W. 1998. Commercial planting
media effective in screening for Verticillium wilt of Capsicum
annuum. HortScience 33:285–286.
of sodium polygalacturonate sources and improved recovery 254 Advanced symptoms and plant collapse of pepper
of Verticillium species from soil. (Abstract) Phytopathology
81:1347. caused by Verticillium wilt.

255
BEET CURLY TOP

Pepper is susceptible to a large number of virus patho-
gens. Over 70 such agents have been documented to
some degree, and other virus-like diseases have yet to be
fully characterized. Many of these diseases are eco-
nomically important worldwide, while certain others
are only significant in particular pepper producing
areas. Beet curly top virus (BCTV) occurs in North and
South America, Asia, the Middle East, and the
Mediterranean region. It is an important pathogen of
many crops such as beet, tomato, and pepper.
255 Leaf rolling symptom of Beet curly top virus of
Symptoms and diagnostic features pepper.
BCTV can result in severely stunted, chlorotic plants if
peppers are infected early in development. Such plants 256
have dull to bright yellow leaves that are brittle,
thickened, and rolled (255, 256). Plants that are
infected later show some degree of reduced growth,
chlorosis, and rolled brittle leaves. Fruit set can be
reduced.

or in pairs. The BCTV genome is a single stranded
circular DNA. BCTV is vectored by either the beet
leafhopper (Circulifer tenellus) in the United States or
C. opacipennis in the Mediterranean region. In the
plant, BCTV is restricted to the phloem tissue. This
virus has many plant hosts. Curly top as a disease may 256 Stunted and chlorotic pepper infected with
actually be caused by one of four different curly top Beet curly top virus.
virus species: Beet curly top virus (BCTV), Beet mild
curly top virus (BMCTV), Beet severe curly top virus References
(BSCTV), and Spinach curly top virus (SCTV). Abdalla, O. A., Desjardins, P. R., and Dodds, J. A. 1991.
Research is on-going to further determine the relation- Identification, disease incidence, and distribution of viruses
infecting peppers in California. Plant Disease 75:1019–1023.
ships of these various viruses. On a molecular level,
Briddon, R. W., Stenger, D. C., Bedford, I. D., Stanley, J.,
researchers have compared strains of BCTV from Izadpanah, K., and Markham, P. G. 1998. Comparison of a
North America and the Middle East and found them to beet curly top virus isolate originating from the old world
with those from the new world. European Journal of Plant
be similar, providing evidence that these various BCTV Pathology104:77–84.
strains share a common origin.
V IRAL D ISEASES
Soto, M. J. and Gilbertson, R. L. 2003. Distribution and rate of

movement of the curtovirus Beet mild curly top virus (family
Control Geminiviridae) in the beet leafhopper. Phytopathology
93:478–484.
Follow general suggestions for managing virus diseases Stenger, D. C., Duffus, J. E., and Villalon, B. 1990. Biological and
(see Part 1). genomic properties of a geminivirus isolated from pepper.
C APSICUM 215
Stenger, D. C. and McMahon, C. L. 1997. Genotypic diversity of

beet curly top virus populations in the western United States. 257
Phytopathology 87:737–744
Wang, H., Gurusinghe, P. de A., and Falk, B. W. 1999. Systemic
insecticides and plant age affect beet curly top virus
transmission to selected host plants. Plant Disease
83:351–355.
CUCUMBER MOSAIC

Cucumber mosaic virus (CMV) is commonly found 257 Necrotic growing point of pepper caused by
throughout the world and can cause disease on perhaps Cucumber mosaic virus.
over 1,000 plant hosts, including pepper and many
other vegetable crops. 258

CMV symptoms on pepper are extremely variable and
can range from mild mosaics, diffuse chlorotic lesions,
necrotic specks, ring spots, and many other manifesta-
tions (257, 258, 259). Infected plants may not produce
as many fruit, or fruit that do develop are small or have
ring spot or other markings.

CMV is a cucumovirus with virions that are isometric
(28–29 nm in diameter) and contain three single
stranded RNAs. A number of CMV strains have been 258 Necrotic spotting on pepper fruit infected with
documented. CMV is transmitted by many aphid Cucumber mosaic virus.
vectors, and in pepper the virus can be seedborne.
259
259 Necrotic veins
Control of pepper leaf
Follow general suggestions for managing virus diseases caused by
(see Part 1). CMV is seedborne in pepper. Use seed that Cucumber mosaic
does not have significant levels of the pathogen. virus.
References
Abdalla, O. A., Desjardins, P. R., and Dodds, J. A. 1991.
Identification, disease incidence, and distribution of viruses
infecting peppers in California. Plant Disease 75:1019–1023.
Gallitelli, D. 2000. The ecology of cucumber mosaic virus and
sustainable agriculture. Virus Research 71:9–21.
Rodriguez-Alvarado, G., Kurath, G., and Dodds, J. A. 1995.
V IRAL D ISEASES
Heterogeneity in pepper isolates of cucumber mosaic virus.

Pepper mild mottle virus

260
PEPPER MILD MOTTLE

Pepper mild mottle virus (PMMV) is a serious pathogen
worldwide.

Foliar symptoms are usually slight and consist of mild
mottles, mosaics, or chlorosis (260). Fruit, however, can
be severely malformed, small, and have necrotic and
off-colored skin (261).

PMMV is a tobamovirus with virions that are rod 260 Chlorotic leaf symptoms on pepper infected with
shaped (312 x 18 nm) and contain an RNA genome. Pepper mild mottle virus.
Four PMMV strains have been documented. This virus
does not have a known vector, but is easily transmitted 261
mechanically and is seedborne.
Control
(see Part 1). PMMV is seedborne in pepper. Use seed
that does not have significant levels of the pathogen.
References
Alonso, E., Garcia-Luque, I., Avila-Rincon, M. J., Wicke, B.,
Serra, M. T., and Diaz-Ruiz, J. R. 1989. A tobamovirus
causing heavy losses in protected pepper crops in Spain.
Journal of Phytopathology 125:67–76.
Alonso, E., Garcia-Luque, I., de la Cruz, A., Wicke, B., Avila-
Rincon, M. J., Serra, M. T., Castresana, C., and Diaz-Ruiz, J.
R. 1991. Nucleotide sequence of the genomic RNA of pepper
261 Chlorotic blotches on pepper fruit infected with
mild mottle virus, a resistance-breaking tobamovirus in
pepper. Journal of General Virology 72:2875–2884. Pepper mild mottle virus.
Wetter, C. 1984. Serological identification of four tobamoviruses
infecting pepper. Plant Disease 68:597–599.
V IRAL D ISEASES
C APSICUM 217
Potato virus Y Causal agent and disease cycle

POTATO VIRUS Y STLCV is a begomovirus with isometric particles that
contain a DNA genome. STLCV is vectored by the
Introduction and significance Bemisia tabaci whitefly.
Potato virus Y (PVY) is a pathogen of solanaceous
plants around the world. Control
Symptoms and diagnostic features (see Part 1).
Symptoms can vary greatly but mostly consists of vein
clearing that later turns into dark green vein banding. References
Mottle and mosaic patterns can also occur. Necrosis Brown, J. K., Idris, A. M., and Fletcher, D. C. 1993. Sinaloa
can develop on petioles and stems. Fruit symptoms, tomato leaf curl virus, a newly discovered geminivirus of
tomato and pepper in west coast Mexico. Plant Disease
when present, appear as mosaic patterns and necrotic 77:1262.
spotting on fruit skin. Idris, A. M., and Brown, J. K. 1998. Sinaloa tomato leaf curl
geminivirus: biological and molecular evidence for a new
subgroup III virus. Phytopathology 88:648–657.
PVY is a potyvirus with long (730 x 11 nm) flexuous
rods that contain single stranded RNA. PVY is vectored
by aphids and is also readily transmitted mechanically. Tobacco etch virus
TOBACCO ETCH
Control
Follow general suggestions for managing virus diseases Introduction and significance
(see Part 1). Tobacco etch virus (TEV) can be a serious virus
pathogen in parts of North and South America.
References
Llave, C., Martínez, B., Díaz-Ruíz, J. R., and López-Abella, D. Symptoms and diagnostic features
1999. Serological analysis and coat protein sequence Leaf mosaics, mottles, and distortions are typical
determination of potato virus Y (PVY) pepper pathotypes and
differentiation from other PVY strains. European Journal of symptoms. Plants can be stunted and produce fruit with
Plant Pathology105:847–857. severe mosaics and deformities.

Sinaloa tomato leaf curl virus TEV is a potyvirus with long (730 x 12 nm) flexuous
SINALOA TOMATO LEAF CURL rods that contain single stranded RNA. TEV is vectored
by aphids. Several TEV strains have been documented.
Introduction and significance Control
This virus is an important pathogen in North and Follow general suggestions for managing virus diseases
Central America. This pathogen appears to infect only (see Part 1).
plants in the Solanaceae and Malvaceae plant families.
References
Symptoms and diagnostic features Ariyaratne, I., Hobbs, H. A., Valverde, R. A., Black, L. L., and
Sinaloa tomato leaf curl virus (STLCV) causes inter- Dufresne, D. J. 1996. Resistance of Capsicum spp. genotypes
to tobacco etch potyvirus isolates from the Western
veinal chlorosis, mosaic patterns, and curling of leaves. hemisphere. Plant Disease 80:1257–1261.
Plants can be stunted and form fruit that are small and
V IRAL D ISEASES
have necrotic tissue on the blossom end.

Tobacco mosaic virus,Tomato mosaic virus Tomato spotted wilt virus

TOBACCO MOSAIC, TOMATO SPOTTED WILT
TOMATO MOSAIC
Introduction and significance This virus can be very common on pepper and tomato
Tobacco mosaic (TMV) and Tomato mosaic (ToMV) crops, as well as on neighboring crops of other types. In
viruses are two closely related virus pathogens. Both some regions, such as California, greenhouse produced
viruses can infect pepper and other solanaceous plants. peppers can be especially hard hit by this disease.
Symptoms and diagnostic features Symptoms and diagnostic features

TMV and ToMV both cause light and dark green Tomato spotted wilt virus (TSWV) causes leaves to
mosaics and distortions of leaves. Necrotic flecks and develop irregularly shaped to circular, black, small
spots can also appear on leaves. Fruit can be small, spots; chlorotic and necrotic ring spots can also occur.
deformed, and show chlorosis and necrosis in the skin. Stems and shoots may have black streaks or lesions on
the epidermis (262). Severely affected plants may wilt
Causal agents and disease cycle or be stunted. Symptomatic fruit will develop chlorotic
TMV and ToMV are viruses in the tobamovirus group. rings, patches, and lesions (263).
These viruses have straight rod particles that measure
300 x 18 nm and contain single stranded, linear RNA Causal agent
genomes. TMV has no known vector, is readily trans- TSWV is a tospovirus and has isometric particles,
mitted mechanically, and is possibly seedborne in measuring approximately 80–110 nm, which are sur-
pepper. ToMV also lacks a known vector, is transmitted rounded with membranes. TSWV has a genome con-
mechanically, and can be seedborne in pepper and sisting of three linear single-stranded RNAs and is
tomato. vectored by several species of thrips; at least eight
species are found to be vectors. The western flower
Control (Frankliniella occidentalis) and tobacco (F. fusca) thrips
Follow general suggestions for managing virus diseases are probably the most important vectors.
(see Part 1). Both ToMV and TMV are seedborne in
pepper. Use seed that does not have significant levels of Disease cycle
the pathogen. TSWV has one of the most extensive host ranges of any
known plant virus and can infect over 900 different cul-
References tivated and weedy plant species. Therefore initial
Broadbent, L. 1976. Epidemiology and control of tomato mosaic inoculum can come from any number of landscape
virus. Annual Review of Phytopathology 14:75–96. plants, weeds, and other plants. Thrips vector the virus
to the pepper crops. It is well documented that thrips
insects can only acquire the virus as larvae that feed on
infected plants; after acquiring the virus, the insects
carry the virus for the rest of their lives. The virus is not
seedborne in pepper.
Control
(see Part 1). The broad host range of TSWV and the dif-
V IRAL D ISEASES
ficulty in controlling thrips makes this disease particu-

larly difficult to manage. Some sweet and hot pepper
cultivars have the Tsw gene that confers resistance to
TSWV. In Italy, however, some resistance breaking (RB)
strains have overcome this resistance.
C APSICUM 219
262 References
Best, R. J. 1968. Tomato spotted wilt virus. Advances in Virus
Cho, J. J., Mau, R. F. L., Gonsalves, D., and Mitchell, W. C.
1986. Reservoir weed hosts of tomato spotted wilt virus.
Greenough, D. R., Black, L. L., and Bond, W. P. 1990.
Aluminum-surfaced mulch: an approach to the control of
tomato spotted wilt virus in solanaceous crops. Plant Disease
74:805–808.
Groves, R. L., Walgenbach, J. F., Moyer, J. W., and Kennedy, G.
G. 2002. The role of weed hosts and tobacco thrips,
Frankliniella fusca, in the epidemiology of tomato spotted
wilt virus. Plant Disease 86:573–582.
Hobbs, H. A., Black, L. L., Story, R. N., Valverde, R. A., Bond,
W. P., Gatti, J. M. Jr., Schaeffer, D. O., and Johnson, R. R.
1993. Transmission of tomato spotted wilt virus from pepper
and three weed hosts by Frankliniella fusca. Plant Disease
77:797–799.
Maris, P. C., Joosten, N. N., Goldbach, R. W., and Peters, D.
2003. Restricted spread of Tomato spotted wilt virus in
thrips-resistant pepper. Phytopathology 93:1223–1227.
Maris, P. C., Joosten, N. N., Goldbach, R. W., and Peters, D.
2004. Tomato spotted wilt virus infection improves host
suitability for its vector Frankliniella occidentalis.
Maris, P. C., Jootsen, N. N., Peters, D., and Goldbach, R. W.
2003. Thrips resistance in pepper and its consequences for the
acquisition and inoculation of Tomato spotted wilt virus by
the western flower thrips. Phytopathology 93:96–101.
Roggero, P., Masenga, V., and Tavella, L. 2002. Field isolates of
tomato spotted wilt virus overcoming resistance in pepper
262 Stem and leaf lesions caused by Tomato spotted and their spread to other hosts in Italy. Plant Disease
wilt virus on pepper. 86:950–954.
263
263 Severe symptoms of Tomato spotted wilt virus on

fruit of jalapeno pepper. Healthy fruit is on the right.
V IRAL D ISEASES
Cucurbitaceae Gourd family
THE CUCURBITACEAE (gourd family) includes a wide variety of vegetable crops that are commercially grown
primarily for their edible fruits and sometimes immature blossoms. Cultivated cucurbits are classified into two
groups, the Cucurbiteae and Sicyoideae. Notable commercial species include the following: cucumber (Cucumis
sativus); muskmelon and other melons (Cucumis melo); cantaloupe (C. melo var. cantalupensis); watermelon
(Citrullus lanatus); summer and winter squashes, gourds, or courgette (Cucurbita pepo); vegetable marrow
(C. pepo var. medullosa); pumpkin (Cucurbita maxima and C. pepo); Chinese winter melon (Benincasa hispida);
bitter melon (Momordica cochinchinensis). It is believed that many of these species originated from tropical
regions in Africa, the Americas, and Asia.
Acidovorax avenae subsp. citrulli 264 Watermelon 264

BACTERIAL FRUIT BLOTCH leaf showing leaf
spots caused by
Introduction and significance Acidovorax avenae
Compared to most cucurbit diseases, bacterial fruit subsp. citrulli.
blotch is a recently described problem, being first
observed and characterized in 1988–1989. Watermelon
is the primary host. However, honeydew and musk
melons, cantaloupe, pumpkin, citron, and squash are
also susceptible.

Symptoms on leaves are not particularly striking and
may resemble other diseases. Leaf spots are small,
water-soaked to brown, irregularly shaped, and with
angular edges. Such spots may sometimes be surrounded
by chlorotic borders (264, 265). The pathogen is 265 Watermelon
265
seedborne, resulting in seedling infections where the leaf showing
cotyledons develop irregularly shaped water-soaked necrotic lesion
lesions (266). Lesions can expand and run along the caused by
cotyledon midrib and become brown to red-brown and Acidovorax avenae
necrotic. Hypocotyls on young seedlings can develop subsp. citrulli.
lesions and subsequently collapse and die.
The most important impact of this disease is on
watermelon fruits. The upper portion develops small
(less than 1 cm) irregularly shaped lesions that rapidly

expand into large blotches that can cover most or all of
the fruit (267). Early in development, blotches appear
either water-soaked, dull gray-green, or dark green in
color. In time the older, central area of lesions can turn
brown to red-brown and necrotic, with the epidermis
cracking and an amber-colored exudate oozing out of
C UCURBITACEAE 221
266 267
266 Watermelon cotyledons infected with the bacterial 267 Fruit lesions of bacterial fruit blotch on
fruit blotch pathogen. watermelon.
the central blotch area. Blotches are shallow infections Apparently this disease does not readily spread in
that usually do not penetrate into the watermelon flesh. storage from diseased to healthy watermelon fruit if
Secondary decay organisms that invade fruit blotch proper postharvest conditions are maintained.
lesions are mostly responsible for fruit breakdown, rot,
and collapse. Triploid (seedless) cultivars of watermel- Control
on may be less susceptible. Use seed that does not have significant levels of the
pathogen. Seed treatments such as bleach, other bacte-
Causal agent ricides, and fermentation plus seed-drying procedures
Bacterial fruit blotch is caused by Acidovorax avenae may be helpful in cleaning up infested seed. Remove
subsp. citrulli (formerly named Pseudomonas pseudoal- cucurbit weeds and volunteer reservoir hosts. Complete
caligenes subsp. citrulli). This bacterium is a Gram- resistance is not yet available for watermelon. Rotate
negative rod having a single polar flagellum, is nonflu- out of cucurbit crops for at least 3 years. Reduce or
orescent in culture, and forms white colonies. When eliminate the use of sprinkler irrigation. For transplant
inoculated into tobacco leaves, this pathogen generally greenhouses, practice good sanitation, reduce humidity
causes a hypersensitive reaction. However, some strains levels, reduce sprinkler irrigation, and remove sympto-
are not able to cause the tobacco hypersensitivity matic plants and surrounding trays. Accept and plant
reaction, and infect watermelon seedlings but not fruit. transplants that do not show symptoms of the disease.
Copper sprays provide some control.
Disease cycle
The pathogen is seedborne in many cucurbit species and References
can therefore be present when seedlings germinate in Frankle, W. G., Hopkins, D. L., and Stall, R. E. 1993. Ingress of
the field or in transplant greenhouses. Warm tempera- watermelon fruit blotch bacterium into fruit. Plant Disease
77:1090–1092.
tures and high humidity favor disease development.
Hopkins, D. L. and Thompson, C. M. 2002. Seed transmission
Splashing water from rain and sprinkler irrigation of Acidovorax avenae subsp. citrulli in cucurbits. HortScience
spread the bacteria from plant to plant. Environmental 37:924–926.
conditions inside transplant greenhouses are particu- Isakeit, T., Black, M. C., Barnes, L. W., and Jones, J. B. 1997.
First report of infection of honeydew with Acidovorax avenae
larly favorable for this disease. The bacterium infects subsp. citrulli. Plant Disease 81:694.
immature fruit through stomata, and young fruit Latin, R. X. and Hopkins, D. L. 1995. Bacterial fruit blotch of
apparently are most susceptible to infection. It appears watermelon: the hypothetical exam question becomes reality.
that the bacterium can infect fruit pulp and seeds if it
Latin, R., Tikhonova, I., and Rane, K. 1995. Factors affecting the
enters through blossoms early in fruit development. The survival and spread of Acidovorax avenae subsp. citrulli in
pathogen survives in infested crop residues and fruit watermelon transplant production facilities. Phytopathology
rinds, and on diseased volunteer and weed cucurbits. 85:1413–1417.
Lovic, B. R. and Hopkins, D. L. 2003. Production steps to reduce Erwinia tracheiphila

seed contamination by pathogens of cucurbits.
HortTechnology 13:50–54. BACTERIAL WILT
Rane, K. K. and Latin, R. X. 1992. Bacterial fruit blotch of
watermelon: association of the pathogen with seed. Plant Introduction and significance
Disease 76:509–512.
Bacterial wilt is a serious disease of cucurbits such as
Rushing, J. W., Keinath, A. P., and Cook, W. P. 1999. Postharvest
development and transmission of watermelon fruit blotch. cucumbers and muskmelons, while it is less of a concern
HortTechnology 9:217–219. on various other cucurbit crops. The disease is more
Somodi, G. C., Jones, J. B., Hopkins, D. L., Stall, R. E., important in North America than in Europe.
Kucharek, T. A., Hodge, N. C., and Watterson, J. C. 1991.
Occurrence of a bacterial watermelon fruit blotch in Florida.
Plant Disease 75:1053–1056. Symptoms and diagnostic features
Sowell, G., Jr. and Schaad, N. W. 1979. Pseudomonas Initial symptoms consist of the wilting of a few to
pseudoalcaligenes subsp. citrulli on watermelon: seed
several leaves along a stem. As disease develops, the
transmission and resistance of plant introductions. Plant
Disease Reporter 63:437–441. foliage will exhibit extensive wilting. The wilting can
Walcott, R. R., Gitaitis, R. D., and Castro, A. C. 2003. Role of occur on individual runners or stems, or throughout an
blossoms in watermelon seed infestation by Acidovorax entire plant’s foliage. Wilting foliage takes on a dark
avenae subsp. citrulli. Phytopathology 93:528–534.
green color, but later can become chlorotic and then
Willems, A., Goor, M., Thielemans, S., Gillis, M., Kersters, K.,
and De Ley, J. 1992. Transfer of several phytopathogenic necrotic. In advanced stages of the disease the entire
Pseudomonas species to Acidovorax as Acidovorax avenae plant will collapse and die (268). Sticky strands of
subsp. avenae subsp. nov., comb. nov., Acidovorax avenae
subsp. citrulli, Acidovorax avenae subsp. cattleyae, and
bacterial ooze can be observed when the cut ends of
Acidovorax konjaci. International Journal of Systematic symptomatic stems are slowly drawn apart (269).
Bacteriology 42:107–119. Squash fruit can be infected and show small, irregular
water-soaked areas on the fruit surface.
268
268 Collapsing oriental melon vines caused by bacterial wilt.

C UCURBITACEAE 223
269
Disease cycle
The complete epidemiology of bacterial wilt has not yet
been determined. The pathogen is apparently not
seedborne, nor does it survive in soil beyond 2 or 3
months. In contrast to earlier studies, it now appears
that the pathogen does not persist within the insect
vector’s intestinal tract. The initial inoculum of bacterial
wilt, therefore, is not known. Infected weed or
volunteer cucurbit hosts may be the source of inoculum
from which insects become infested. The pathogen may
survive in dried plant tissues for a limited time.
Control
Plant resistant cultivars as they become available.
269 Bacterial strands extending from cut ends of melon Control the vector insects by applying systemic insecti-
stem infected with bacterial wilt. cides to the soil or contact insecticides to host plants.
References
Leach, J. G. 1964. Observations on cucumber beetles as vectors
Causal agent of curcurbit wilt. Phytopathology 54:606–607.
Main, C. E. and Walker, J. C. 1971. Physiological responses of
The cause of bacterial wilt is the Gram-negative
susceptible and resistant cucumber to Erwinia tracheiphila.
bacterium Erwinia tracheiphila, which is classified Phytopathology 61:518–522.
in the Erwinia amylovora taxonomic group. This
pathogen differs from most Erwinia species in that E.
tracheiphila does not liquefy gelatin, shows weak action
in milk, does not reduce nitrates, and does not metabo-
lize inorganic nitrogen sources. This pathogen is host
specific to the Cucurbitaceae. Erwinia tracheiphila is
mechanically transmitted by a number of insects,
primarily the striped cucumber beetle (Acalymma
vittatum) and the spotted cucumber beetle (Diabrotica
undecimpunctata). Insects that are in contact with and
feed on diseased plant tissue become contaminated with
the pathogen. These insects move to other plants and
inoculate them when their infested mouthparts feed on
the plants. The bacteria enter the xylem via these
feeding wounds and become systemic within the plant.
Wilting occurs when the multiplying bacteria and
resulting resins plug the vascular tissue of the host plant.
This disease develops most rapidly in young, succulent
cucurbit plants.
Pseudomonas syringae pv. lachrymans Causal agent

ANGULAR LEAF SPOT The pathogen is the aerobic, Gram-negative bacterium
Pseudomonas syringae pv. lachrymans, strains of which
Introduction and significance are host specific to cucurbit plants. When cultured on
Angular leaf spot occurs on cucurbits throughout the Kings medium B, this organism produces a diffusible
world and is particularly serious in more humid, pigment that fluoresces blue under ultraviolet light.
warmer regions. The disease can be severe on cucumber Other Pseudomonas pathogens affect the cucurbit
grown outside in fields, but is less commonly found on group of plants, though in many reports it is not clear
cucurbits grown inside greenhouses. exactly which species and pathovars are involved.
Recently a Pseudomonas disease has been reported on
Symptoms and diagnostic features cantaloupe in Europe. The pathogen is a pathovar of P.
Initial symptoms occur on leaves and consist of small, syringae and causes necrotic leaf spots with water-
irregularly shaped, water-soaked to gray-colored soaked margins, stem and petiole cankers, and sunken
lesions. As these lesions expand, they become angular fruit lesions. Fruit infection can cause immature fruit to
in shape as the lesion edges become delimited by leaf drop and more mature fruit to develop dry rot cavities.
veins (270). On some cultivars the lesions can be sur- The bacterium is also pathogenic to sugar beet and
rounded by chlorotic borders. As lesions age they turn therefore may be P. syringae pv. aptata. Another
tan to gray and become dry. The dried tissue often tears bacterium, P. syringae pv. syringae, is reported to also
and falls out, resulting in a ‘shot hole’ or tattered cause disease on cantaloupe and squash in the USA.
appearance (271). If conditions are wet or humid,
bacterial exudates can ooze onto lesion surfaces and dry Disease cycle
into a white residue. Lesions and bacterial ooze can also This pathogen is internally seedborne, which results in
develop on petioles and stems. infection of the seedling cotyledons upon germination.
Early symptoms of fruit infections consist of typically Bacteria are splashed from plant to plant by splashing
oval to circular lesions that are small (1 to 5 mm in water from rain and sprinkler irrigation. Insects and
diameter) and water-soaked. The water-soaked appear- physical contact from passing equipment and har-
ance can later turn into a brown discoloration of fruit vesters can also spread the pathogen. Warm, humid
tissues. Exudates sometimes collect on these fruit spots. conditions favor disease development. Optimum tem-
Lesions can later develop into deep internal rots; such peratures for disease development are 24–28° C,
infections, along with the activity of secondary decay though the pathogen can survive at higher (36° C) tem-
organisms, result in unmarketable fruit. peratures. The pathogen can also survive in the soil on
infested plant residues for perhaps up to 2 years.
270 271
F UNGAL D ISEASES
270 Leaf lesions of angular leaf spot on cucumber. 271 Advanced symptoms of angular leaf spot on
cucumber.
C UCURBITACEAE 225

Use seed that does not have significant levels of the Initial symptoms usually occur 10 to 15 days before
pathogen. Seed treatments for this disease usually fruit maturity. Foliage rapidly turns a lime green, then
consist of hot water that has been acidified, or heated bright yellow. Plants show stunted growth and eventual
zinc or manganese sulfate solutions. Rotate crops so decline. Older leaves can be blighted or burned in
that seed and fruit production plantings are placed in appearance, and younger leaves on vine tips can curl
fields that have not had cucurbits for 2 years. Do not and not properly expand. A characteristic symptom is
use overhead sprinkler irrigation. Conduct production the gold to honey-brown-colored phloem in the main
and harvesting procedures only when the foliage is dry. roots and crowns of diseased plants. In advanced stages
Use resistant cultivars if they are available. The appli- of CYVD, the root systems will rot; however, this is
cation of copper sprays may also be useful. Do not over thought to be due to secondary decay organisms in the
fertilize the crop with high nitrogen fertilizers, as soil. In Oklahoma, watermelon and cantaloupe fields
excessive nitrogen may increase disease severity, espe- that are planted before 15 June show the greatest
cially on younger leaves. disease severity.
In some cases, at the time of flowering and fruit set,
References plants will not turn chlorotic but instead will wilt and
Grogan, R. G., Lucas, L. T., and Kimble, K. A. 1971. Angular collapse in a day or two. Fruit appear normal in shape,
leaf spot of cucumber in California. Plant Disease Reporter but in the case of watermelon the fruit lose their green
55:3–6.
color and become unmarketable. Because this
Hopkins, D. L. and Schenck, N. C. 1972. Bacterial leaf spot of
watermelon caused by Pseudomonas lachrymans. bacterium is vectored by an insect, symptoms often
Phytopathology 62:542–545. appear in aggregated small patches or along the edges
Kritzman, G. and Zutra, D. 1983. Survival of Pseudomonas of fields; such patterns are related to the movement of
syringae pv. lachrymans in soil plant debris, and the
rhizosphere of nonhost plants. Phytoparasitica 11:99–108. the insect.
Langston, D. B., Jr., Sanders, F. H., Brock, J. H., Gitaitis, R. D.,
Flanders, J. T., and Beard, G. H. 2003. First report of a field Causal agent
outbreak of a bacterial leaf spot of cantaloupe and squash
caused by Pseudomonas syringae pv. syringae in Georgia.
The pathogen is the aerobic, rod shaped, Gram-
Plant Disease 87:600. negative bacterium Serratia marcescens that inhabits
Morris, C. E., Glaux, C., Latour, X., Gardan, L., Samson, R., and the phloem tissue of cucurbit hosts. The pathogen can
Pitrat, M. 2000. The relationship of host range, physiology, be isolated by grinding phloem tissue in buffer and then
and genotype to virulence on cantaloupe in Pseudomonas
syringae from cantaloupe blight epidemics in France. streaking the resulting suspension onto potato dextrose
Phytopathology 90:636–646. agar, nutrient agar, or purple agar. The bacterium can
be maintained on nutrient agar. This bacterium is
vectored by the squash bug (Anasa tristis).
Serratia marcescens Serratia marcescens is interesting in that strains of
CUCURBIT YELLOW VINE this bacterium are found in a number of diverse envi-
DISEASE ronments. On plants, S. marcescens is a non-pathogen-
ic endophyte in cotton and rice, a crown rot pathogen
Introduction and significance of alfalfa and sainfoin (Onobrychis vicifolia), and now
A relatively newly discovered disease, cucurbit yellow an important cucurbit pathogen. Other strains cause
vine disease (CYVD) was first seen on squash and disease in insects, are opportunistic pathogens on
pumpkin plantings in the USA (Oklahoma, Texas) in humans, and inhabit water and soil ecosystems. Unlike
1988. The disease has since been documented in other many other S. marcescens strains, cucurbit strains do
F UNGAL D ISEASES
states in the southeastern USA as well as in not produce the red prodigiosin pigment. While genetic
Massachusetts. Levels of damage vary, but CYVD can analysis shows that the cucurbit strains are
cause extensive crop loss to cantaloupe, pumpkin, S. marcescens, other experiments show that the
squash, and watermelon. cucurbit strains form a distinct group and differ from
other non-CYVD strains in biochemical and physio-
logical aspects.
The host range of this cucurbit pathogen has not yet Acremonium cucurbitacearum,
been determined. Researchers found, however, that the Fusarium spp., Phytophthora spp., Pythium spp.,
S. marcescens endophyte strains from rice were not Rhizoctonia solani, Rhizopycnis vagum
pathogenic to cucurbits. DAMPING-OFF, ROOT ROTS
Disease cycle Introduction and significance

The disease epidemiology of CYVD has not been deter- A number of soilborne pathogens cause seed and
mined. There is no evidence that the pathogen is seedling diseases of cucurbits. Pathogens include species
seedborne. It appears that the squash bug vector is the of Acremonium, Fusarium, Phytophthora, Pythium,
most important factor in pathogen survival and distri- Rhizoctonia, and Rhizopycnis. Some of these patho-
bution. Overwintering populations of this insect can gens are also implicated in the vine decline complex that
transmit the pathogen to new crops in the spring. affects mature plants.

Manage the squash bug vector by spraying insecticides, These diseases have various phases. Cucurbit seeds can
plowing down old cucurbit plantings, and removing be infected prior to germination and result in seed
vegetation habitats that might help the insect over- death. Newly germinated seedlings can be infected to
winter. such a degree that plants do not emerge above the soil
(pre-emergence damping-off). Finally, seedlings might
References emerge from the ground but become diseased after soil
Avila, F. J., Bruton, B. D., Fletcher, J., Sherwood, J. L., Pair, S. D., emergence (post-emergence damping-off) (272). Initial
and Melcher, U. 1998. Polymerase chain reaction detection symptoms of post-emergence damping-off generally
and phylogenetic characterization of an agent associated with
yellow vine disease of cucurbits. Phytopathology consist of yellow or light tan to dark brown lesions of
88:428–436. the root and hypocotyl tissues (273). With time the
Bruton, B. D., Fletcher, J., Pair, S. D., Shaw, M., and Sittertz- hypocotyl shrivels, roots decay further, and the cotyle-
Bhatkar, H. 1998. Association of a phloem-limited bacterium
with yellow vine disease in cucurbits. Plant Disease
dons and leaves wilt and collapse. Some pathogens
82:512–520. initially attack the tissue where the seed coat is in
Bruton, B. D., Mitchell, F., Fletcher, J., Pair, S. D., Wayadande, contact with the hypocotyl after germination.
A., Melcher, U., Brady, J., Bextine, B., and Popham, T. W. Damping-off diseases often result in death of the
2003. Serratia marcescens, a phloem-colonizing, squash bug-
transmitted bacrerium: causal agent of cucurbit yellow vine seedling and subsequent reduction of plant stands
disease. Plant Disease 87:937–944. (274). However, even if plants do not succumb to these
Lukezic, F. L., Hildebrand, D. C., Schroth, M. N., and Shinde, P. pathogens, the surviving plant may be stunted and
A. 1982. Association of Serratia marcescens with crown rot of
alfalfa in Pennsylvania. Phytopathology 72:714–718.
delayed in development.
Pair, S. D., Bruton, B. D., Mitchell, F., Fletcher, J., Wayadande, Older, mature plants can also be attacked by these
A., and Melcher, U. 2004. Overwintering squash bugs harbor seedling pathogens. The feeder roots of mature plants
and transmit the causal agent of cucurbit yellow vine disease. will discolor and turn a water-soaked, tan to brown
Journal of Economic Entomology 97:74–78.
Rascoe, J., Berg, M., Melcher, U., Mitchell, F. L., Bruton, B. D.,
color. The root tissue becomes soft and can slough
Pair, S. D., and Fletcher, J. 2003. Identification, phylogenetic away. Upper taproot and lower stem tissue in contact
analysis, and biological characterization of Serratia with the soil can become first gray-green, then brown to
marcescens strains causing cucurbit yellow vine disease.
Phytopathology 93:1233–1229. red-brown, soft in texture, and rotted. Fruit in contact
with the soil develop irregularly shaped, water-soaked
to brown lesions. These fungi, along with Verticillium
F UNGAL D ISEASES
dahliae, are implicated in the vine decline disease that is

caused by a complex of fungi.
C UCURBITACEAE 227
Causal agents 272

Acremonium cucurbitacearum produces conidiophores
that are simple, awl-shaped, erect monophialides
measuring 13–54 μm long. Conidia collect in slimy
aggregations and are usually one-celled, hyaline, oblong
to cylindrical, and measure 5–7.5 x 2–4 μm. This
pathogen produces chlamydospores that allow it to
survive in the soil. Optimum disease development
occurs at 24–27° C, though infection takes place over a
broader temperature range (12-30° C).
Fusarium equiseti and F. solani can cause seedling
diseases of cucurbits. However, even Fusarium wilt 272 Muskmelon seedlings affected by Pythium
pathogens (various forma speciales of F. oxysporum), damping-off.
may sometimes cause damping-off. Fusarium species
have branched or unbranched conidiophores that have 273 Rhizoctonia 273
phialides as conidiogenous cells. Phialides produce root rot on young
either small, one- to two-celled microconidia or larger, watermelon
fusoid, curved, multicelled macroconidia. Macro- seedlings.
conidiophores grow in clustered groups called sporo-
dochia. Resilient chlamydospores enable Fusarium
species to survive for long periods of time in the soil.
Phytophthora and Pythium species belong in the
oomycete group of organisms. Phytophthora drechsleri
has been reported to cause seedling damping-off.
A number of Pythium species cause damping-off:
P. aphanidermatum, P. irregulare, P. myriotylum,
P. ultimum. All these pathogens survive in the soil as
saprophytes and are favored by wet soil conditions.
With the exception of P. ultimum, these organisms
usually produce zoospores that swim to and infect sus-
ceptible tissues. Sexual structures (antheridia, oogonia,
and oospores) are produced by all species. In addition
to cucurbits, these pathogens can infect numerous other
plants.
274
Rhizoctonia solani is a soilborne fungus with a very
broad host range. R. solani has no asexual fruiting
structures or spores, but produces characteristically
coarse, brown, right-angle branching hyphae. The
hyphae are distinctly constricted at branch points, and
cross walls with dolipore septa are deposited just after
the branching. Hyphal cells are multi-nucleate. Small,
tan to brown loosely aggregated clumps of mycelia
F UNGAL D ISEASES
function as sclerotia. This fungus can survive by

infecting and thriving on a great number of plant hosts,
besides cucurbits, and can also persist in the soil as
a saprophyte. The teleomorph stage, Thanatephorus 274 Watermelon seedlings affected by Pythium
cucumis, is not commonly observed. damping-off.
Disease cycle Cladosporium cucumerinum

Most of these soilborne pathogens survive in fields for SCAB
indefinite amounts of time. Wet soil conditions and cool
temperatures (15–20° C) generally favor these fungi Introduction and significance
and their ability to grow and infect host cucurbits. Scab can be an important foliar and fruit disease in
However, for pathogens such as Fusarium, Pythium some regions of the world, and losses can sometimes
aphanidermatum and Pythium myriotylum, warmer exceed 50%. The disease affects most cucurbit crops,
soil conditions (32–37° C) are favorable. Seedlings are although resistant cultivars have made scab less
the most susceptible to infection, though these patho- important for cucumber production.
gens can infect the feeder roots of mature plants.
Control Initial symptoms on leaves consist of water-soaked, pale
Control damping-off by creating conditions unfavor- green lesions that are irregularly shaped. As the disease
able for the pathogens. For transplant production, develops, lesions enlarge, turn gray to brown in color
practice good sanitation (keep growing areas and (275). Eventually the inner tissue of the lesion breaks
benches clean, use either new or thoroughly disinfected and falls out, resulting in irregularly shaped holes and
trays, do not reuse rooting media). Plant on raised beds tears in the leaf (276). Leaf lesions may also have
and in well draining soils so that overly wet soil condi- chlorotic borders around them. If newly expanded
tions are avoided. Carefully irrigate so that excess water leaves are infected with numerous lesions, the leaves
is not applied. Plant fungicide-treated seed, and avoid may twist and become deformed. Lesions on petioles
planting seed too deeply, which delays seedling and stems tend to be more elongated in shape but have
emergence and increases the chance of infection. Post- the same initially water-soaked, then brown, color.
plant fungicides may provide control for some of these Under humid conditions, the leaf, petiole, and stem
pathogens. Avoid planting too soon into fields that still lesions can be covered with the powdery, dark green
have extensive crop residue in the soil. Some rotation fungal growth of the pathogen. Severe infection and
crops can exacerbate the damping-off problems for subsequent profuse production of conidia can result in
cucurbits. If melons are planted after cotton, root rot allergic reactions in sensitive individuals.
caused by F. equiseti can be severe; melons following The greatest economic impact of scab is on the fruit
alfalfa might have increased Pythium problems. (277, 278). Fruit infections begin as minute (2–4 mm ),
greasy looking, sunken specks on the fruit surface.
References These enlarge, become circular to oval in shape, gray in
Adams, G. C., Gubler, W. D., and Grogan, R. G. 1987. Seedling color, and remain sunken. Dark green sporulation may
disease of muskmelon and mixed melons in California caused appear on the lesions, and such fruit lesions often ooze
by Fusarium equiseti. Plant Disease 71:370–374.
sticky exudates, hence the use of the additional name of
Aegerter, B. J., Gordon, T. R., and Davis, R. M. 2000.
Occurrence and pathogenicity of fungi associated with melon ‘gummosis’ for this disease. In severe cases, the lesions
root rot and vine decline in California. Plant Disease will coalesce and form large sunken craters and cavities.
84:224–230.
Secondary decay organisms will colonize infected fruit
Armengol, J., Vicent, A., Martínez-Culebras, P., Bruton, B. D.,
and García-Jiménez, J. 2003. Identification, occurrence and tissue and contribute further to fruit rot.
pathogenicity of Rhizopycnis vagum on muskmelon in Spain.
Plant Pathology 52:68–73. Causal agent
Garcia-Jimenez, J., Velacruz, M. T., Jorda, C., and Alfaro-Garcia,
A. 1994. Acremonium species as the causal agent of
Scab is caused by the fungus Cladosporium cucumer-
muskmelon collapse in Spain. Plant Disease 78:416–419. inum. Cultures appear olivaceous brown to greenish
F UNGAL D ISEASES
black at maturity. Conidia form in long, acropetal

chains and are branched and olive-brown in color.
Lower conidia are larger, have one or two septa, and are
called ramoconidia. Upper conidia are smaller, one-
celled, ellipsoidal to cylindrical to fusiform, and
measure 4–9 x 3–5 μm. Another Cladosporium species,
C UCURBITACEAE 229
275 276
275 Leaf spots of scab on squash. 276 Tattered leaf symptoms of scab on squash.
C. tenuissimum, has been associated with small 277 Fruit lesions 277
(3 mm in diameter), circular swellings on cucumber of scab on yellow
fruit grown in Israel. squash.
Disease cycle
The scab pathogen can survive on old crop residues and
other organic matter in the soil. Survival in some cases
can reach up to 3 years. Conidia are dispersed long
distances in the air, land on susceptible tissues, and
germinate and infect the host if conditions are
favorable. The pathogen requires 100% relative
humidity or free moisture for infection. Optimum tem-
peratures for the fungus are between 17–27° C, though
growth can occur in the range of 5–30° C. The
pathogen may be seedborne.
Control
Plant resistant cultivars if available. Rotate crops so that
2 or more years pass between susceptible cucurbit 278
crops. Use seed that does not have significant levels of
the pathogen. Avoid using sprinkler irrigation. Some
fungicides may provide control if applied prior to fruit
development.
References
Batta, Y. A. 2004. Cladosporium tenuissimum Cooke
(Deuteromycotina: Hyphomycetes) as a causal organism of
new disease on cucumber fruits. European Journal of Plant
F UNGAL D ISEASES
Pathology 110:1003–1009.
Crossan, D. F. and Sasser, J. M. 1969. Effect of rotation with corn
on cucurbit scab. Plant Disease Reporter 53:452–453.
McKemy, J. M. and Morgan-Jones, G. 1992. Studies in the genus
Cladosporium sensu lato. VII. Concerning Cladosporium
cucumerinum, causal organism of crown blight and scab or
gummosis of cucurbits. Mycotaxon 43:163–170. 278 Fruit lesions of scab on immature zucchini squash.
Didymella bryoniae Causal agent

(anamorph = Phoma cucurbitacearum) Gummy stem blight is caused by the fungus Didymella
GUMMY STEM BLIGHT, bryoniae. In older references the fungus is referred to as
BLACK ROT Mycosphaerella melonis. Didymella bryoniae forms
dark, ostiolate pseudothecia that have bitunicate asci.
Introduction and significance Each ascus contains eight ascospores that are hyaline,
Gummy stem blight is one of the most important oval, one-septate, and measure 14–18 x 4–7 μm.
diseases of cucurbits and affects leaves, stems, and fruits Ascospores have constrictions at the septa, and the
of most of these species. If environmental conditions upper cell is wider than the lower cell. The anamorph,
favor disease development, significant damage can Phoma cucurbitacearum, is usually more commonly
occur to susceptible crops. Greenhouse-grown found in the diseased tissue. Pycnidia of P. cucur-
cucumbers are also affected. bitacearum produce conidia that are hyaline, cylindri-
cal, are often one-septate, and measure 6–13 x 2–4 μm.
Symptoms and diagnostic features Researchers have found that some isolates are more
Early leaf symptoms consist of circular, water-soaked to virulent than others, showing that there is some
gray green spots on cotyledons and true leaves. Such diversity within pathogen populations.
spots enlarge quickly, can become irregular in shape,
and turn tan to dark brown. When spots coalesce, the Disease cycle
entire leaf can become blighted. Leaf spots can be The fungus can survive in the soil and on crop residue.
colonized with the small, dark fruiting bodies (pycnidia) Studies indicate that the pathogen can persist in fields
of the fungus perfect stage (279). Stem infections consist for 2 years without a host. Rains and winds blow
of oblong water-soaked lesions that later turn brown to ascospores or conidia from inoculum sources onto new
dark brown (280). As disease develops, such infections crops. The fungus is most damaging with warm, moist
turn into cankers that can girdle the entire stem and weather, and optimum conditions for infection include
result in wilting of the attached foliage and death of the free moisture and temperatures in the 20–24° C range.
seedling or plant. A brown, sticky exudate often oozes The pathogen may be seedborne, resulting in diseased
from stem cankers. Stem infections also support the seedlings and transplants. Fruit can rot 2–3 days after
development of pycnidia. On occasion, leaf and stem first becoming infected.
lesions contain the structures of the perfect stage
(pseudothecia) of the pathogen. In greenhouses, Control
cucumber plants are often first infected on the cut stubs To reduce soilborne inoculum, rotate crops on a 2-year
left where fruit were harvested or shoots were pruned. cycle without cucurbit hosts. Apply protectant fungi-
Lesions on these cut stubs can expand and girdle the cides; such chemicals are especially needed to protect
entire stem. wounds that function as infection sites. Note that there
On fruit (281, 282), the disease is called black rot are reports of the apparent failure of a strobilurin
and initially appears as water-soaked, dark green fungicide to control the disease, indicating that resistant
circular spots. Spots expand, darken, and have pycnidia isolates are present. In the USA, a disease forecasting
and pseudothecia in the lesion centers. Depending on program (Melcast) has been used to schedule fungicide
the crop species, the fruit rot may eventually take on a applications for controlling gummy stem blight and
black color. If stored under humid conditions, fruit anthracnose of melons.
lesions may develop a white, cottony mycelial growth. Use seed that does not have significant levels of the
Older fruit lesions can become leathery in texture and pathogen. Carefully examine transplants and remove
F UNGAL D ISEASES
cracked. Infected, rotted fruit enables the pathogen to diseased plants. Greenhouse production of transplants
become seedborne. Black rot can be severe on Hubbard or crops should include increased ventilation and
pumpkin and butternut, acorn, and buttercup squashes. reduced sprinkler irrigation. Avoid injuring fruit before
or during harvest, as wounds enable the pathogen to
enter fruit during storage.
C UCURBITACEAE 231
279 281
279 Leaf spot of gummy stem blight on cucumber. 281 Black rot fruit lesions on butternut squash.
280 282
280 Stem lesion of gummy stem blight on cucumber. 282 Cut cantaloupe showing black rot lesions.
References
Arny, C. J. and Rowe, R. C. 1991. Effects of temperature and Somai, B. M., Dean, R. A., Farnham, M. W., Zitter, T. A., and
duration of surface wetness on spore production and Keinath, A. P. 2002. Internal transcribed spacer regions 1 and
infection of cucumbers by Didymella bryoniae. 2 and random amplified polymorphic DNA analysis of
Phytopathology 81:206–209. Didymella bryoniae and related Phoma species isolated from
Gleason, M. L., Parker, S. K., Pitblado, R. E., Latin, R. X., cucurbits. Phytopathology 92:997–1004.
Speranzini, D., Hazzard, R. V., Maletta, M. J., Cowgill, W. P., Svedelius, G. 1990. Effects of environmental factors and leaf age
and Biederstedt, D. L. 1997. Validation of a commercial on growth and infectivity of Didymella bryoniae.
system for remote estimation of wetness duration. Plant Mycological Research 94:885–889.
Disease 81:825–829. Utkhede, R. S. and Koch, C. A. 2002. Chemical and biological
Keinath, A. P. and DuBose, V. B. 2004. Evaluation of fungicides treatments for control of gummy stem blight of greenhouse
for prevention and management of powdery mildew on cucumbers. European Journal of Plant Pathology
watermelon. Crop Protection 23:35–42. 108:443–448.
Keinath, A. P., Farnham, M. W., and Zitter, T. A. 1995. van Steekelenburg, N. A. M. 1982. Factors influencing external
Morphological, pathological, and genetic differentiation of fruit rot of cucumber caused by Didymella bryoniae.
Didymella bryoniae and Phoma sp. isolated from cucurbits. Netherlands Journal of Plant Pathology 88:47–56.
F UNGAL D ISEASES
van Steekelenburg, N. A. M. 1985. Influence of humidity on

Kothera, R. T., Keinath, A. P., Dean, R. A., and Farnham, M. W. incidence of Didymella bryoniae on cucumber leaves and
2003. AFLP analysis of a worldwide collection of Didymella growing tips under controlled conditions. Netherlands
bryoniae. Mycological Research 107:297–304. Journal of Plant Pathology 91:277–283.
St. Amand, P. C. and Wehner, T. C. 1995. Eight isolates of Zhang, J. X., Bruton, B. D., Miller, M. E., and Isakeit, T. 1999.
Didymella bryoniae from geographically diverse areas exhibit Relationship of developmental stages of cantaloupe fruit to
variation in virulence but no isolate by cultivar interaction on black rot susceptibility and enzyme production by Didymella
Cucumis sativus. Plant Disease 79:1136–1139. bryoniae. Plant Disease 83:1025–1032.
Erysiphe cichoracearum Causal agents

(= Golovinomyces cichoracearum), There are two main powdery mildew pathogens that
Sphaerotheca fuliginea (= Podosphaera xanthii), infect cucurbits: Sphaerotheca fuliginea and Erysiphe
Leveillula taurica (anamorph = Oidiopsis taurica) cichoracearum. Both of these species produce a whitish,
POWDERY MILDEW epiphytic mycelium that grows superficially on host
surfaces. Conidiophores of both species are borne on
Introduction and significance this surface mycelium. For E. cichoracearum, conidia
Most of the various cucurbit crops are susceptible to are produced in long chains, are hyaline, ellipsoid to
powdery mildew, which is a prevalent foliar disease barrel-shaped, and measure 25–45 x 14–25 μm. Edge
worldwide. If not managed, this disease can cause early line shapes of immature conidial chains are sinulate,
plant senescence and reduction in yields. Several and conidia lack fibrosin bodies. Erysiphe cichora-
powdery mildew fungi infect the cucurbits. cearum conidia germinate with straight germ tubes and
unlobed appressoria. Cleistothecia are not commonly
Symptoms and diagnostic features observed but are globose, have numerous hypha-
The first sign of the pathogen is the white, powdery like appendages, and contain up to 10–25 unitunicate
growth of the fungus that occurs on both top and asci. Asci contain two ascospores that are ovoid to
bottom leaf surfaces and on petioles and stems (283). ellipsoid. Recently researchers have reclassified E.
Older, lower leaves are the first leaves to show infection cichoracearum and recommend the name Golovino-
(284). Powdery mildew leaf colonization can cause the myces cichoracearum.
underlying leaf tissue to turn chlorotic and later The conidia of S. fuliginea are produced in long
necrotic. In severe cases, the entire leaf can be covered chains, are hyaline, ellipsoid to barrel-shaped, and
with the white growth, turn brown, and die. Severely measure 25–37 x 14–25 μm. Edge line shapes are
infected plants can be stunted, have smaller fruit and crenate, and freshly produced conidia contain fibrosin
reduced yields, and senesce early. Loss of foliage can bodies. Sphaerotheca fuliginea conidia germinate by
result in sunburned fruit because of exposure to direct producing forked germ tubes but no appressoria.
sunlight. Fruit are rarely colonized. Cleistothecia are rare and are globose, have numerous
hypha-like appendages, and contain a single unitunicate
ascus. Asci contain eight ascospores that are ovoid to
ellipsoid. Sphaerotheca fuliginea appears to be more
prevalent worldwide on cucurbits. This pathogen has
recently been reclassified as Podosphaera xanthii.
283 284
F UNGAL D ISEASES
283 Powdery mildew sporulation on squash leaf. 284 Older squash foliage infected by powdery mildew.
Healthy leaf on right.
C UCURBITACEAE 233
While both S. fuliginea and E. cichoracearum are References

reported as having broad host ranges, these are El-Ammari, S. S. and Khan, M. W. 1983. Leveillula taurica on
complex organisms, and sub-populations within each greenhouse cucumber in Libya. Plant Disease 67:553–555.
Epinat, C., Pitrat, M., and Bertrand, F. 1993. Genetic analysis of
species are probably host specific to various plant
resistance of five melon lines to powdery mildews. Euphytica
groups. Therefore the S. fuliginea and E. cichoracearum 65:135–144.
isolates that infect cucurbits most likely do not infect Keinath, A. P. and DuBose, V. B. 2004. Evaluation of fungicides
non-cucurbit plants, and vice versa. On melons, the for prevention and management of powdery mildew on
watermelon. Crop Protection 23:35–42.
S. fuliginea pathogen has five described races, and
Kiss, L. and Szentivanyi, O. 2001. Infection of bean with
E. cichoracearum has two described races. cucumber powdery mildew, Podosphaera fusca. Plant
Some cucurbit crops (such as cucumber) are also sus- Pathology 50:411.
ceptible to a third powdery mildew fungus, Leveillula Kobori, R. F., Suzuki, O., Wierzbicki, R., Della Vecchia, P. T., and
Camargo, L. E. A. 2004. Occurrence of Podosphaera xanthii
taurica (anamorph: Oidiopsis taurica). However, this Race 2 on Cucumis melo in Brazil. Plant Disease 88:1161.
particular fungus, which is an endophytic powdery McGrath, M. T. 2001. Fungicide resistance in cucurbit powdery
mildew species, is of minor economic importance for mildew: experiences and challenges. Plant Disease
85:236–245.
cucurbit production. The fungus causes chlorotic, vein-
McGrath, M. T. and Shishkoff, N. 2003. First report of the
delimited leaf lesions; profuse white sporulation cucurbit powdery mildew fungus (Podosphaera xanthii)
develops on the undersides of these angular spots. resistant to strobilurin fungicides in the United States. Plant
Disease 87:1007.
McGrath, M. T. and Staniszewska, H. 1996. Management of
Disease cycle powdery mildew in summer squash with host resistance,
As obligate pathogens, all powdery mildew species disease threshold-based fungicide programs, or an integrated
overwinter on volunteer or weed host plants that then program. Plant Disease 80:1044–1052.
serve as sources of initial inoculum. Greenhouse grown McGrath, M. T., Staniszewska, H., and Shishkoff, N. 1996.
Fungicide sensitivity of Sphaerotheca fuliginea populations in
cucurbits or cucurbit crops grown beyond the produc- the United States. Plant Disease 80:697–703.
tion region may also be sources of initial inoculum. McGrath, M. T., Staniszewska, H., Shishkoff, N., and Casella, G.
Conidia are wind blown for long distances. High 1996. Distribution of mating types of Sphaerotheca fuliginea
in the United States. Plant Disease 80:1098–1102.
relative humidity favors infection, though conidia can
Menzies, J., Bowen, P., Ehret, D., and Glass, A. D. M. 1992.
germinate and infect plants at 50% or lower relative Foliar applications of potassium silicate reduce severity of
humidity. Disease development is optimum at temper- powdery mildew on cucumber, muskmelon, and zucchini
atures of 20–27° C. Sphaerotheca development can be squash. Journal of the American Society for Horticultural
Science 117:902–905.
quite rapid, with germ tubes appearing within 2 hours, Romero, D., Rivera, M. E., Cazorla, F. M., De Vicente, A., and
conidiophores developing within 4 days after infection, Pérez-García, A. 2003. Effect of mycoparasitic fungi on the
and cleistothecia being produced after several weeks. development of Sphaerotheca fusca in melon leaves.
Mycological Research 107:64–71.
Reuveni, M., Agapov, V. and Reuveni, R. 1995. Suppression of
Control cucumber powdery mildew (Sphaerotheca fuligena) by foliar
Plant resistant cultivars and apply protectant fungicides sprays of phosphate and potassium salts. Plant Pathology
44:31–39.
such as sulfur. Resistance to systemic fungicides has
Sowell, G., Jr. 1982. Population shift of Sphaerotheca fuliginea
been widespread for S. fuliginea. In some cases, on muskmelon from race 2 to race 1 in the southeastern
breeding programs did not recognize that cucurbit United States. Plant Disease 66:130–131.
powdery mildew was caused by different pathogens; Vakalounakis, D. J. and Klironomou, E. 1995. Race and mating
type identification of powdery mildew on cucurbits in Greece.
therefore, some early information regarding cultivar
resistance may not be reliable. Vakalounakis, D. J. and Klironomou, E. 2001. Taxonomy of
Golovinomyces on cucurbits. Mycotaxon 80:489–491.
F UNGAL D ISEASES
Fusarium oxysporum f. sp. cucumerinum, Symptoms and diagnostic features

f. sp. melonis, f. sp. niveum, f. sp. radicis-cucumerinum These three wilt diseases show a similar range of
FUSARIUM WILT, symptoms, though particular expressions of disease
FUSARIUM ROOT/STEM ROT vary depending upon the host, age of the plant, envi-
ronmental conditions, abundance of the pathogen in
Introduction and significance soil, and virulence of the prevalent strains.
Cucurbits are susceptible to several vascular wilt Seedlings can develop damping-off and lower stem
diseases caused by different formae speciales of the infections due to Fusarium wilt pathogens; high
Fusarium oxysporum fungus. Cucumber, melon (or damping-off incidence has been observed if watermelon
muskmelon), and watermelon are each subject to their is planted during warm weather and fields have high
own particular F. oxysporum pathogen. Squash appar- inoculum levels. However, the typical problem occurs
ently does not have its own specific F. oxysporum on older seedlings and further advanced plants.
pathogen, but can be infected by the watermelon Initial symptoms include dull green to gray-green
pathogen. coloring of foliage, yellowing of older leaves, and
temporary wilting of shoot tips and young leaves during
the warmer time of the day. Symptoms initially may be
285
one sided and only affect vines on a particular side of
the plant. As disease develops, a wilting symptom may
affect all leaves and shoots (285). Plants might be
stunted, show a stiff appearance, and suffer from poor
growth and reduced fruit set, while leaves become
necrotic, brown, and dried up. Fruit that are present
might become sunburned due to loss of functional
foliage that covers the fruit. The vines will subsequent-
ly collapse and die (286). Symptom expression may be
initiated, and most severe, when plants are stressed or
when fruit set and development are taking place. An
important diagnostic feature is the light to dark brown
to red-brown discoloration of the xylem tissue in the
285 Wilting of watermelon vines caused by Fusarium taproot, crown, and lower stem; however, on some
wilt. cultivars the vascular discoloration may be subtle or
absent. On occasion a longitudinal, necrotic lesion
286
occurs on the external surface of lower stems (287);
such lesions might be more common on muskmelon.
Causal agents
The pathogen morphology and colony characteristics
of these pathogens are similar to other F. oxysporum
fungi. The fungus forms one- or two-celled, oval to
kidney shaped microconidia on monophialides, and
three- to five-celled, fusiform, curved macroconidia.
Macroconidia are usually produced in cushion shaped
F UNGAL D ISEASES
structures called sporodochia. Resilient chlamydo-

spores are also formed. The pathogen is usually readily
isolated from symptomatic vascular tissue, though
semi-selective media like Komada’s medium can be
286 Advanced symptoms of Fusarium wilt of helpful to reduce interference from secondary rot
watermelon. organisms.
C UCURBITACEAE 235
287 Stem 287 the host via roots, colonize the xylem, and become sys-
symptoms caused temically distributed. Fusarium wilt is more severe if
by Fusarium wilt cucurbits are planted in sandy, porous soils that have
on cucumber. high nitrogen content and acidic pH values
(pH 5.0–6.0). Optimum soil temperatures for disease
development are between 20-27° C. Fusarium
oxysporum f. sp. melonis occurs early in the season in
cooler soils (18–22° C). After an infected plant dies or
is incorporated into the soil, the fungus produces
chlamydospores that are returned to the soil and
increase the pathogen population. Fungal propagules
are distributed whenever infested, contaminated soil is
moved by equipment, vehicles, and water. Fusarium
wilt severity increases when the host plant is stressed
due to unfavorable growing conditions such as temper-
ature extremes and heavy fruit loads.
Fusarium wilt of cucumber (Cucumis sativus) is Control

caused by F. oxysporum f. sp. cucumerinum. This Use resistant cultivars, when available. Note that the
pathogen primarily infects cucumber, though some performance of a resistant cultivar is influenced by the
isolates can infect watermelon and melon. Presently inoculum level in the soil. Grafting to resistant root-
three races have been documented. Melon and stocks (e.g. melon to Benincasa cerifera roots) has
muskmelon (both Cucumis melo plants) Fusarium wilt proven successful in combating Fusarium wilt. Use seed
is caused by F. oxysporum f. sp. melonis. Four races of that does not have significant levels of the pathogen.
this pathogen are currently recognized and are desig- Practice crop rotations so that pathogen populations
nated as 0, 1, 2, and 1–2. Fusarium oxysporum f. sp. are allowed to decline. In California, a 3-year rotation
niveum is the causal agent of Fusarium wilt of water- out of susceptible cucurbits is sufficient to avoid
melon (Citrullus lanatus). Three races (races 0, 1, and economic damage of the crop. Some soils show natural
2) are documented. While this pathogen is generally suppressiveness to these Fusarium pathogens. Fumi-
considered host specific to watermelon, there are gation of field soils can effectively lower soil popula-
several reports of isolates being able to infect cucumber, tions of the pathogen, though such soils may be
melon, and summer squash (Cucurbita pepo). re-invaded. Researchers found that F. oxysporum f. sp.
A different F. oxysporum pathogen causes a distinct melonis rapidly recolonized soils treated with various
disease called Fusarium root and stem rot. The patho- fumigants.
gen, F. oxysporum f. sp. radicis-cucumerinum, causes
tan to brown lesions at the plant crown and upper root References
areas. Affected plants grow poorly and can later Gerlagh, M. and Blok, W. 1988. Fusarium oxysporum f. sp.
collapse. This pathogen affects cucumber, muskmelon, cucurbitacearum n. f. embracing all formae speciales of F.
oxysporum attacking cucurbitaceous crops. Netherlands
squash, and other cucurbits. This disease is similar to Journal of Plant Pathology 94:17–31.
crown and root rot of tomato. Gordon, T. R., Okamoto, D., and Jacobson, D. J. 1989.
Colonization of muskmelon and nonsusceptible crops by
Fusarium oxysporum f. sp. melonis and other species of
Disease cycle Fusarium. Phytopathology 79:1095–1100.
F UNGAL D ISEASES
All wilt pathogens infecting cucurbits share very similar Gordon, T. R. and Okamoto, D. 1990. Colonization of crop
epidemiologies. The pathogens are true soilborne residue by Fusarium oxysporum f. sp. melonis and other
organisms and can persist in the soil for long periods of species of Fusarium. Phytopathology 80:381–386.
Gubler, W. D. and Grogan, R. G. 1976. Fusarium wilt of
time as saprobes. Chlamydospores also enable these muskmelon in the San Joaquin Valley, California. Plant
fungi to survive in the soil without a host. The Disease Reporter 60:742–744.
pathogens can be seedborne. Fusarium wilt fungi enter
Jenkins, S. F., Jr. and Wehner, T. C. 1983. Occurrence of Fusarium solani f. sp. cucurbitae
Fusarium oxysporum f. sp. cucumerinum on greenhouse- (teleomorph = Nectria haematococca)
grown Cucumis sativus seed stocks in North Carolina. Plant
Disease 67:1024–1025. FUSARIUM CROWN & FOOT ROT
Kim, D. H., Martyn, R. D., and Magill, C. W. 1993.
Mitochondrial DNA (mtDNA)—relatedness among formae
speciales of Fusarium oxysporum in the Cucurbitaceae. Introduction and significance
Phytopathology 83:91–97. Fusarium crown and foot rot is primarily a squash and
Larkin, R. P., Hopkins, D. L., and Martin, F. N. 1990. Vegetative pumpkin problem, though other cucurbits can become
compatibility within Fusarium oxysporum f. sp. niveum and
infected. Quality of the squash or pumpkin fruit can be
its relationship to virulence, aggressiveness, and race.
Canadian Journal of Microbiology 36:352–358. severely affected.
Leary, J. V. and Wilbur, W. D. 1976. Identification of the races of
Fusarium oxysporum f. sp. melonis causing wilt of Symptoms and diagnostic features
muskmelon in California. Phytopathology 66:15–16.
Initial symptoms occur on the crown and upper root
Louvet, J., Alabouvette, C., and Rouxel, F. 1981.
Microbiological suppressiveness of some soils to Fusarium tissues of seedlings as well as older plants. Crown and
wilts. In: Fusarium: Disease, Biology and Taxonomy (Eds upper root infections appear as water-soaked lesions
R.E. Nelson, T.A. Tousoun, and R.J. Cooke) pp. 262–275.
Pennsylvania State University Press.
near or beneath the soil line. With time, the lesions
Marois, J. J., Dunn, M. T., and Papavizas, G. C. 1983. become darker and above-ground parts of the plants
Reinvasion of fumigated soils by Fusarium oxysporum f. sp. can wilt and eventually die. Lesions may girdle the plant
melonis. Phytopathology 73:680–684. and result in a sunken, shriveled appearance. Crowns in
Martyn, R. D. and Bruton, B. D. 1989. An initial survey of the
United States for races of Fusarium oxysporum f. sp. niveum.
this condition can easily break off. White to pink
HortScience 24:696–698. mycelial growth may develop on symptomatic tissues.
Martyn, R. D. and McLaughlin, R. J. 1983. Susceptibility of The pathogen generally does not infect upper stem or
summer squash to watermelon wilt pathogen (Fusarium lower root tissues. The surfaces of squash and pumpkin
oxysporum f. sp. niveum). Plant Disease 67:263–266.
Martyn, R. D. and McLaughlin, R. J. 1983. Effects of inoculum
fruit that are in contact with the soil can develop
concentration on the apparent resistance of watermelon to circular to oblong, tan to brown, firm, dry, sunken
Fusarium oxysporum f. sp. niveum. Plant Disease lesions. Such lesions may have concentric rings within
67:493–495.
them (288, 289). These spots remain firm unless
McKeen, C. D. and Wensley, R. N. 1962. Cultural and
pathogenic variation in the muskmelon wilt fungus, Fusarium secondary decay organisms enter the infected area and
oxysporum f. sp. melonis. Canadian Journal of Microbiology cause soft, wet rots.
8:769–784.
Punja, Z. K. and Parker, M. 2000. Development of Fusarium
root and stem rot, a new disease on greenhouse grown
Causal agent
cucumbers in British Columbia caused by Fusarium The pathogen is Fusarium solani f. sp. cucurbitae. The
oxysporum f. sp. radicis-cucumerinum. Canadian Journal of fungus forms one- or two-celled, ovoid to oblong
microconidia on elongated monophialides, and three-
Risser, G., Banihashemi, Z., and Davis, D. W. 1976. A proposed
nomenclature of Fusarium oxysporum f. sp. melonis races to five-celled, fusiform, slightly curved macroconidia on
and resistance genes in Cucumis melo. Phytopathology multi-branched polyphialides. Macroconidia are
66:1105–1106.
usually produced in cushion-shaped structures called
Rose, S. and Punja, Z. K. 2004. Greenhouse cucumber cultivars
differ in susceptibility to Fusarium root and stem rot. sporodochia. Chlamydospores are also formed. Two
HortTechnology 14:240–242. races of this pathogen have been identified. Race 1
Vakalounakis, D. J. 1996. Root and stem rot of cucumber caused infects all plant parts and is distributed worldwide,
by Fusarium oxysporum f. sp. radicis-cucumerinum f. sp. nov.
while race 2 only infects the fruit and is apparently
Wensley, R. N. and McKeen, C. D. 1962. Rapid test for
limited to California and Ohio in the USA. The teleo-
pathogenicity of soil isolates of Fusarium oxysporum f. sp. morph, Nectria haematococca, has not been observed
F UNGAL D ISEASES
melonis. Canadian Journal of Microbiology 8:818–819. in the field on infected cucurbits.

Zink, F. W. and Gubler, W. D. 1986. Inheritance of resistance to
races 0 and 2 of Fusarium oxysporum f. sp. melonis in a
gynoecious muskmelon. Plant Disease 70:676–678.
C UCURBITACEAE 237
288 References
Champaco, E. R., Martyn, R. D., and Miller, M. E. 1993.
Comparison of Fusarium solani and F. oxysporum as causal
agents of fruit rot and root rot of muskmelon. HortScience
28:1174–1177.
Nagao, H., Sato, K., and Ogiwara, S. 1994. Susceptibility of
Cucurbita spp. to the cucurbit root-rot fungus, Fusarium
solani f. sp. cucurbitae race 1. Agronomie 2:95–102.
Nash, S. M. and Alexander, J. V. 1965. Comparative survival of
Fusarium solani f. sp. cucurbitae and F. solani f. sp. phaseoli in
soil. Phytopathology 55:963–966.
Sumner, D. R. 1976. Etiology and control of root rot of summer
squash in Georgia. Plant Disease Reporter 60:923–927.
Toussoun, T. A. and Snyder, W. C. 1961. The pathogenicity,
distribution, and control of two races of Fusarium
(Hypomyces) solani f. sp. cucurbitae. Phytopathology
51:17–22.
288 Fruit lesions on pumpkin caused by Fusarium

solani.
289
289 Fruit lesions on spaghetti squash caused by

Fusarium solani.
Disease cycle
The pathogen can survive in the soil for a maximum of
2 to 3 years. For fruit infections to occur, the fruit must
be in contact with moist soil that harbors inoculum.
Fusarium solani f. sp. cucurbitae can also be seedborne.
Control
F UNGAL D ISEASES
Rotate crops to non-cucurbits for 3 or more years. Use

seed that does not have significant levels of the
pathogen. Treat infested seed with hot water (15 minute
soak at 55° C) or fungicides.
Glomerella lagenarium Symptoms and diagnostic features

(anamorph = Colletotrichum orbiculare) Initial symptoms appear as irregularly shaped water-
ANTHRACNOSE soaked leaf lesions that soon turn chlorotic. Lesions can
expand, become greater than 1 cm in diameter, and turn
Introduction and significance tan to brown in color (290). On watermelon, such
Anthracnose disease occurs worldwide on a number of lesions are darker and appear brown to black.
cucurbit crops and some wild cucurbit species. The Extensive lesion development will cause the leaf to
disease is usually of minor importance in arid regions, buckle and become distorted. Lesion tissue dries,
but can be very damaging in high humidity cucurbit cracks, and falls out (291). Lesions can also occur on
production areas such as the southeast USA. petioles and stems and start out as elongated, oval to
Anthracnose is widespread as far west as Oklahoma. diamond- shaped, water-soaked lesions that later turn
tan to brown. Stem lesions can be covered with the
minute black fungal structures (acervuli) and pink spore
masses that are exuded by these fruiting bodies. Clear,
290
brown exudates can also collect on these stem lesions.
Fruit symptoms are circular water-soaked areas that
later become dark brown to black sunken lesions (292,
293). If high humidity and water are present, acervuli
of the pathogen will grow in the fruit lesions and exude
gelatinous pink spore masses.
Causal agent
Anthracnose is caused by the fungus Colletotrichum
orbiculare. Older references use the name Colletotrich-
um lagenarium. Colletotrichum orbiculare produces
microscopic, black, cup-shaped structures (acervuli)
that contain conidiophores and conidia. Conidia are
hyaline, straight, cylindrical, nonseptate, with blunt
ends, and measure 4–6 x 13–19 μm. Collectively,
290 Leaf spot caused by the anthracnose pathogen on conidia are produced in pink gelatinous droplets. Black
cucurbits. setae are usually present in the acervuli. The teleomorph
Glomerella lagenarium is rarely found in association
291
with cucurbit hosts. Distinct races of C. orbiculare have
been identified.
Disease cycle
The pathogen overwinters on infected crop residues,
volunteer cucurbit plants, and wild hosts. Conidia from
these sources move to uninfected plants by splashing
water, contact with contaminated tools and workers,
and perhaps by insects. To germinate and infect the
host, conidia require 24 hours of 100% relative
F UNGAL D ISEASES
humidity and optimum temperatures of 22–27° C.

Spores can take up to 72 hours to infect the host, and
symptoms first appear 4 days after infection. Sub-
sequent disease development is dependent on warm,
wet weather, and spread of secondary inoculum is
291 Leaf spots of anthracnose on cucumber. primarily achieved via splashing rain or irrigation water.
C UCURBITACEAE 239
292 293
292 Fruit lesions caused by Colletotrichum orbiculare 293 Fruit lesions on spaghetti squash caused by
on acorn squash. anthracnose.
The pathogen can also be seedborne and result in early References

infections on germinating seedlings or transplants Gleason, M. L., Parker, S. K., Pitblado, R. E., Latin, R. X.,
placed into production fields. The pathogen infects Speranzini, D., Hazzard, R. V., Maletta, M. J., Cowgill, W. P.,
and Biederstedt, D. L. 1997. Validation of a commercial
several wild cucurbit species, which in turn can act as system for remote estimation of wetness duration. Plant
inoculum sources for production cucurbits. Disease 81:825–829.
Koike, S. T., Tidwell, T. E., Fogle, D. G., and Patterson, C. L.
1991. Anthracnose of greenhouse-grown watermelon
Control transplants caused by Colletotrichum orbiculare in
Use resistant cultivars as they are available. Use seed California. Plant Disease 75:644.
that does not have significant levels of the pathogen. Leben, C. and Daft, G. C. 1968. Cucumber anthracnose:
Practice crop rotations in which cucurbits are not influence of nightly wetting of leaves on numbers of lesions.
planted for 2 years. Apply protectant fungicides. In the Monroe, J. S., Santini, J. B., and Latin, R. 1997. A model defining
USA, a disease forecasting program (Melcast) has been the relationship between temperature and leaf wetness
used to schedule fungicide applications for controlling duration, and infection of watermelon by Colletotrichum
orbiculare. Plant Disease 81:739–742.
anthracnose and gummy stem blight of melons. Avoid
Thompson, D. C. and Jenkins, S. F. 1985. Effects of temperature,
irrigating with overhead sprinklers. moisture, and cucumber cultivar resistance on lesion size
increase and conidial production by Colletotrichum
lagenarium. Phytopathology 75:828–832.
Thompson, D. C. and Jenkins, S. F. 1985. Influence of cultivar
resistance, initial disease, environment, and fungicide
concentration and timing on anthracnose development and
yield loss in pickling cucumbers. Phytopathology
75:1422–1427.
Wasilwa, L. A., Correll, J. C., Morelock, T. E., and McNew, R. E.
1993. Reexamination of races of the cucurbit anthracnose
pathogen Colletotrichum orbiculare. Phytopathology
83:1190–1198.
F UNGAL D ISEASES
Macrophomina phaseolina 294 Early crown

294
CHARCOAL ROT symptoms of
charcoal rot on
Introduction and significance cantaloupe.
Charcoal rot is usually most serious on melon hosts.
The disease is usually of minor importance, but can be
confused with other diseases.

Initial symptoms consist of chlorosis, wilting, and
necrosis of lower, older leaves near the crown. The
crown and lower stem will develop a dark green, water-
soaked lesion (294) that can eventually cover the entire
crown and extend up to 15–20 cm above the ground.
Brown exudates will collect on the lesion surfaces. Vines
can be stunted or wilt, collapse, and die. In later stages
of the disease (295), the stem and crown lesion will dry,
crack, and support the development of minute, black 295
295 Advanced
microsclerotia of the pathogen. Other structures cracking and
(pycnidia) might also form in the lesions. Roots can be bleeding of
extensively colonized. Fruit in contact with soil can also charcoal rot on
develop a firm decay. cantaloupe.
Causal agent
Charcoal rot is caused by the fungus Macrophomina
phaseolina, which is a soilborne fungus that has a wide
host range but occurs mainly in hot climates where soil
temperatures reach at least 28º C. The fungus produces
spherical, dark brown, ostiolate pycnidia and single-
celled conidia that are hyaline, ellipsoidal to ovoid, and
measure 14–30 x 5–10 μm. In diseased tissues, profuse
microsclerotia are produced that are irregular in shape,
black, and range in length from 100–1000 μm.
Disease cycle
The pathogen persists in the soil and crop residue as References
microsclerotia. Roots become infected first and the Bruton, B. D., Jeger, M. J., and Reuveni, R. 1987.
fungus later progresses into the plant crown. Macrophomina phaseolina infection and vine decline in
cantaloupe in relation to planting date, soil environment, and
plant maturation. Plant Disease 71:259–263.
Control Bruton, B. D. and Reuveni, R. 1985. Vertical distribution of
Rotate with non-host crops so that soil inoculum does microsclerotia of Macrophomina phaseolina under various
soil types and host crops. Agriculture, Ecosystems, &
not build up to high levels. Some cultivars may have Environment 12:165–169.
F UNGAL D ISEASES
tolerance or resistance to this pathogen. Minimize plant Reuveni, R., Krikum, J., Machimias, A., and Shelvin, E. 1982.
stress by irrigating and fertilizing properly. The role of Macrophomina phaseolina in a collapse of melon
plants in Israel. Phytoparasitica 10:51–56.
C UCURBITACEAE 241
Monosporascus cannonballus symptoms progress up the vines until many or most of

MONOSPORASCUS ROOT ROT the leaves wilt and die (297, 298). Fruit on affected
AND VINE DECLINE vines may be smaller, or cracked and sunburned due to
exposure. Symptoms on roots include tan to red-brown
Introduction and significance lesions (299). These necrotic spots can expand and
Monosporascus root rot and vine decline affects a result in the death of small feeder roots. In severe cases
number of cucurbit crops, but is most severe on melons the taproot and entire root system may rot and the plant
and watermelons. The disease has been detected in dies. An important sign is the development of minute,
India, Israel, Japan, Spain, Taiwan, Tunisia, and the black erumpent fungal structures (perithecia) in the
USA (in the southwest part of the country, including the brown root lesions. With a hand lens, clusters of the
states of California, Arizona, and Texas). A similar round, black spores of the fungus can be observed at the
disease, reportedly caused by M. eutypoides, is docu- perithecial openings.
mented in Israel.
Causal agent
Symptoms and diagnostic features The disease is caused by the fungus Monosporascus
Initial symptoms include the stunting and poor growth cannonballus. This pathogen is a soilborne ascomycete
of young plants. The older, lower leaves then begin to that forms globose, brown perithecia. Perithecia
turn chlorotic, wilt, and collapse (296). These leaf contain clavate to pyriform, unitunicate asci that each
296 298
296 Chlorosis and decline of old cantaloupe leaves 298 Foliage collapse of cantaloupe caused by
caused by Monosporascus. Monosporascus.
297 299 F UNGAL D ISEASES
297 Dead cantaloupe vines killed by Monosporascus. 299 Root lesions of root rot and vine decline of
cantaloupe.
hold a single, one-celled, thick-walled, spherical, black 300

ascospore that measures 35–50 μm in diameter (300,
301). A dark, periapical ring surrounds the perithecial
opening. An anamorph stage has not been identified.
The fungus grows well under warm conditions and
optimum in vitro growth takes place at 30–35° C.
Disease cycle
The complete epidemiology of Monosporascus root rot
and vine decline is not yet documented. Mycelium or
ascospores in soil presumably infect roots early in the
season, with disease development and fungal growth
encouraged by warmer temperatures later in the 300 Ascospores of Monosporascus on infected root.
summer. Roots in the upper soil profile are affected first.
Plant stress may make disease symptoms more severe. 301
Ascospore production takes place in infected roots of
declining and senescent plants. Monosporascus
cannonballus is distributed wherever infested, contami-
nated soil is moved by equipment, vehicles, and water.
Non-cucurbits such as wheat, corn, and sorghum may
also be hosts to this pathogen.
Control
The fungus appears to survive in the soil for extended
periods, so avoid planting melons and watermelons in
known infested fields. Enhance plant growth by 301 Asci and single ascospores of Monosporascus.
employing good production practices. Avoid excessive
irrigation. In Israel, experiments demonstrated that
Radewald, K. C., Ferrin, D. M., and Stanghellini, M. E. 2004.
reduced, less frequent irrigations helped delay plant Sanitation practices that inhibit reproduction of
collapse, though yields and fruit quality were also Monosporascus cannonballus in melon roots left in the field
reduced. Recent research finds that pathogen inoculum after crop termination. Plant Pathology 53:660–668.
production is reduced if old crop roots are dried out by Pivonia, S., Cohen, R., Cohen, S., Kigel, J., Levita, R., and Katan,
J. 2004. Effect of irrigation regimes on disease expression in
cultivating fields after harvest or by applying fumigants melon plants infected with Monosporascus cannonballus.
(metam sodium) immediately after harvest. European Journal of Plant Pathology 110:155–161.
Pivonia, S., Cohen, R., Kigel, J., and Katan, J. 2002. Effect of soil
temperature on disease development in melon plants infected
References by Monosporascus cannonballus. Plant Pathology
Martyn, R. D. and Miller, M. E. 1996. Monosporascus root rot 51:472–479.
and vine decline: an emerging disease of melons worldwide. Pollack, F. G. and Uecker, F. A. 1974. Monosporascus
Plant Disease 80:716–725. cannonballus, an unusual ascomycete in cantaloupe roots.
Mertely, J. C., Martyn, R. D., Miller, M. E., and Bruton, B. D. Mycologia 66:346–349.
1991. Role of Monosporascus cannonballus and other fungi Stanghellini, M. E., Ferrin, D. M, Kim, D. H., Waugh, M. M.,
in a root rot/vine decline disease of muskmelon. Plant Disease Radewald, K. C., Sims, J. J., Ohr, H. D., Mayberry, K. S.,
75:1133–1137. Turini, T., and McCaslin, M. A. 2003. Application of
Mertely, J. C., Martyn, R. D., Miller, M. E., and Bruton, B. D. preplant fumigants via drip irrigation systems for the
F UNGAL D ISEASES
1993. An expanded host range for the muskmelon pathogen management of root rot of melons caused by Monosporascus
Monosporascus cannonballus. Plant Disease 77:667–673. cannonballus. Plant Disease 87:1176–1178.
Mertely, J. C., Martyn, R. D., Miller, M. E., and Bruton, B. D. Stanghellini, M. E., Kim, D. H., and Rasmussen, S. L. 1996.
1993. Quantification of Monosporascus cannonballus Ascospores of Monosporascus cannonballus: germination
ascospores in three commercial muskmelon fields in south and distribution in cultivated and desert soils in Arizona.
Texas. Plant Disease 77:766–771. Phytopathology 86:509–514.
C UCURBITACEAE 243
Phytophthora capsici
303
PHYTOPHTHORA
CROWN AND ROOT ROT

Phytophthora crown and root rot affects most cucurbit
crops, with squash perhaps being the most sensitive.
In several states in the USA, this pathogen has increased
in importance in recent years.

Initial symptoms consist of wilting of young shoots and
leaves, followed by wilting and collapse of all foliage
(302). The lower stem and crown turns tan to brown in
color and is soft and rotted. The root system turns tan 303 Phytophthora capsici causing aerial blight
to brown and is rotted. When dug out of the ground, symptoms on hard squash.
the small feeder roots break off and outer tissue of the
larger roots sloughs off. The crown and root rot 304
pathogen can also cause seedling damping-off, foliar
blight, and fruit rot diseases (303, 304, 305).
Causal agent
The main pathogen is the oomycete Phytophthora
capsici. Optimum growth occurs at 25–28° C. Phyto-
phthora capsici produces sporangia that release
zoospores that swim to and infect susceptible tissues.
Also, sporangia are deciduous and can be aerially
dispersed. As a heterothallic species, both mating
types (A1 and A2) must be present for oospore produc-
tion. In addition to cucurbits, P. capsici can infect
aubergine (eggplant), pepper, tomato, and other crops.
304 Phytophthora capsici infecting cucumber fruit.
302 305
F UNGAL D ISEASES
302 Phytophthora crown and root rot in squash field. 305 Phytophthora capsici infecting pumpkin fruit.
Other Phytophthora species, such as P. drechsleri, also Pseudoperonospora cubensis

have been reported to cause crown and root rot of DOWNY MILDEW
cucurbits.
Disease cycle Downy mildew is a major foliar disease of the various
Phytophthora capsici survives in the soil as a sapro- cucurbit crops and is particularly severe in warm
phyte and pathogen of several host plants. If wet soil temperate or tropical environments. Watermelon and
conditions persist, zoospores move to, and infect, the some Cucurbita species (C. maxima and C. moschata)
crown and root tissues of the host. Oospores are may less susceptible.
important sources of initial inoculum because they can
survive as dormant propagules in soil for extended Symptoms and diagnostic features
periods of time. Initial symptoms are found on the top surfaces of leaves
and consist of small, pale green to greasy looking,
Control angular or rectangular spots that are delimited by leaf
Do not plant cucurbits in fields that have poorly veins (306, 307). These patches later turn slightly
draining, heavy textured soils. Prepare seed and trans- chlorotic to bright yellow. The early symptoms can give
plant beds so that drainage is enhanced. Schedule irri- the leaf a mosaic or mottled appearance. As downy
gations so that excess water is not applied and fields mildew lesions age, the tissue turns brown and necrotic.
drain properly. Rotate crops so that cucurbits and other Lesions can expand and coalesce, resulting in the shriv-
hosts are not planted within 3 years of the previous sus- eling and death of large areas of leaf surface.
ceptible planting. Some fungicides may also be helpful If environmental conditions are favorable, the lower
in controlling this disease, though resistance to pheny- leaf surfaces of infected areas will support the growth of
lamide fungicides has been found. light gray to dark purple sporulation that will also be
delimited by leaf veins and therefore result in angular or
References rectangular patterns (308). Downy mildew can cause
Cafe-Filho, A. C., Duniway, J. M., and Davis, R. M. 1995. stunting or even death if young plants are infected early
Effects of the frequency of furrow irrigation on root and fruit and severely. Fruit maturation and production might be
rots of squash caused by Phytophthora capsici. Plant Disease
79:44–48. prevented and fruit flavor and sugar content could also
Hausbeck, M. K. and Lamour, K. H. 2004. Phytophthora capsici be affected.
on vegetable crops: research progress and management
challenges. Plant Disease 88:1292–1303.
Ho, H. H., Lu, J., and Gong, L. 1984. Phytophthora drechsleri
causing blight of Cucumis species in China. Mycologia
76:115–121.
306
Lamour, K. H. and Hausbeck, M. K. 2003. Susceptibility of
mefenoxam-treated cucurbits to isolates of Phytophthora
capsici sensitive and insensitive to mefenoxam. Plant Disease
87:920–922.
Lamour, K. H. and Hausbeck, M. K. 2003. Effect of crop
rotation on the survival of Phytophthora capsici in Michigan.
Polach, F. J. and Webster, R. K. 1972. Identification of strains and
inheritance of pathogenicity in Phytophthora capsici.
Ristaino, J. B. 1990. Intraspecific variation among isolates of
Phytophthora capsici from pepper and cucurbit fields in
F UNGAL D ISEASES
North Carolina. Phytopathology 80:1253–1259.

Tian, D. and Babadoost, M. 2004. Host range of Phytophthora
capsici from pumpkin and pathogenicity of isolates. Plant
Disease 88:485–489.
306 Downy mildew on summer squash. Upper surface

of leaf showing angular lesions of downy mildew.
C UCURBITACEAE 245
307 308
307 Angular lesions of downy mildew of squash. 308 Downy mildew sporulation on leaf underside of
cucumber.

Downy mildew is caused by the oomycete Pseudo- Plant resistant cultivars, though these are currently only
peronospora cubensis, which is an obligate pathogen available for cucumber and melon. Apply protectant
that is host specific to cucurbits. Sporangiophores fungicides; however, some resistance to such materials
emerge from leaf stomates, branch dichotomously, and has been documented. Avoid using overhead sprinkler
terminate in slender curved tips. The sporangial tips irrigation. Ventilate greenhouses to reduce humidity
bear a single, gray to purple, ovoid to ellipsoidal levels.
sporangium that measures 20–40 x 14–25 μm.
Sporangia have a papilla on the distal end. When References
produced, oospores measure 22–42 μm in diameter; Cohen, Y. 1977. The combined effects of temperature, leaf
however, these sexual structures are rarely found. Five wetness, and inoculum concentration on infection of
cucumber with Pseudoperonospora cubensis. Canadian
distinct physiological races or pathotypes have been Journal of Botany 55:1478–1487.
reported for P. cubensis, each of which is host specific to Katan, T. and Bashi, E. 1981. Resistance to metalaxyl in isolates
particular cucurbit plants. of Pseudoperonospora cubensis, the downy mildew pathogen
of cucurbits. Plant Disease 65:798–800.
Palti, J. and Cohen, Y. 1980. Downy mildew of cucurbits.
Disease cycle Phytoparasitica 8:109–147.
As an obligate pathogen, P. cubensis overwinters on Thomas, C. E., Inaba, T., and Cohen, Y. 1987. Physiological
volunteer or weedy cucurbit plants that then serve specialization in Pseudoperonospora cubensis.
as sources of initial inoculum. Greenhouse-grown
cucurbits or cucurbit crops grown far beyond the pro-
duction region may also be sources of initial inoculum.
Sporangia are produced if humidity is at 100% for
6 hours and temperatures are between 15–20° C; these
spores are wind blown or splashed onto susceptible
host tissue and germinate if free moisture is present for
at least 2 hours at 20–25° C. Sporangia germinate by
F UNGAL D ISEASES
releasing 2–15 motile zoospores that swim towards,

and encyst on, leaf stomates. Cysts germinate with germ
tubes that penetrate the stomates and initiate coloniza-
tion of the leaf. The incubation period prior to symp-
tom expression is 3–12 days depending on temperature,
relative humidity, and inoculum concentration.
Verticillium dahliae though semi-selective media such as NP-10 can be

VERTICILLIUM WILT useful for isolation and for purifying cultures. On
general purpose media, the pathogen forms the charac-
Introduction and significance teristic hyaline, verticillate conidiophores bearing three
Verticillium wilt affects most species in this crop group. to four phialides at each node, and hyaline, single-
The disease is found throughout the world. celled, ellipsoidal conidia that measure 2–8 x 1–3 μm.
Older cultures form dark brown to black torulose
Symptoms and diagnostic features microsclerotia that consist of groups of swollen cells
Initial symptoms typically occur after plants are estab- formed by repeated budding. Microsclerotia size varies
lished and have set fruit. Lower leaves will become off greatly and ranges from 15 to 100 μm in diameter.
green and wilt during the warmer part of the day. As Microsclerotia enable the pathogen to survive in the soil
disease progresses, the leaves become chlorotic, for extended periods of time (up to 8 to 10 years). The
withered, and later necrotic and dry. Such symptoms pathogen has a very wide host range.
progress and affect all leaves and the tips of plant
runners. Wilt symptoms are sometimes one sided and Disease cycle
affect only the vines on one side of the plant. Plants Roots of susceptible plants grow near microsclerotia
eventually collapse and die (309, 310). An important that are dormant in the soil. Microsclerotia are stimu-
symptom is the tan to brown discoloration of the xylem lated to germinate and infect the roots. The pathogen
tissues in roots and stems. Verticillium dahliae, along subsequently invades xylem tissue and becomes
with a series of other soilborne pathogens, is implicated systemic in the plant. Disease progresses most rapidly
in the vine decline disease that is caused by a complex during relatively cool temperatures (20–23° C) and
of fungi. This pathogen has been found to cause when plants are undergoing stress, such as during
an internal fruit decay on Chinese winter melon flower and fruit formation. Diseased plants become
(Benincasa hispida). colonized with microsclerotia, which are returned to the
soil during crop residue incorporation.
Causal agent
The causal agent is Verticillium dahliae. The pathogen Control
can be isolated on standard microbiological media, Plant resistant or tolerant cultivars as they become
available. Rotate crops so that cucurbits are not planted
in fields having a history of the problem. Soil tests have
been developed that can estimate the numbers of
309
microsclerotia per gram of soil; such tests may be useful
for giving indications of potential risk of this disease.
Minimize spread of infested soil to uninfested areas.
References
Aegerter, B. J., Gordon, T. R., and Davis, R. M. 2000.
Occurrence and pathogenicity of fungi associated with melon
root rot and vine decline in California. Plant Disease
84:224–230.
Gubler, W. D. and Bernhardt, E. A. 1992. Cavity rot of winter
melon caused by Verticillium dahliae. Plant Disease
76:416–417.
F UNGAL D ISEASES
of sodium polygalacturonate sources and improved recovery

of Verticillium species from soil. (Abstract) Phytopathology
81:1347.
309 Declining vines of Verticillium wilt of

watermelon.
C UCURBITACEAE 247
310 Control
(see Part 1). Virus resistant, transgenic squash cultivars
are available. These plants derive their resistance from
genes of the virus pathogen itself.
References
Alonso-Prados, J. L., Luis-Arteaga, M., Alvarez, J. M.,
Moriones, E., Batlle, A., Laviña, A., García-Arenal, F., and
Fraile, A. 2003. Epidemics of aphid-transmitted viruses in
melon crops in Spain. European Journal of Plant Pathology
109:129–138.
Arce-Ochoa, J. P., Dainello, F., Pike, L. M., and Drews, D. 1995.
Field performance comparison of two transgenic summer
squash hybrids to their parental hybrid line. HortScience
30:492–493.
Dodds, J. A., Lee, J. G., Nameth, S. T., and Laemmlen, F. F. 1984.
Aphid- and whitefly-transmitted cucurbit viruses in the
Imperial Valley, California. Phytopathology 74:221–225.
coat protein genes. Plant Disease 82:1350–1356.
Karchi, Z., Cohen, S., and Govers, A. 1975. Inheritance of
310 Collapsed plants of Verticillium wilt of cucumber. resistance to cucumber mosaic virus in melons.
Nameth, S. T., Dodds, J. A., Paulus, A. O., and Laemmlen, F. F.
Cucumber mosaic virus 1986. Cucurbit viruses of California. Plant Disease 70:8–12.
Provvidenti, R. 1993. Resistance to viral diseases of cucurbits.
CUCUMBER MOSAIC Pages 8–43 in: Resistance to Viral Diseases of Vegetables:
Genetics and Breeding. M. M. Kyle, editor. Timber Press,
Introduction and significance Portland, Oregon.
Cucumber mosaic virus (CMV) is commonly found

throughout the world and infects over 800 plant (crop
and weed) hosts, including cucurbits.

CMV severely stunts plant growth and causes leaves to
be distorted, reduced in size, curled or rolled, and show
a yellow mosaic or mottle pattern with chlorotic
patches (311). Young leaves at the growing point may
form a rosette. Flowers can be distorted and may have
green petals. Fruit can be small, malformed, and show
various discolorations.

(29 nm in diameter) and contain three single-stranded
V IRAL D ISEASES
RNAs. A number of CMV strains have been docu-

mented. CMV is transmitted in a nonpersistent manner
by a number of aphid vectors and is probably the most
commonly encountered virus on cucurbit crops. CMV 311 Cucumber mosaic virus affecting garden
occurs in many weed hosts and can also be seedborne. marrow.
Papaya ringspot virus type W Causal agent and disease cycle

PAPAYA RINGSPOT PRSV-W was previously named Watermelon mosaic
virus I (WMV-1). It is a potyvirus, with filamentous
Introduction and significance virions measuring 760–800 x 12 nm and containing
This virus can result in significant crop loss in temperate single-stranded RNA. The host range of PRSV-W
as well as subtropical and tropical regions. appears to be limited to cucurbits and does not include
papaya. The papaya pathotype PRSV-P is serologically
Symptoms and diagnostic features identical to PRSV-W but has the ability to infect
Papaya ringspot virus type W (PRSV-W) causes severe cucurbits and papaya. PRSV-P is less important eco-
stunting of the plant. Extremely malformed leaves have nomically for cucurbit production. PRSV-W is vectored
reduced lamina and irregular, dark green blisters (312, by aphid species.
313). Fruit are distorted, knobby, and show color
breaks. Control
Follow general suggestions in Part 1.
312
References
Aphid- and whitefly-transmitted cucurbit viruses in the
Wang, Y. J., Provvidenti, R., and Robinson, R. W. 1984.
Inheritance of resistance to watermelon mosaic virus 1 in
cucumber. HortScience 19:587–588.
Webb, R. E. and Scott, H. A. 1965. Isolation and identification of
watermelon mosaic viruses 1 and 2. Phytopathology
55:895–900.
Squash leaf curl virus

SQUASH LEAF CURL

312 Distorted pumpkin leaves affected by papaya Squash leaf curl virus (SLCV) was first seen in the 1970s
ringspot. in the southwest region of the USA. Presently this virus
is found in various cucurbit growing areas in the USA,
313
Mexico, and Central America.

SLCV causes leaves to take on a bright yellow mosaic
or mottle symptom. Leaves can be curled or slightly
distorted. Plants are stunted. Flowers produced on
diseased plants may be late in opening or fall off. Fruit
may not mature or can be malformed, bumpy, and have
a break in color.

V IRAL D ISEASES
SLCV is a geminivirus with isometric particles that

measure 20 x 30 nm and contain a single stranded,
circular DNA genome. It is vectored by various bio
types in the Bemisia tabaci whitefly group and appears
313 Foliar symptoms of papaya ringspot on squash. to primarily infect plants in the cucurbit family.
C UCURBITACEAE 249
Control can be mechanically transmitted through production

Follow general suggestions in Part 1. and harvest procedures. This virus naturally infects
plants in the cucurbit and chenopodium families.
References
Cohen, S., Duffus, J. E., Larsen, R. C., Liu, H. Y., and Flock, R. Control
A. 1983. Purification, serology, and vector relationships of Follow general suggestions in Part 1. Use seed that has
squash leaf curl virus, a whitefly-transmitted geminivirus.
Phytopathology 73:1669–1673. been tested and certified to be free of the virus.
Aphid- and whitefly-transmitted cucurbit viruses in the References
Alvarez, M. and Campbell, R. N. 1978. Transmission and
Flock, R. A. and Mayhew, D. E. 1981. Squash leaf curl, a new distribution of squash mosaic virus in seeds of cantaloupe.
disease of cucurbits in California. Plant Disease 65:75–76. Phytopathology 68:257–263.
Nameth, S. T., Dodds, J. A., Paulus, A. O., and Laemmlen, F. F. Nelson, M. R. and Knuhtsen, H. K. 1973. Squash mosaic virus
1986. Cucurbit viruses of California. Plant Disease 70:8–12. variability: review and serological comparisons of six
Polston, J. E., Dodds, J. A., and Perring, T. M. 1989. Nucleic acid biotypes. Phytopathology 63:920–926.
probes for detection and strain discrimination of cucurbit Nolan, P. A. and Campbell, R. N. 1984. Squash mosaic virus
geminiviruses. Phytopathology 79:1123–1127. detection in individual seeds and seed lots of cucurbits by
Provvidenti, R. 1993. Resistance to viral diseases of cucurbits. enzyme-linked immunosorbent assay. Plant Disease
Pages 8–43 in: Resistance to Viral Diseases of Vegetables: 68:971–975.
Portland, Oregon.
Tobacco ringspot virus

Squash mosaic virus TOBACCO RINGSPOT
SQUASH MOSAIC
Introduction and significance Tobacco ringspot virus (TRSV) is found throughout the
This disease has been known since the early 1900s. Its USA and has also been reported around the world.
importance in many countries has decreased due to the
use of virus-free seed. However, some cucurbit Symptoms and diagnostic features
producing regions still experience losses from this virus. TRSV causes a very bright chlorosis on young foliage
that takes the form of mosaics, mottles, and ring spots.
Symptoms and diagnostic features Fruit will either abort, not grow to full size, or develop
Squash mosaic virus (SqMV) symptoms are extremely bumps, ring spots, mottles, and other distortions.
variable. Leaves show a variety of mosaic, mottle, dark
green vein banding, ring spot, and other virus-like foliar Causal agent and disease cycle
symptoms. Leaf enations can also develop. Plants are TRSV is a nepovirus that has isometric particles
stunted and fruit are malformed and have color breaks. measuring 25–29 nm and a genome of two single-
stranded RNAs. Various strains have been differentiat-
Causal agent ed. This pathogen has a broad host range that includes
SqMV is a comovirus that has isometric particles plants in over 20 families and is vectored primarily by
measuring 28–30 nm in diameter and a genome of two the soilborne dagger nematode (Xiphinema ameri-
single-stranded linear RNAs. Distinct strains exist and canum). TRSV has been reported to be vectored non-
cause different symptoms on different cucurbits. specifically by aphids and mites; it can also be
seedborne and pollen borne.
Disease cycle
V IRAL D ISEASES
The virus is vectored by the western striped cucumber Control

beetle (Acalymma trivittatum) and the spotted Follow general suggestions in Part 1. Do not plant sus-
cucumber beetle (Diabrotica undecimpunctata). As a ceptible crops in fields having a history of this disease.
seedborne pathogen, an important means of spread is Use seed that does not have significant levels of the
by the use of infested seed. The virus is very stable and pathogen.
Watermelon mosaic virus Causal agent and disease cycle

WATERMELON MOSAIC VIRUS WMV is a potyvirus that has filamentous particles
measuring 730–765 nm long and single stranded linear
Introduction and significance RNA genomes. WMV infects cucurbits, legumes, and
Watermelon mosaic virus (WMV) was previously other plants and has a host range of over 150 species.
named Watermelon mosaic virus 2 (WMV-2) and is This pathogen is vectored by aphids.
found in cucurbit producing areas throughout the
world. Control
Symptoms and diagnostic features (see Part 1). Virus resistant, transgenic squash cultivars
WMV causes leaves to develop mosaics, vein banding, are available. These plants derive their resistance from
rings, light green patches, and other symptoms (314). genes of the virus pathogen itself.
Leaves are sometimes crinkled. Fruit can be distorted or
have color breaks (315). References
Alonso-Prados, J. L., Luis-Arteaga, M., Alvarez, J. M.,
Moriones, E., Batlle, A., Laviña, A., García-Arenal, F., and
Fraile, A. 2003. Epidemics of aphid-transmitted viruses in
314 melon crops in Spain. European Journal of Plant Pathology
109:129–138.
30:492–493.
Mclean, G. D., Burt, J. R., Thomas, D. W., and Sproul, A. N.
1982. The use of reflective mulch to reduce the incidence of
watermelon mosaic virus in Western Australia. Crop
Protection 1:491–496.
314 Deformed squash leaf infected with Watermelon

mosaic virus. Zucchini yellow mosaic virus
ZUCCHINI YELLOW MOSAIC
315
Zucchini yellow mosaic virus (ZYMV) is an important
cucurbit virus throughout the world and can at times
cause tremendous crop loss. The disease first appeared
in northern Italy and southern France in the late 1970s,
spread world-wide during the 1980s, and reached the
UK in 1987.

Leaves are severely distorted and develop dark green
blisters, strip-like lamina (called laciniate or filiform),
V IRAL D ISEASES
315 Deformed serrated edges, necrosis, enations, and other malforma-

squash fruit tions (316). Plants can be extremely stunted and stem
infected with internodes are very short. In severe cases, most of the
Watermelon leaves have the laciniate or filiform distortion; in this
mosaic virus. case overall plant canopy and leaf surface area are
C UCURBITACEAE 251
significantly reduced. Fruit can be greatly distorted and 316

have knobs, swellings, and cracks (317).

ZYMV is a potyvirus that has filamentous virions
measuring 750 x 11 nm and single-stranded linear
RNA genomes. Some strains have been differentiated.
Information is lacking on the natural host range of this
pathogen. ZYMV is vectored by aphids, can be
seedborne within the seed coat, and may be spread on
cutting knives during harvesting.
Control
(seePart 1). Resistant cultivars are available and mild- 316 Leaf symptoms of cucumber infected with Zucchini
strain inoculation of seedlings has been shown to yellow mosaic virus.
protect plants against severe strains. Virus resistant,
transgenic squash cultivars are also available. These 317
plants derive their resistance from genes of the virus
pathogen itself.
References
30:492–493.
Blua, M. J. and Perring, T. M. 1989. Effect of zucchini yellow
mosaic virus on development and yield of cantaloupe. Plant
Disease 73:317–320.
Desbiez, C. and Lecoq, H. 1997. Zucchini yellow mosaic virus.
Lisa, V., Boccardo, G., D’Agostino, G., Dellavalle, G., and
d’Aquilio, M. 1981. Characterization of a potyvirus that
causes zucchini yellow mosaic. Phytopathology 71:667–672.
Nameth, S. T., Dodds, J. A., Paulus, A. O., and Kishaba, A. 1985.
Zucchini yellow mosaic virus associated with severe diseases
of melon and watermelon in Southern California desert
valleys. Plant Disease 69:785–788.
Nameth, S. T., Dodds, J. A., Paulus, A. O., and Laemmlen, F. F.
1986. Cucurbit viruses of California. Plant Disease 70:8–12.
Provvidenti, R. 1991. Inheritance of resistance to the Florida
strain of zucchini yellow mosaic virus in watermelon.
HortScience 26:407–408. 317 Cucumber fruit deformed by Zucchini yellow
Provvidenti, R. 1993. Resistance to viral diseases of cucurbits. mosaic virus.
V IRAL D ISEASES
Pages 8–43 in: Resistance to Viral Diseases of Vegetables:

Portland, Oregon.
Purcifull, D. E., Adlertz, W. C., Simone, G. W., Hiebert, E., and Walkey, D. G. A., Lecoq, H., Collier, R., and Dobson, S. 1992.
Christie, S. R. 1984. Serological relationships and partial Studies on the control of zucchini yellow mosaic virus in
characterization of zucchini yellow mosaic virus isolated from courgettes by mild strain protection. Plant Pathology
squash in Florida. Plant Disease 68:230–233. 41:762–771.
Fabaceae Pea family
THE FABACEAE (pea family) is the second largest of the flowering plant familes,
with over 16,000 species in 750 genera. Commonly known as legumes or pulses, they are
second only to cereals in their economic and nutritional importance in the human diet.
This chapter has individual sections on the diseases of broad bean, pea, and bean.
The bean group is diverse and the genus Phaseolus comprises over 150 species. Common or
snap bean (P. vulgaris) is primarily grown for its green pods that are used for fresh markets or for
freezing and canning. Common bean is generally divided into several categories: French bean
(both pods and under-developed seeds are consumed); haricot filet bean (only immature pods
are eaten because fully mature pods are stringy); haricot bean (only fresh seed are eaten); dry
field bean (dry seed are used for consumption, and the pods are not eaten). Scarlet runner bean
(Phaseolus coccineus) is probably native to Central American and Mexico. This species is
sometimes used as an ornamental plant, but is also grown for its young pods that are used in
similar ways as common bean. The lima bean (P. lunatus) is grown for its large seeds, and the
pods are not consumed. Lima beans are used for canned, frozen, and fresh
market products.
Pea (Pisum sativum) is a familiar vegetable commodity that is used fresh, frozen, canned,
and dried. Some cultivars are grown for their immature, edible pods and under-developed seed.
Other cultivars are grown for the seed, as the pods are not consumed.
Broad bean (Vicia faba), also known as faba bean, horsebean, or English bean, is grown
commercially for the very large seeds that are shelled and used for frozen, fresh, and dried beans.
Broad bean is an important vegetable in the UK and other European countries. In the USA, in
addition to being considered a specialty vegetable, broad bean is used as a cover crop for adding
organic matter to the soil.
PHASEOLUS SPECIES (BEANS)
Pseudomonas syringae pv. phaseolicola Symptoms and diagnostic features

HALO BLIGHT Early symptoms appear as greasy looking, water-
soaked, angular leaf lesions (318). The young lesions
Introduction and significance expand and coalesce into larger lesions that are brown
This seedborne bacterial disease is an important and and can reach 2–3 cm in diameter. Old lesions dry and
widespread problem in both common and scarlet become red to brown. Developing and older leaf spots
runner bean. It may be the most important disease usually are surrounded by a distinct yellow halo, which
of Phaseolus species in Europe. Halo blight is also is a conspicuous feature of this disease (319). In severe
damaging in cooler, high altitude climates in the tropics. cases, the bean plant can show systemic chlorosis in
FABACEAE 253
318 319
318 Leaf lesions of halo blight of bean. 319 Chlorosis or ‘halo’ of halo blight of bean.
which much of the foliage turns yellow. Seedlings Some strains of a different Pseudomonas pathogen,
grown from infected seed may be stunted and have a Pseudomonas syringae pv. syringae, are pathogenic to
‘snake’s head’ symptom because leaf tissue (plumules) bean and cause bacterial brown spot disease. Symptoms
has been destroyed. Water-soaked or yellow-brown of bacterial brown spot can be somewhat similar to
lesions also develop at the primary leaf node, which those of halo blight. Spots tend to be more circular, are
girdle and weaken the stem so that plants eventually brown in color, and a yellow halo can also surround the
snap off at this node. The disease may cause a red dis- lesion.
coloration in the interveinal leaf tissue and elongated
red streaks on stems. Leaf veins may also take on a red Disease cycle
discoloration. Pods develop water-soaked, round to Infected seed is the most important source of inoculum,
oval spots on sides of pods, and elongated lesions along as there appears to be limited survival on crop residues
the sutures. Early pod infection may cause seeds to rot or in soil. Weed hosts may be important in some
or to remain immature. A cream or silver-colored regions. The pathogen is spread by splashing water
bacterial ooze may be exuded from pod lesions. from rain or sprinkler irrigation. In field crops, only one
infected plant in 10,000 is sufficient to cause an
Causal agent epidemic. The bacterium invades through stomata or
Halo blight is caused by the bacterium Pseudomonas wounds and then spreads through the vascular system.
syringae pv. phaseolicola. This pathogen is an aerobic, It is able to break out of the xylem and into the
Gram-negative, rod-shaped bacterium. The pathogen parenchyma where it causes tissue collapse. The disease
can be isolated on standard microbiological media and cycle takes less than 7 days under optimum conditions.
produces cream-colored colonies typical of most Disease development is most pronounced at cooler tem-
pseudomonads. When cultured on Kings medium B, it peratures, 16–20º C; however, the production of toxin
produces a diffusible pigment that fluoresces blue under and appearance of halo symptoms develop at warmer
ultraviolet light. Strains of this pathogen are host temperatures: 20–23º C. Seeds are infected through the
specific to bean, hence the pathovar (pv.) designation. vascular tissues or by direct infection through pod
This pathogen is seedborne. There are several races of walls.
this pathogen; the particular strain of the pathogen and
environmental conditions influence the development Control
and degree of the yellow halo, which is due to the pro- Use seed that does not have significant levels of the
duction of the bacterial toxin phaseolotoxin. pathogen. Apply copper sprays to foliage, though such
treatments may be only marginally effective. Choose Xanthomonas campestris pv. phaseoli
resistant cultivars. Irrigate with furrow or drip irriga- COMMON BACTERIAL BLIGHT
tion, and avoid the use of overhead sprinklers.
Eliminate volunteer and other hosts. Introduction and significance
Like halo blight, this seedborne bacterial disease is a
References very important and widespread problem on bean. The
Cheng, G. Y., Legard, D. E., Hunter, J. E., and Burr, T. E. 1989. disease is damaging in humid environments and is
Modified bean pod assay to detect strains of Pseudomonas found in most bean production areas. This disease is
syringae pv. syringae that cause bacterial brown spot of snap
bean. Plant Disease 73:419–423. actually caused by two very closely related, but distinct
Hirano, S. S., Rouse, D. I., Clayton, M. K., and Upper, C. D. bacterial pathogens.
1995. Pseudomonas syringae pv. syringae and bacterial
brown spot of snap bean: a study of epiphytic
phytopathogenic bacteria and associated disease. Plant
Disease 79:1085–1093. Early symptoms are water-soaked, angular leaf lesions.
Legard, D. E. and Schwartz, H. F. 1987. Sources and The young lesions expand and coalesce into larger
management of Pseudomonas syringae pv. phaseolicola and lesions that are gray-brown and irregular in shape. Leaf
Pseudomonas syringae pv. syringae epiphytes on dry beans in
Colorado. Phytopathology 77:1503–1509. spots are usually surrounded by a narrow yellow halo
Lindemann, J., Arny, D. C., and Upper, C. D. 1984. Epiphytic (320). Pods develop water-soaked, round to oval spots
population of Pseudomonas syringae pv. syringae on snap on sides of pods (321). Pod lesions later turn brown to
beans and nonhost plants and the incidence of bacterial
brown spot. Phytopathology. 74:1329–1333.
red-brown. Bacterial ooze may be exuded from pod
Rico, A., Lopez, R., Asenio, C., Aizpun, M. T., Asensio-S.- lesions.
Manzanera, M. L., and Murillo, J. 2003. Nontoxigenic
strains of Pseudomonas syringae pv. phaseolicola are a main Causal agents
cause of halo blight of beans in Spain and escape current
detection methods. Phytopathology 93:1553–1559. Common bacterial blight is caused by the bacterium
Schaad, N. W., Azad, H., Peet, R. C., and Panopoulos, N. J.1989. Xanthomonas campestris pv. phaseoli. This pathogen
Identification of Pseudomonas syringae pv. phaseolicola by a is an aerobic, Gram-negative, rod-shaped bacterium.
DNA hybridization probe. Phytopathology 79: 903–907.
Serfontein, J. J. 1994. Occurrence of bacterial brown spot of dry
beans in Transvaal province of South Africa. Plant Pathology logical media and produces yellow, mucoid, slow
43: 597–599. growing colonies typical of most xanthomonads. This
Taylor, J. D. 1972. Field studies on halo-blight of beans bacterium hydrolyzes starch, so starch-based semi-
(Pseudomonas phaseolicola) and its control by foliar sprays.
Annals of Applied Biology 70:191–197. selective media such as SX and MXP media are useful
Taylor, J. D., Dudley, C. L., and Presly, L. 1979. Studies of halo- for isolating and identifying this pathogen. Strains of
blight infected seed and disease transmission in dwarf beans. this pathogen are restricted to hosts in the Fabaceae
Annals of Applied Biology 93: 267–277.
family. This pathogen is seedborne.
Taylor, J. D., Phelps, K., and Dudley, C. L. 1979. Epidemiology
and strategy for the control of halo-blight of beans. Annals of
Taylor, J. D., Teverson, D. M., Allen, D. J., and Pastor–Corrales,
M. A. 1996. Identification and origin of races of
Pseudomonas syringae pv. phaseolicola from Africa and other
bean growing areas. Plant Pathology 45: 469–478.
Taylor, J. D., Teverson, D. M., and Davis, J. H. C. 1996. Sources
of resistance to Pseudomonas syringae pv. phaseolicola races
in Phaseolus vulgaris. Plant Pathology 45:479–485.
Webster, D. M., Atkin, J. D., and Cross, J. E. 1983. Bacterial
blights of snap beans and their control. Plant Disease

67:935–940.
Yessad-Carreau, S., Manceau, C., and Luisetti, J. 1994.
Occurrence of specific reactions induced by Pseudomonas
syringae pv. syringae on bean pods, lilac and pear plants.
FABACEAE 255
320 321
320 Angular lesions and surrounding yellow borders on 321 Bean pod lesions caused by the common bacterial
bean leaves caused by common bacterial blight. blight pathogen.
Common bacterial blight is also caused by a variant References

of X. campestris pv. phaseoli. This variant causes the Audy, P., Laroche, A., Saindon, G., Huang, H. C., and
same disease symptoms, and has the same host range Gilbertson, R. L. 1994. Detection of bean common blight
bacteria, Xanthomonas campestris pv. phaseoli and
and similar biochemical profile. However, in culture Xanthomonas campestris pv. phaseoli var. fuscans, using the
this variant produces a brown pigment on tyrosine polymerase chain reaction. Phytopathology 84:1185–1192.
medium. The pigment is called fuscous, meaning dusky Birch, P. R. J., Hyman, L. J., Taylor, R., Opio, A. F., Bragard, C.,
and Toth, I. K. 1997. RAPD PCR-based differentiation of
brown in color. This pathogen is named X. campestris Xanthomonas campestris pv. phaseoli and Xanthomonas
pv. phaseoli var. fuscans. There is genetic evidence (in campestris pv. phaseoli var. fuscans. European Journal of
the form of low DNA–DNA homology) that these two Plant Pathology 103:809–814.
variants are genetically distinct from each other. Chan, J. W.Y.F. and Goodwin, P. H. 1999. Differentiation of
Xanthomonas campestris pv. phaseoli from Xanthomonas
campestris pv. phaseoli var. fuscans by PFGE and RFLP.
Disease cycle European Journal of Plant Pathology 105:867–878.
Infected seed is an important source of inoculum. Weed Claflin, L. E., Vidaver, A. K., and Sasser, M. 1987. MXP,
semiselective medium for Xanthomonas campestris pv.
hosts may be important in some regions. In temperate phaseoli. Phytopathology 77:730–734.
climates, the pathogen may survive in crop residue and Gilbertson, R. L., Maxwell, D. P., Hagedorn, D. J., and Leong, S.
provide another source of inoculum. The pathogen is A. 1989. Development and application of plasmid DNA
spread by splashing water from rain or sprinkler irriga- probe for detection of bacteria causing common bacterial
blight of bean. Phytopathology 79:518–525.
tion. Disease development is most pronounced at Gilbertson, R. L., Rand, R. E., and Hagedorn, D. J. 1990.
warmer temperatures of 28–32º C with high humidity. Survival of Xanthomonas campestris pv. phaseoli and
pectolytic strains of X. campestris in bean debris. Plant
Disease 74:322–327.
Control
Malin, E. M., Roth, D. A., and Belden, E. L. 1983. Indirect
Use seed that does not have significant levels of the immunofluorescent staining for detection and identification
pathogen. Rotate crops so that beans are not planted of Xanthomonas campestris pv. phaseoli in naturally infected
bean seed. Plant Disease 67:645–647.
into fields having infested crop residues. Apply copper
Mkandawire, A. B. C., Mabagala, R. B., Guzman, P., Gepts, P.,
sprays to foliage, though such treatments may be only and Gilbertson, R. L. 2004. Genetic diversity and pathogenic
marginally effective. Choose resistant cultivars. Irrigate variation of common blight bacteria (Xanthomonas
with furrow or drip irrigation, and avoid the use of campestris pv. phaseoli and Xanthomonas campestris pv.
phaseoli var. fuscans) suggests pathogen coevolution with the
overhead sprinklers. Eliminate volunteer and other common bean. Phytopathology 94:593–603.
hosts.
Aphanomyces euteiches, Fusarium oxysporum f. sp. different isolates, or anastomosis groups (AGs) can
phaseoli, Phoma medicaginis var. pinodella, Pythium infect bean. See the pea section on foot rot complex for
spp., Rhizoctonia solani,Thielaviopsis basicola
more details (page 272).
ROOT/FOOT ROT COMPLEX
Disease cycle
Introduction and significance Inoculum resides in the soil in the form of various
Foot rot disease is extremely common, and symptoms survival structures, spores, or mycelium. Nutrients and
of this problem can be found in most crops. The foot rot exudates released from germinating bean seeds and
complex of pathogens is probably one of the most roots stimulate pathogen activity and germination of
important disease problems in legumes. chlamydospores, oospores, and spores. Disease devel-
opment occurs at a wide range of temperatures. Overly
Symptoms and diagnostic features wet or poorly draining soils enhance disease severity
This group of pathogens causes damping-off of seeds and incidence. Other factors that increase the problem
and seedlings, and brown to red-brown, sunken lesions include compacted soils, acid soils, low soil fertility, and
on plant hypocotyls and taproots below the soil surface frequent plantings of legumes. Bean hypocotyls become
(322, 323, 324, 325, 326). Lesions may continue to less susceptible to R. solani approximately 2 weeks after
develop until the stem base and roots are severely dis- planting; this increase in resistance is associated with
colored, shriveled, and nonfunctional. Affected plants calcification of the middle lamella between plant cells.
may be stunted, unproductive, and in some cases will
wither and die. Control
Rotate crops and avoid over planting legumes. A
Causal agents minimum of 4 years between such crops is needed to
The main pathogens include Fusarium solani f. sp. help reduce disease pressure. Avoid growing beans in
phaseoli, Rhizoctonia solani, Phoma medicaginis var. fields having histories of severe foot rot. Correct poor
pinodella (formerly known as Ascochyta pinodella), drainage and soil compaction problems. Irrigate fields
Thielaviopsis basicola (cause of black root rot), so that excess water is not applied. Fungicide seed treat-
Aphanomyces euteiches, and Pythium species. The ments are useful in reducing damping-off and
Fusarium and Rhizoctonia pathogens are particularly improving crop establishment; however, these materials
common in California. For R. solani a number of have little effect on the foot rot phase of the disease.
322
322 Hypocotyl
323
lesions due to
Fusarium root rot
of bean.
F UNGAL D ISEASES
323 Hypocotyl lesions due to Rhizoctonia root rot of

bean.
FABACEAE 257
324 References
Alves-Santos, F. M., et al 2002. Pathogenicity and race
characterization of Fusarium oxysporum f. sp. phaseoli
isolates from Spain and Greece. Plant Pathology 51:605–611.
Burke, D. W. and Miller, D. E. 1983. Control of Fusarium root
rot with resistant beans and cultural management. Plant
Disease 67:1312–1317.
Datnoff, L. E. and Sinclair, J. B. 1988. Interaction of Fusarium
oxysporum and Rhizoctonia solani in causing root rot of
soybeans. Phytopathology 78:771–777.
France, R. A. and Abawi, G. S. 1994. Interaction between
Meloidogyne incognita and Fusarium oxysporum f. sp.
phaseoli on selected bean genotypes. Journal of Nematology
26:467–474.
324 Infected hypocotyls of Pythium root rot of bean. Godoy-Lutz, G., Steadman, J. R., Higgins, B., and Powers, K.
2003. Genetic variation among isolates of the web blight
pathogen of common bean based on PCR-RFLP of its ITS-
rDNA region. Plant Disease 87:766–771.
325 Hall, R. and Phillips, L. G. 1992. Effects of crop sequence and
rainfall on population dynamics of Fusarium oxysporum f.
sp. phaseoli in soil. Canadian Journal of Botany
70:2005–2008.
Henis, Y. and Ben-Yephet, Y. 1970. Effect of propagule size of
Rhizoctonia solani on saprophytic growth, infectivity, and
virulence on bean seedlings. Phytopathology 60:1351–1356.
Lloyd, A. B. and Lockwood, J. L. 1963. Effect of soil
temperature, host variety, and fungus strain on Thielaviopsis
root rot of peas. Phytopathology 53:329–331.
Maier, C. R. 1961. Black root-rot development on pinto beans,
incited by Thielaviopsis basicola isolates, as influenced by
different soil temperatures. Plant Disease Reporter
45:804–807.
Miller, D.E. and Burke, D. W. 1986. Reduction of Fusarium root
rot and Sclerotinia wilt in beans with irrigation, tillage, and
bean genotype. Plant Disease 70:163–166.
325 Blackening at stem base of bean caused by Muyolo, N. G., Lipps, P. E., and Schmitthenner, A. F. 1993.
Reactions of dry bean, lima bean, and soybean cultivars to
Thielaviopsis basicola. Rhizoctonia root and hypocotyl rot and web blight. Plant
Disease 77:234–238.
Papavizas, G. C. and Adams, P. B. 1969. Survival of root-
infecting fungi in soil: XII. Germination and survival of
326 endoconidia and chlamydospores of Thielaviopsis basicola in
fallow soil and in soil adjacent to germinating bean seed.
Papavizas, G. C., Adams, P. B., Lumsden, R. D., Lewis, J. A.,
Dow, R. L., Ayers, W. A., and Kantzes, J. G. 1975. Ecology
and epidemiology of Rhizoctonia solani. Phytopathology
65:871–877.
Paulus, A. O., Brendler, R. A., Nelson, J., and Otto, H. W. 1985.
Rhizoctonia stem canker on beans. California Agriculture 39
(11/12):13–14.
Pfender, W. F. and Hagedorn, D. 1982. Aphanomyces euteiches f.
sp. phaseoli, a causal agent of bean root and hypocotyl rot.
F UNGAL D ISEASES
Silbernagel, M. J. and Mills, L. J. 1990. Genetic and cultural

control of Fusarium root rot in bush snap beans. Plant
Disease 74:61–66.
Snapp, S., Kirk, W., Roman-Aviles, B., and Kelly, J. 2003. Root
traits play a role in integrated management of Fusarium root
326 Lower stem lesion of bean caused by Thielaviopsis
rot in snap beans. HortScience 38:187–191.
basicola.

327
GRAY MOLD

Gray mold is frequently damaging on common bean
grown under cool temperate conditions. Botrytis
cinerea is a weak pathogen, and problems are usually
associated with damaged tissues. Crop loss occurs from
diseased pods and also when it proves impractical for
processors to pick out and remove infected pods.
327 Bean pod lesion caused by Botrytis cinerea and
Symptoms and diagnostic features associated with adhering petal.
Young plants that are damaged during crop manage-
ment operations or from environmental extremes are
328
subject to infection by Botrytis, which can infect and
girdle stems and other compromised tissues. Such
plants can die. Leaves are subject to gray mold if they
are damaged by winds and other abrasion factors, or if
fallen petals adhere to leaves. The pathogen colonizes
damaged leaf tissue, or grows on the nutrient-rich petal
tissue and then bridges into healthy leaf tissue. In either
case, the result is a water-soaked lesion that rapidly
turns into a brown lesion that supports the gray growth
of the fungus. However, the most serious problem
involves infection of flowers and developing bean pods.
Pod lesions often develop where floral tissues adhere to
the base or tips of developing pods (327). Once pods
have been colonized, there is rapid enlargement of
water-soaked lesions and the development of the char- 328 Bean pods infected with Botrytis cinerea.
acteristic gray fungal growth (328). Direct contact
between infected and healthy pods enables secondary
spread to take place.
Causal agent
Gray mold is caused by the ascomycete fungus fungus produces characteristically profuse sporulation
Botryotinia fuckeliana. The disease is more commonly that is dense, velvety, and grayish brown in color.
associated with the asexual form Botrytis cinerea.
Conidiophores of B. cinerea are long (1–2 mm), become Disease cycle
gray-brown with maturity, and branch irregularly near Under moderate (15–20º C) and wet conditions with
the apex. Conidia are clustered at the branch tips and high humidity (90–95% relative humidity), disease
are single-celled, pale brown, ellipsoid to obovoid, and development can be rapid. Botrytis is also important on
measure 6–18 x 4–11 μm. The pathogen can be isolated bean in storage and in transit as even a low level of
F UNGAL D ISEASES
on standard microbiological media. Some isolates infection can result in crop rejection. Under dry and
sporulate poorly in culture unless incubated under warm conditions, the pathogen is inhibited and lesions
lights (12 h light/12 h dark). If formed, sclerotia are dry out and become bleached. Botrytis requires
black, oblong or dome-shaped, and measure 4–10 mm. wounded tissue or a food base, such as detached petals,
The fungus grows best at 18–23º C but is inhibited at to incite disease.
warm temperatures above 32º C. On host tissue the
FABACEAE 259
Control Erysiphe polygoni

Plant cultivars that have some tolerance to Botrytis; POWDERY MILDEW
such differences in susceptibility have been seen in
common bean. Cultivars that bear pods high off the Introduction and significance
ground may be less prone to pod infection. Manage the Powdery mildew has a worldwide distribution on bean
crop to avoid damage to the plants. Select sites that have and in some areas is a common problem. However,
good air movement that allows foliage to dry, and plant significant yield losses due to powdery mildew are rare.
crop rows parallel to prevailing winds. Apply fungicides
at early flowering; however, B. cinerea is widely known Symptoms and diagnostic features
to develop resistance to many fungicides. Early symptoms are darkened, discolored areas on the
upper surfaces of the oldest leaves. Such spots become
References colonized with diffuse, white radiating fungal colonies
Johnson, K. B. and Powelson, M. L. 1983. Influence of prebloom (329). Severe powdery mildew growth may cause
disease established by Botrytis cinerea and environmental and foliage to twist, become distorted, and turn yellow. The
host factors on gray mold pod rot of snap bean. Plant Disease
67:1198–1202. fungus colonizes stems and pods, causing pods to be
Polach, F. J. and Abawi, G. S. 1975. The occurrence and biology small and deformed.
of Botryotinia fuckeliana on beans in New York.
Causal agents
Vulsteke, G. and Meeus, P. 1982. Chemical control of Botrytis
cinerea and Sclerotinia sclerotiorum on dwarf snap beans. Powdery mildew is caused by the obligate fungus
Netherlands Journal of Plant Pathology 88:79–85. Erysiphe polygoni. Conidia are ellipsoidal, typically
measure 26–52 x 15–23 μm, and are produced in
chains. The perfect stage appears as small black fruiting
bodies (cleistothecia) but is rarely formed on green
foliage of bean. Distinct races may exist.
Recently a second powdery mildew was reported on
bean in Hungary. Symptoms and signs of this mildew
are similar to those of E. polygoni. This second
powdery mildew pathogen is Podosphaera fusca (pre-
viously named Sphaerotheca fuliginea or S. fusca).
Disease cycle
Disease is favored by warm, dry days and cooler nights,
leading to dew formation. The fungus overwinters on
diseased hosts, and sometimes as cleistothecia on plant
329
debris. Conidia are air dispersed. Powdery mildew
usually occurs on bean late in the production season.
Control
Plant resistant cultivars or cultivars that are less severely
affected by powdery mildew. Early planting and irri-
gating with overhead sprinklers can lower disease
severity. Apply sulfur and other fungicides when early
F UNGAL D ISEASES
stages of disease are observed.
References
Kiss, L. and Szentivanyi, O. 2001. Infection of bean with
cucumber powdery mildew, Podosphaera fusca. Plant
Pathology 50:411.
329 Powdery mildew of bean.
Fusarium oxysporum f. sp. phaseoli Glomerella lindemuthiana

FUSARIUM WILT, (anamorph = Colletotrichum lindemuthianum)
FUSARIUM YELLOWS ANTHRACNOSE
Introduction and significance Introduction and significance

Fusarium wilt of bean is found in North America, South This is an important disease of common bean
America, Africa, and Europe. The disease can be severe (Phaseolus vulgaris) and also occurs on scarlet runner
in parts of Africa, Spain, Brazil, Colombia, Panama, bean (P. coccineus), other Phaseolus species (including
and Costa Rica. P. aureus, P. lunatus, P. mungo, P. radiatus), broad bean
(Vicia faba), and cowpea (Vigna unguiculata). It occurs
Symptoms and diagnostic features in all production areas except hot, dry regions where
Early symptoms include chlorosis of leaves and furrow irrigation is used.
premature senescence of lower foliage. As the disease
progresses, foliage can become bright yellow. Vascular Symptoms and diagnostic features
tissue of main taproot, crown, and lower stem turns Leaf symptoms are angular red-brown spots and red-
red-brown in color. brown sections of leaf veins (330). Stems and petioles
have brown, sunken, elliptical or circular lesions with
Causal agent darker red-brown margins (331). Similar lesions form
Fusarium wilt is caused by the fungus Fusarium oxy- on the hypocotyl when spores wash down from the
sporum f. sp. phaseoli. From diseased vascular tissue in cotyledons or leaves. These lesions are typically 1–2 cm
stems, the pathogen can be isolated onto standard agar long and cause stem collapse when they girdle the stem.
media such as potato dextrose agar. Pathogen mor- As disease progresses, dark brown fruiting bodies
phology and colony characteristics are similar to other develop in the lesions; lesions later ooze pink to orange
F. oxysporum fungi. For more information see the spore exudates. Pods also develop the sunken, brown,
section on Fusarium wilt of pea in this chapter. At least circular lesions and fruiting bodies (332, 333). Seed
five distinct races have been documented. This patho- infection occurs where pod lesions extend through the
gen can survive in the soil for many years. pod wall. Affected seeds have yellow or brown lesions
and can be shriveled, under developed, and result in
Disease cycle poor germination. Severely affected plants show con-
The fungus infects bean roots and travels up the siderable loss of foliage and pod distortion.
vascular tissue and into the stem and above ground
tissues. Disease development is favored by soil temper-
atures around 20º C.
330 330 Leaf vein
Control discoloration from
Use resistant cultivars if such are available. Rotate crops anthracnose of
away from bean, though such rotations do not bean.
eliminate soil inoculum.
References
Alves-Santos, F. M., et al. 2002. Pathogenicity and race
characterization of Fusarium oxysporum f. sp. phaseoli
isolates from Spain and Greece. Plant Pathology 51:605–611.
F UNGAL D ISEASES
Salgado, M. O. and Schwartz, H. F. 1993. Physiological

specialization and effects of inoculum concentration of
Fusarium oxysporum f. sp. phaseoli on common beans. Plant
Disease 77:492–496.
Woo, S. L., et al. 1996. Characterization of Fusarium oxysporum
f. sp. phaseoli by pathogenic races, VCGs, RFLPs, and RAPD.
FABACEAE 261
Causal agent 332

Anthracnose is caused by the ascomycete fungus
Glomerella lindemuthiana. However, the disease is
more commonly associated with the asexual stage
Colletotrichum lindemuthianum. Colletotrichum lin-
demuthianum produces cup-shaped fruiting bodies
called acervuli. Each acervulus consists of a cluster of
conidiophores, long dark setae, and masses of pink
conidia. The conidia are aseptate, cylindrical with
rounded ends, and measure 11–20 x 2.5–5 μm. This is
a complex pathogen and consists of many races,
genotypes, and anastomosis groups.
Disease cycle 332 Pod lesions of anthracnose on bean.

Anthracnose is primarily a seedborne disease, and
survival on crop residues is limited. In temperate regions
the fungus survives in the soil on residues for only a few and new ones continue to appear; therefore, the appro-
months during cold winter conditions. However, if priate resistance must be deployed. The dominant ARE
residues remain dry and undecomposed, the fungus can gene has been important in European cultivars, but in
remain viable for as long as 5 years. In tropical and sub- South and Central America, races have emerged that
tropical areas it is common to have crop-free periods can overcome it. Use seed that does not have significant
lasting only a few months; in such cases, the anthrac- levels of the pathogen. Fungicides have been used suc-
nose fungus can easily persist and infect subsequent cessfully as seed treatments and as foliar sprays, but
bean plantings. In humid conditions, the fungus sporu- they may not be required on resistant cultivars. Ensure
lates on infected seedlings and other tissues. Spores are that there is a rotation of at least 2 years between sus-
then splash-dispersed to surrounding plants. ceptible bean crops.
Control References
Use resistant cultivars, as these are important for the Ansari, K. I., Palacios, N., Araya, C., Langin, T., Egan, D., and
management of anthracnose. Breeding resistant culti- Doohan, F. M. 2004. Pathogenic and genetic variability
among Colletotrichum lindemuthianum isolates of different
vars has been very successful, but there are many races geographic origins. Plant Pathology 53:635–642.
333 Dried bean 333

331
pods showing
anthracnose
lesions.
F UNGAL D ISEASES
331 Stem lesions of anthracnose on bean.

Dillard, H. R. and Cobb, A. C. 1993. Survival of Colletotrichum Sclerotinia minor, S. sclerotiorum, S. trifoliorum
lindemuthianum in bean debris in New York state. Plant
Disease 77:1233–1238. WHITE MOLD
Drijfhout, E. and Davis, J. H. C. 1989. Selection of a new set of
homogeneously reacting bean (Phaseolus vulgaris) Introduction and significance
differentials to differentiate races of Colletotrichum
lindemuthianum. Plant Pathology 38:391–396. White mold or Sclerotinia rot is an important disease on
Mahuku, G. S. and Riascos, J. J. 2004. Virulence and molecular many legume crops, including bean, pea, and broad
diversity within Colletotrichum lindemuthianum isolates bean. Serious attacks can occur on common bean
from Andean and Mesoamerican bean varieties and regions.
grown in temperate areas and on scarlet runner bean.
European Journal of Plant Pathology 110 (3):253–263.
Menezes, J. R. and Dianese, J. C. 1988. Race characterization of Sclerotinia sclerotiorum is the species most commonly
Brazilian isolates of Colletotrichum lindemuthianum and found on bean, broad bean, and pea; S. minor also
detection of resistance to anthracnose in Phaseolus vulgaris. affects bean, causing occasional problems in parts of
North America and Europe. Older references refer to
Rodríguez–Guerra, R., Ramírez-Rueda, M-T., Martínez de la
Vega, O., and Simpson, J. 2003. Variation in genotype, this group of pathogens as belonging in the genus
pathotype and anastomosis groups of Colletotrichum Whetzelinia.
lindemuthianum isolates from Mexico. Plant Pathology
52:228–235.
Schwartz, H. F., Pastor-Corrales, M. A., and Singh, S. P. 1982. Symptoms and diagnostic features
New sources of resistance to anthracnose and angular The first symptoms on bean are small, irregularly
leafspot of beans. Euphytica 31:741–754. shaped, water-soaked areas on stems, leaves, or pods.
Stonehouse, J. 1994. Assessment of Andean bean diseases using
visual keys. Plant Pathology 43:519–527.
These quickly develop into soft, pale brown lesions.
Tu, J. C. 1981. Anthracnose on white bean in Southern Ontario: Lesions eventually support white mycelium, white
spread of the disease from an infection locus. Plant Disease mycelial mounds that are immature sclerotia, and
65:477–480. finally mature, hard, black sclerotia (334, 335). Mature
Tu, J. C. 1982. Effect of temperature on incidence and severity of
anthracnose on white bean. Plant Disease 66:781–783.
sclerotia usually form after tissues are rotted and
Tu, J. C. 1983. Epidemiology of anthracnose caused by breaking down. Plants with stem infections can com-
Colletotrichum lindemuthianum on white bean in southern pletely collapse and dry out. The soilborne S. minor
Ontario: Survival of the pathogen. Plant Disease 67:402–404. only causes infection on stems and crowns in contact
with soil. In these situations, stems develop a brown
decay that later is covered with white mycelium and
small black sclerotia (336).
On broad bean, both young and mature plants can
be affected and rapidly developing, brown lesions occur
on stems, leaves, and pods. Infection often takes place
at soil level, which results in watery lesions at the base
of the stem and subsequent wilting and collapse of the
plants. White mycelium and black sclerotia form on
soft-rotted tissue.
On pea, initial symptoms are water-soaked lesions
on the foliage that can quickly be covered with white
mycelium. Leaf and stem lesions are pale brown, but
have a bleached appearance under dry conditions. Pod
lesions are pale to dark brown in color. Once estab-
lished, there is rapid enlargement of leaf, stem, and pod
F UNGAL D ISEASES
lesions under humid conditions. When lesions girdle the

stem, plants wilt and die. White mycelium and black
sclerotia develop on the surface and inside rotted
tissues.
FABACEAE 263
334 337
334 Pod infections of white mold (Sclerotinia sclerotio- 337 The fruiting bodies, or apothecia, emerging from a
rum) on bean. sclerotium of Sclerotinia sclerotiorum.
335
335 Bean pods Causal agents
and stems infected White mold on legumes is caused by three species of the
with Sclerotinia ascomycete fungus Sclerotinia: S. sclerotiorum, S. trifo-
sclerotiorum. liorum, and S. minor. Sclerotinia minor is readily dis-
tinguished from the other two species because sclerotia
are significantly smaller, usually up to 2–4 mm in
diameter, and are more numerous on plant tissue and in
culture. In addition, S. minor for the most part does not
produce apothecia in nature, while both S. sclerotiorum
and S. trifoliorum produce these sexual fruiting bodies
(337). Sclerotinia minor has a relatively narrow host
range and in addition to occasional infections on
legumes can infect a few other plants like lettuce,
pepper, radicchio, tomato, basil, and cauliflower.
In contrast to S. minor, S. sclerotiorum has an
extremely broad host range and has significantly larger
(5–10 mm long) sclerotia. Sclerotia germinate car-
pogenically by forming small, tan apothecia that are
336
336 Hypocotyl cup-shaped and stalked. Optimum conditions for car-
infection of white pogenic germination are soil temperatures of 15º C and
mold (Sclerotinia soil water potentials between –0.03 and –0.07 MPa.
minor) on bean. Mature apothecia contain cylindrical to clavate asci.
Each ascus contains eight ascospores that are single-
celled, hyaline, elliptical, and measure 9–13 x 4–5 μm.
All eight ascospores are fairly uniform in size.
Sclerotinia trifoliorum forms sclerotia and apothecia
that appear very similar to those of S. sclerotiorum.
F UNGAL D ISEASES
However, the eight ascospores in each ascus sometimes

occur in two distinct sizes (dimorphic). In culture the
mycelial growth of S. trifoliorum on potato dextrose
agar at 26º C is more sparse and slower that of S. scle-
rotiorum. Sclerotinia trifoliorum has a restricted host
range and is generally limited to legume plants.
Disease cycle Overall disease incidence in any particular field

Sclerotinia sclerotiorum and S. trifoliorum survive in the varies from season to season, and a field having severe
soil as sclerotia which can remain viable from a few white mold in one year may or may not have a similar
months to perhaps 10 years, depending on soil condi- severity the following year.
tions, soil moisture, and depth of burial. Percent germi-
nation decreases with increasing time and burial depth. Control
Sclerotia that are kept dry tend to survive for longer Do not plant seed that is contaminated with sclerotia.
periods of time. Direct infection by soilborne sclerotia Avoid planting susceptible legumes in severely infested
apparently is less important for these species. However, fields or locations with a history of white mold
if sufficient soil moisture is present, shallowly buried problems. In a related strategy, practice crop rotations
sclerotia germinate carpogenically by forming small, that use non-hosts, though crop rotations will not
tan apothecia that are cup-shaped and stalked. prevent disease due to the airborne nature of
Ascospores are released from apothecia and carried ascospores. Differences in cultivar susceptibility are
by winds to the host plant. Recent research suggests associated with differences plant growth habit; varieties
that ascospores can survive for several weeks on leaf with open crop canopies may be less susceptible.
surfaces and require very high humidity but not neces- Therefore, choose cultivars that may develop less severe
sarily free moisture to germinate. Nutrients derived white mold disease. Truly resistant cultivars, however,
from senescent or damaged tissues are required for are not readily available. Irrigate in the morning so that
ascospores to germinate and initiate infection. Pea and plant foliage and the soil surface dry quickly. Or irrigate
bean petals are particularly good nutrient sources for with subsurface drip systems so the soil surface is drier.
these pathogens. Secondary spread occurs by mycelium Avoid excessive nitrogen fertilization, which encourages
where there is direct contact between diseased and production of dense foliage, and ensure that potash
healthy plant organs. In bean crops, moderate temper- levels are adequate. For S. minor, deep plowing soils to
atures (20–25º C) and moist soils provide optimal con- bury sclerotia below the root zone has been helpful for
ditions for the pathogen. Synchrony of sclerotial crops such as lettuce.
germination and ascospore production with flowering In some cases, foliar fungicides applied during
of bean flowers is an important aspect of white mold flowering provide effective control, and new products
disease epidemiology. are becoming available for control of Sclerotinia. Foliar
Infective propagules of S. minor are sclerotia that are fungicides include triazole, benzimidazole, dicarbox-
buried in the soil. Duration of soil survival depends on imide, and strobilurin products. However, it is unlikely
the same factors that govern S. sclerotiorum survival. that fungicides will successfully prevent secondary
These sclerotia germinate eruptively by producing spread among senescent leaves. Soil sterilization with
mycelial plugs that directly infect taproots and crowns. chemical, steam or heat treatments can significantly
To successfully infect hosts, the germinating sclerotia reduce sclerotia in the soil, but such treatments are
must be within 2 cm of the taproot, crown or senescing usually too expensive to use in legume crops and will
leaf. Optimum conditions for sclerotial germination are not affect airborne ascospore inoculum entering from
soil temperatures between 10–15º C and soil water beyond the treated field. Biological control with
potential of -0.033 MPa. Once infection has occurred, commercial formulations of the mycoparasite Conio-
the pathogen causes a soft rot decay and production of thyrium minitans has shown some promise against
additional sclerotia. When these decayed tissues are S. sclerotiorum, but not for S. minor.
incorporated back into the field, sclerotia are buried Researchers find that incorporating the biomass
and increase soil inoculum. Under field conditions the from brassica cover crops or crops such as broccoli can
F UNGAL D ISEASES
sclerotia of S. minor rarely produce apothecia with the also reduce soil inoculum and subsequent disease
notable exception of apothecial development in New caused by S. minor. Researchers are attempting to
Zealand. Recent studies indicate that if S. minor define conditions required for ascospore infection and
sclerotia form in aggregations, such clusters might have onset of symptoms; therefore, forecasting systems may
enough resources to produce apothecia. contribute to disease control in the future.
FABACEAE 265
References Uromyces appendiculatus

Abawi, G. S. and Grogan, R. G. 1975. Source of primary RUST
inoculum and effects of temperature and moisture on
infection of beans by Whetzelinia sclerotiorum.
Phytopathology 65:300–309. Introduction and significance
Abawi, G. S., Polach, F. J., and Molin, W. T. 1975. Infection of Most beans are susceptible to rust disease, which occurs
bean by ascospores of Whetzelinia sclerotiorum. worldwide. There are at least 35 recognized pathotypes
of this pathogen, which makes it a challenge to develop
Ferraz, L. C. L., Café Filho, A. C., Nasser, L. C. B., and Azevedo,
J. 1999. Effects of soil moisture, organic matter and grass resistant varieties. Rust can cause severe damage to
mulching on carpogenic germination of sclerotia and foliage and pods and result in significant crop loss.
infection of bean by Sclerotinia sclerotiorum. Plant Pathology Outbreaks of rust are sporadic and associated with
48:77–82.
Fuller, P. A., Steadman, J. R., and Coyne, D. P. 1984.
extended periods of warm temperatures and high
Enhancement of white mold avoidance and yield in dry bean humidity. Rust is increasing in importance in the UK on
by canopy elevation. HortScience 19:78–79. both common and scarlet runner beans.
Gerlagh, M., Goossen-van de Geijn, H. M., Hoogland, A. E., and
Vereijken, P. F. G. 2003. Quantitative aspects of infection of
Sclerotinia sclerotiorum sclerotia by Coniothyrium minitans – Symptoms and diagnostic features
timing of application, concentration and quality of conidial Symptoms develop on leaves and pods, but do not
suspension of the mycoparasite. European Journal of Plant usually affect the stems. Initial symptoms appear about
Hannusch, D. J. and Boland, G. J. 1996. Influence of air
5 days after infection on the undersides of leaves and
temperature and relative humidity on biological control of appear as small, raised white spots. The spot develops
white mold of bean (Sclerotinia sclerotiorum). into a pustule (sorus), or uredinium, measuring 1–2 mm
or larger in diameter, and erupts through the leaf
broccoli rotation on lettuce drop caused by Sclerotinia minor epidermis to release red-brown powdery urediniospores
and on the population density of sclerotia in soil. Plant (338).
Disease 87:159–166.
Kerr, E. D., Steadman, J. R., and Nelson, L. A .1978. Estimation
of white mold disease reduction on yield and yield
components of dry edible beans. Crop Science 18:275–279.
338
Kohn, L. M. 1979. A monographic revision of the genus
Sclerotinia. Mycotaxon 9:365–444.
Nasser, L. C. B. and Hall, R. 1997. Practice and precept in
cultural management of bean diseases. Canadian Journal of
Phillips, A. J. L. 1994. Influence of fluctuating temperatures and
interrupted periods of plant surface wetness on infection of
bean leaves by ascospores of Sclerotinia sclerotiorum. Annals
of Applied Biology 124, 413–427.
Saindon, G., Huang, H. C., and Kozub, G. C. 1995. White mold
avoidance and agronomic attributes of upright common
beans grown at multiple planting densities in narrow rows.
Journal of the American Society for Horticultural Science
120:843–847.
Tu, J. C. 1989. Management of white mold of beans in Ontario.
Willetts, H. J. and Wong, J. A–L. 1980. The biology of Sclerotinia
sclerotiorum, S. trifoliorum, and S. minor with emphasis on
specific nomenclature. The Botanical Review 46:101–165.
F UNGAL D ISEASES
338 Rust of bean.

Uredinia may be surrounded by yellow tissue (339) 339

or additional uredinia. Extensive rust development
causes the leaf to turn chlorotic, dry, and decline. Black
teliospores of the second spore stage are later formed in
these same pustules.
Causal agent
Rust is caused by the basidiomycete fungus Uromyces
appendiculatus. This rust is autoecious, meaning that it
completes its life cycle on one host. Urediniospores are
light to gold-brown, echinulate, thin-walled, unicellu-
lar, measure 18–24 x 20–37 μm, and have two pores.
Teliospores are globoid to ellipsoid, unicellular, measure
20–28 x 25–35 μm, with a hemispherical hyaline
papilla over the pore, and thick cell walls that are
3–4 μm. Both urediniospores and teliospores can occur
in the same sorus. Urediniospores are important in both
the early spread and the wider dispersal of rust, while
teliospores enable the pathogen to survive between
infecting crops.
Disease cycle
Optimum conditions for germination are temperatures
of 17–23º C and leaf wetness duration of 6–8 hours.
The fungus has low survival and infectivity rates if con-
ditions are dry, which accounts for the seasonal vari-
ability in this disease, especially in dry regions. 339 Climbing French bean infected with rust.
Temperature, light intensity, and age of host influence
teliospore formation. Races may differ in their ability to
form teliospores. References
Bassanezi, R. B., Amorim, L., Bergamin,Filho, A., Hau, B., and
Control Berger, R. D. 2001. Accounting for photosynthetic efficiency
of bean leaves with rust, angular leaf spot and anthracnose to
Plant resistant cultivars, though the emergence of new assess crop damage. Plant Pathology 50:443–452.
races may overcome the resistance genes and create the Stavely, J. R. 1984. Pathogenic specialization in Uromyces
need for new varieties. Bury or otherwise destroy crop phaseoli in the United States and rust resistance in beans.
residues, which may reduce teliospore inoculum. Avoid
Stavely, J. R., Steadman, J. R., and McMillan, R. T. 1989. New
over-fertilizing the crop, as high nitrogen levels will pathogenic variation in Uromyces appendiculatus in North
increase bean susceptibility. Interestingly, increasing America. Plant Disease 73:428–432.
potash levels may lower disease severity. Apply fungi- Tomkins, F. D., Canary, D. J., Mullins, C. A., and Hilty, J. W.
1983. Effect of liquid volume, spray pressure and nozzle
cides if available; sulfur and triazoles may provide some arrangement on coverage of plant foliage and control of snap
protection. bean rust with chlorothalonil. Plant Disease 67:952–953.
F UNGAL D ISEASES
FABACEAE 267
Bean common mosaic virus

340
BEAN COMMON MOSAIC

Bean common mosaic virus (BCMV) occurs worldwide
and is primarily seedborne, with transmission rates
sometimes exceeding 80%. On susceptible cultivars,
seed yield may be reduced by more than 50%.

Symptoms consist of leaf chlorosis and mottling,
downward cupping of leaves, and some reduction in
leaflet size (340, 341). Seedborne infection can result in
young plants having a leaf mosaic of light and dark
green areas, with paler sections near the leaf margin.
The first true leaf shows dark green blistering. Aphid-
borne infection on older plants produces crinkled,
chlorotic leaves with a stiff appearance, but does not
cause the mottling or downward rolling of the leaf
margin associated with seedborne infection. The rolling
symptom is useful in distinguishing BCMV from Bean
yellow mosaic virus. Symptoms tend to become less
pronounced as the season progresses. Severe stunting
and black root symptoms are produced at temperatures
of 20º C or greater with virulent strains, and at higher
temperatures (30º C) with less severe strains. Local vein
necrosis occurs as a hypersensitive reaction in some 340 Bean seedlings infected with Bean common
resistant cultivars and this provides field resistance. mosaic virus.
Causal agent and disease cycle 341

BCMV is a potyvirus that is transmitted in a nonpersis-
tent manner by several aphid species, including the pea
aphid (Acyrosiphum pisi), Aphis fabae, and Myzus
persicae. Particle shape is filamentous (flexuous rods).
BCMV is rarely found in broad bean.
Control
(see Part 1).
References
Spence, N. J. and Walkey, D. G. A. 1995. Variation for
pathogenicity among isolates of bean common mosaic virus
V IRAL D ISEASES
in Africa and a reinterpretation of genetic relationships

between cultivars of Phaseolus vulgaris and pathotypes of 341 Foliar symptoms of bean infected with Bean
BCMV. Plant Pathology 44:527–546. common mosaic virus.
Van Rheenen, H. A. and Muigai, S. G. S. 1984. Control of bean
common mosaic virus by deployment of dominant gene I.
Bean yellow mosaic virus

342
BEAN YELLOW MOSAIC

Bean yellow mosaic virus (BYMV) is a common
potyvirus that affects many cultivated and weed
legumes, Iridaceae plants such as gladiolus, and globe
artichoke (Cynara scolymus).

On bean, BYMV reduces pod numbers and overall
yield may be lowered by 40%. BYMV occurs in most
countries where legumes are grown. On common bean,
infected leaves develop small yellow spots, and the plant 342 Leaf symptoms of Bean yellow mosaic virus of
eventually develops a general chlorosis (342). Plants bean.
become brittle during the early stages of infection. In
contrast to BCMV, symptoms tend to become more 343
severe as the season progresses. Affected plants have a
stunted, bushy appearance because there is shortening
of the internodes and proliferation of lateral shoots.
BYMV is the most common cause of mosaic symptoms
in broad bean (343), where symptoms depend on
whether ‘typical’ or ‘pea mosaic’ strains are involved.
Pea mosaic strains usually produce a distinct green and
yellow mosaic, while typical strains result in a mild
green mosaic, green vein banding, or a general
chlorosis. Vein clearing occurs in the younger leaves
7–10 days after infection. Early infections may cause
some stunting of plant growth and slight narrowing
and crinkling of the leaflets. Some severe strains cause
local lesions, and in the USA there is a top-rolling strain 343 Foliar symptoms on broad bean caused by Bean
that causes mosaic and upward rolling of the leaves. yellow mosaic virus.
Causal agent and disease cycle References

BYMV is a potyvirus and is transmitted by many aphid Bos, L., Kowalska, C. Z., and Maat, D. Z. 1974. The
species, including Acyrosiphum pisi, Aphis fabae, identification of bean mosaic, pea yellow mosaic and pea
necrosis strains of bean yellow mosaic virus. Netherlands
Macrosiphum euphorbiae, and Myzus persicae. Particle Journal of Plant Pathology 80:173–191.
shape is filamentous (flexuous rods). Seed transmission Tu, J. C. 1989. Role of temperature and inoculum concentration
is uncommon. Clover (especially Trifolium pratense), in the development of tip necrosis and seedling death of beans
infected with bean yellow mosaic virus. Plant Disease
vetch, and gladiolus are major sources of inoculum, so 73:405–407
bean should not be grown near these plants.
Control
V IRAL D ISEASES

(see Part 1).
FABACEAE 269
PISUM SATIVUM (PEA)

Pseudomonas syringae pv. pisi
344
BACTERIAL BLIGHT

This is an important seedborne disease of pea, which is
widely distributed in pea-growing regions throughout
the world. Bacterial blight can cause extensive crop loss
if environmental conditions are favorable. Significant
losses were recorded in overwintered peas in the UK.

Initial symptoms are water-soaked, angular spots that
become darker and develop necrotic centers. Older
lesions are papery in texture, with a pale center and
darker brown margin (344). The angular shape of older 344 Bacterial blight on pea leaves.
lesions and a water-soaked margin are retained.
Because the pathogen is seedborne, disease may be
initiated when emerging seedlings are infected by
bacteria from the seed coat. In these situations, the
lowest stipules become the initial infection sites. The
pathogen spreads from stipule lesions to the adjacent
stem and other foliage. Diseased flowers may die and
small, developing pods can have circular, sunken Disease cycle
lesions. Where the pod is diseased, underlying seed may Transmission from infested seed to the emerging
be killed or develop dark spots near the seed hilum. seedling is favored if soils and weather conditions are
Severe infection can cause stand loss at the seedling wet. Bacteria enter through stomata or wounds.
stage or result in significant loss of yield and quality if Bacterial blight can spread very rapidly from infected
foliage and pods are damaged. Bacterial blight seedlings to nearby plants if there is rainy weather and
symptoms can be confused with spots caused by crop injury from driving rain, high winds, hail, wind-
Mycosphaerella pinodes. blown soil particles, and frosts. Infection also takes
place at sites of pest damage, such as the leaf notches
Causal agent caused by the weevil Sitona lineatus. The pathogen is
Bacterial blight is caused by Pseudomonas syringae pv. spread between fields on machinery or clothing that has
pisi. This pathogen is a Gram-negative rod that has one passed through the diseased crop, and in drainage or
to five polar flagella. The pathogen can be isolated on irrigation water. Seed may be contaminated due to
standard microbiological media and produces cream- contact with infested dust during harvesting.
colored colonies typical of most pseudomonads. When Actual seed infection occurs close to harvest when
cultured on Kings medium B, this organism produces a dew or rain allows bacteria to penetrate the pod and
diffusible pigment that fluoresces blue under ultraviolet colonize the seed coat. The pathogen can remain viable
light. Strains of this pathogen are host specific to pea on the seed for at least 3 years. The ability to survive in
and related legume plants. This pathogen is seedborne. the soil appears to be very limited, and in most situa-
There are several races of this pathogen that infect tions the pathogen does not survive through the winter
Lathyrus, Vicia, red clover (Trifolium arvense), and unless there are intact crop residues or diseased
soybean (Glycine max). volunteer plants.
Control Aphanomyces euteiches

Use seed that does not have significant levels of the APHANOMYCES ROOT ROT,
pathogen. However, even a very low seed infestation COMMON ROOT ROT
level (0.01%) is able to cause significant problems if
environmental conditions favor disease development. Introduction and significance
Avoid walking through or driving equipment into fields This disease is important in North America, Australia,
having obvious symptoms, as clothing and equipment New Zealand, Japan, and northern Europe. Sometimes
can become contaminated with the bacteria. Sanitize extensive crop loss can occur in badly infested fields. In
harvest and seedcleaning machinery that is used to the Great Lakes area and northeastern states of the
process pea seed. Seed treatments with dry heat, hot USA, Aphanomyces root rot may be the most
water, or sodium hypochlorite are reported to reduce important disease of pea.
seedborne infection. There are both race-specific and
nonspecific resistance sources for pea. Symptoms and diagnostic features
Aphanomyces can infect pea at any age, though the
References most severe problems occur as seedlings emerge. Root
Elvira-Recuenco, M., Bevan, J. R., Taylor, J. D. 2003. cortex tissue turns yellow brown 7 to 14 days after
Differential responses to pea bacterial blight in stems, leaves infection and gradually darkens. The cortex softens and
and pods under glasshouse and field conditions. European
Journal of Plant Pathology 109:555–564. eventually rots away, leaving only thin strands of
Roberts, S. J. 1992. Effect of soil moisture on the transmission of vascular tissue (345). Similar decay occurs on the lower
pea bacterial blight (Pseudomonas syringae pv. pisi) from seed parts of stems. Secondary decay organisms contribute
to seedling. Plant Pathology 41:136–140.
to the darkening and rot of affected tissues. Severely
Roberts, S. J. 1997. Effect of weather conditions on local spread
and infection by pea bacterial blight (Pseudomonas syringae affected plants are stunted and may produce few pods.
pv. pisi). European Journal of Plant Pathology 103:711–719.
Roberts, S. J., Reeves, J. C., Biddle, A. J., Taylor, J. D., Higgins, P. Causal agent
1991. Prevalence of pea bacterial blight in UK seed stocks,
1986–1990. Aspects of Applied Biology 27:327–332.
The cause of Aphanomyces root rot is the oomycete
Taylor, J. D. 1986. Bacterial blight of compounding pea. Aphanomyces euteiches. The sexual stage develops
Proceedings of the 1986 British Crop Protection Conference when antheridia fuse with the homothallic oogonium
– Pests and Diseases 2:733–736. and an oospore is produced. Oospores are hyaline to
Taylor, J. D., Bevan, J. R., Crute, I. R., and Reader, S. L. 1989.
Genetic relationship between races of Pseudomonas syringae
yellow, measure 25–35 μm in diameter, form in rotted
pv. pisi and cultivars of Pisum sativum. Plant Pathology tissues, and can survive for over 10 years in soil. The
38:364–375. asexual stage consists of long, filamentous zoo-
sporangia that may be up to 3–4 mm long. Swimming
primary zoospores are released from the tips of the zoo-
sporangia. These primary zoospores measure 8–11 μm,
usually encyst, and later germinate and release
secondary zoospores. Secondary zoospores produce
hyphae that invade host tissues.
Aphanomyces root rot can be misdiagnosed because
root rot symptoms resemble those caused by other soil
pathogens, and nonpathogenic soil fungi are often
isolated from Aphanomyces-infected roots. Micro-
scopic examination of the root cortex should reveal the
F UNGAL D ISEASES
oospores of A. euteiches with their characteristic

smooth outer wall and wavy (sinuous) inner wall.
These features distinguish A. euteiches oospores from
oospores of Pythium spp. or the larger (8–30 μm in
diameter) resting sporangia of Olpidium brassicae.
Isolate A. euteiches by placing symptomatic tissue from
FABACEAE 271
345 346
345 Aphanomyces root rot. 346 Field of peas showing severe disease caused by Aphanomyces root rot.
Affected plants on the left.
young lesions onto water agar or a semi-selective media Control

such as corn meal agar amended with antibiotics (van- Fungicide seed treatments and resistant cultivars have
comycin) and fungicides. not provided good control in heavily infested fields.
Aphanomyces euteiches affects alfalfa, bean, pea, Avoid planting pea and other susceptible crops in fields
clover, and leguminous weeds. Even cereals such as having a history of this problem. Prepare fields so that
barley and oats can be hosts. Physiological races have drainage is enhanced. Irrigate properly so that excess
been proposed based on variation in host ranges and water is not applied. Long rotations with non-host
virulence. One study characterized 11 such virulence crops are required to reduce soilborne inoculum.
types. Isolates also differ in host preferences; for
example, isolates obtained from pea plants in France References
were preferentially pathogenic on pea. Holub, E. B., Grau, C. R., and Parke, J. L. 1991. Evaluation of
the forma specialis concept in Aphanomyces euteiches.
Mycological Research 95:147–157.
Disease cycle
Kraft, J. M. and Boge, W. L. 1996. Identification of
Oospores germinate to produce hyphae and zoospo- characteristics associated with resistance to root rot caused by
rangia. Infection by zoospores requires moist, cool soils; Aphanomyces euteiches in pea. Plant Disease 80:1383–1386.
optimum temperature for infection is 16º C. Rain and Muehlchen, A. M., Rand, R. E., and Parke, J. L. 1990.
Evaluation of crucifer green manures for controlling
irrigation saturate the soil and allow for rapid disease Aphanomyces root rot of peas. Plant Disease 74:651–654.
spread (346). Damaging attacks occur when cool wet Malvick, D. K., Percich, J. A., Pfleger, F. L., Givens, J., and
springs are followed by warm dry summers, which Williams, J. L. 1994. Evaluation of methods for estimating
inoculum potential of Aphanomyces euteiches in soil. Plant
create water stress for the diseased plants. Diseased Disease 78:361–365.
plants release additional oospore inoculum when they Pfender, W. F. and Hagedorn, D. J. 1983. Disease progress and
are disked back into the soil. Mature oospores form in yield loss in Aphanomyces root rot of peas. Phytopathology
diseased tissues within 2 weeks of infection. 73:1109–1113.
Wicker, E. and Rouxel, F. 2001. Specific behaviour of French
Aphanomyces euteiches Drechs. populations for virulence
F UNGAL D ISEASES
and aggressiveness on pea, related to isolates from Europe,

America and New Zealand. European Journal of Plant
Wicker, E., Hullé, M., and Rouxel, F. 2001. Pathogenic
characteristics of isolates of Aphanomyces euteiches from pea
in France. Plant Pathology 50:433–442.
Aphanomyces euteiches, Fusarium solani f. sp. pisi, Symptoms and diagnostic features
Phoma medicaginis var. pinodella, Pythium spp., In the field, pea stands are reduced due to seed death
Rhizoctonia solani,Thielaviopsis basicola
and poor plant emergence. Plants that do emerge but
FOOT ROT COMPLEX are infected grow poorly, are stunted, and result in fields
having patches of uneven plants (347). Individual plants
Introduction and significance show yellow foliage, premature ripening, and possible
The complex of root pathogens affecting pea is similar wilting (348). In advanced stages of the disease, foliage
to that described for bean. Foot rot disease is extremely can turn gray-green due to water stress and plants can
common, and symptoms of this problem can be found collapse (349). Roots develop brown or black discol-
in most crops. Severe yield loss occurs where soilborne oration, and crown and lower stem tissues have brown
inoculum is high. to black sunken lesions (350). For plants infected with
Fusarium solani f. sp. pisi, the stem and crown lesions
tend to be red-brown. Vining pea is usually more sus-
ceptible to foot rot that other types of pea. Yield losses
347
can be high in varieties grown for dry pea products.
One foot rot pathogen, Phoma medicaginis var.
pinodella, can cause foliar symptoms as well. Lesions
initially appear as small, irregularly shaped flecks that
are dark brown in color. Lesions on leaves and pods
enlarge, generally are round to oval in shape, and
contain concentric rings of alternating shades of brown.
Lesions on stems may become purple in color, and can
enlarge and girdle the stem (351). Foliar symptoms
caused by P. medicaginis var. pinodella are difficult to
differentiate from those caused by Mycosphaerella
pinodes (see the Ascochyta blight section on pea in this
chapter, page 278).
347 Poor establishment and weak growth of pea
seedlings affected by the foot rot complex of Pythium
spp., Fusarium solani f. sp. pisi, and Phoma medicaginis
var. pinodella.
348 349
F UNGAL D ISEASES
348 Garbanzo beans (chickpeas) infected with black 349 Collapsing sugar pea plants affected by Fusarium
root rot. root rot.
FABACEAE 273
350 Garbanzo 350

351 Lower stem 351
bean root infected and root of pea
with black root rot. affected by Phoma
medicaginis var.
pinodella and
Fusarium spp.
Causal agents Control

Foot rot is caused by one or more of the following See the bean section on foot rot complex for more
complex of soilborne fungi: Fusarium solani f. sp. pisi, details.
Phoma medicaginis var. pinodella, Thielaviopsis
basicola, Aphanomyces euteiches, Pythium species., References
Rhizoctonia solani. These fungi are usually readily Biddle, A.J. 1984. A prediction test for pea foot rot and the
isolated by culturing affected tissue on agar media. effects of previous legumes. Proceedings of the British Crop
Protection Conference – Pests & Diseases 3:773–777.
Fusarium solani f. sp. pisi and P. medicaginis var.
Bowden, R. L., Wiese, M. V., Crock, J. E., and Auld, D. L. 1985.
pinodella are particularly important. Fusarium solani f. Root rot of chickpeas and lentils caused by Thielaviopsis
sp. pisi persists in soil for long periods of time due to basicola. Plant Disease 69:1089–1091.
formation of chlamydospores. Phoma medicaginis var. Kraft, J. M. 1986. Seed electrolyte loss and resistance to
Fusarium root rot of peas. Plant Disease 70:743–745.
pinodella can be seedborne and is capable of killing
Kraft, J. M. 1996. Fusarium root rot of peas. Proceedings of the
seedlings. This fungus also survives by means of Brighton Crop Protection Conference – Pests & Diseases
chlamydospores and affects other legumes such as 2:503–509.
clover (Trifolium spp.). This pathogen is considered a Kraft, J. M. and Wilkins, D. E. 1989. The effects of pathogen
numbers and tillage on root disease severity, root length, and
part of the Ascochyta disease complex that affects peas seed yields in green peas. Plant Disease 73:884–887.
grown in most production areas. Phoma medicaginis Levenfors, J. P., Wikström, M., Persson, L., and Gerhardson, B.
var. pinodella was previously named Ascochyta 2003. Pathogenicity of Aphanomyces spp. from different
leguminous crops in Sweden. European Journal of Plant
pinodella. Pathology 109:535–543.
Different isolates, or anastomosis groups (AGs), of Miller, D. E., Burke, D. W., and Kraft, J. M. 1980. Predisposition
R. solani infect legumes. For A. euteiches, the pathogen of bean roots to attack by the pea pathogen, Fusarium solani
survives in the soil via resilient oospores. Different pop- f. sp. pisi, due to temporary oxygen stress. Phytopathology
70:1221–1224.
ulations appear to exist for this organism, as A. Miller, D. E. and Burke, D. W. 1974. Influence of soil bulk
euteiches isolates from pea tend to infect pea but not density and water potential on Fusarium root rot of beans.
F UNGAL D ISEASES
vetch, and vetch isolates infect vetch but not pea. Phytopathology 64:526–529.
Miller, D. E. and Burke, D. W. 1975. Effect of soil aeration on
Fusarium root rot of beans. Phytopathology 65:519–523.
Disease cycle
See the bean section on foot rot complex for more
details (page 256).
Ascochyta pisi
352
LEAF AND POD SPOT

In the late 1920s, researchers described three pea
diseases caused by different Ascochyta fungi. Presently
the pathogen names comprising this former Ascochyta
complex have been changed. Leaf and pod spot, con-
sidered here, is caused by A. pisi. Ascochyta blight (page
278) is caused by Mycosphaerella pinodes; the asexual
stage is A. pinodes. The foot rot pathogen A. pinodella
is now classified as Phoma medicaginis var. pinodella.
These three pathogens can occur together on pea crops,
making it difficult to differentiate the various diseases.
352 Leaf lesion caused by Aschochyta pisi.
Foliar symptoms caused by A. pisi are distinct from 353
those caused by the other two pathogens. Leaf and pod
spot lesions are sunken, tan to light brown, and sur-
rounded by a darker brown to red-brown border (352,
353). Lesions usually contain numerous fruiting bodies
(pycnidia) of the fungus. On leaves and pods, the lesions
tend to be round, while stem lesions are elongated.
Ascochyta pisi does not cause a foot rot disease. Leaf
and pod spots of Ascochyta blight tend to be darker
brown to purple-brown in color.
Causal agent
Leaf and pod spot is caused by A. pisi. The pathogen
forms light brown pycnidia within leaf and pod lesions.
Pycnidia produce conidia that are hyaline, mostly 353 Diseased pea pod affected by Ascochyta pisi.
two-celled, and measure 10–16 x 3–5 μm. Conidia
are exuded out of pycnidia in orange-red masses.
Ascochyta pisi has no known sexual stage, so perithecia Control
are not present in leaf and pod lesions or on pea crop Use seed that does not have significant levels of the
residues. Various races of this fungus have been docu- pathogen. The current practices of growing pea seed
mented. Other Ascochyta species infect different crops in arid regions and treating pea seed with fungi-
legumes such as lentil and chickpea. cides has greatly reduced the incidence and importance
of this disease.
Disease cycle
In contrast to M. pinodes, A. pisi does not overwinter or References
survive in the soil. This pathogen is seedborne and Biddle, A. J. 1994. Seed treatment usage on peas and beans in the
F UNGAL D ISEASES
primary inoculum comes from conidia and other fungal UK. In: Seed Treatment: Progress and Prospects.T. J. Martin
(ed.). BCPC Monograph No. 57: 143–149. BCPC
structures that are on the outside of the seedcoat. Publications, Farnham, UK.
Secondary spread is by splash dispersal of conidia that Bowen, J. K., Peart, J., Lewis, B. G., Cooper, C., Matthews, P.
germinate and penetrate host tissue via stomata or the 1996. Development of monoclonal antibodies against fungi
of the ‘Ascochyta’ complex. Plant Pathology 45:393–406.
cuticle.
FABACEAE 275
Darby, P., Lewis, B. G., and Matthews, P. 1986. Diversity of problem difficult. Infected pods have brown to red-
virulence within Ascochyta pisi and resistance in the genus
Pisum. Plant Pathology 35:214–223. brown, circular to irregular lesions that can exhibit gray
Kaiser, W. J. and Hannan, R. M. 1988. Seed transmission of sporulation in the center of the lesions (354). On
Ascochyta rabiei in chickpea and its control by seed-treatment occasion, black sclerotia develop in the pod lesions. In
fungicides. Seed Science and Technology 16:625–637.
storage, Botrytis can continue to rot the pods but forms
Kaiser, W. J. and Hannan, R. M. 1986. Incidence of seedborne
Ascochyta lentis in lentil germ plasm. Phytopathology white, not gray, mycelial growth. Botrytis is able to
76:355–360. penetrate through the pod wall to produce chalky seeds
Khan, M. S. A., Ramsey, M. D., Corbière, R., Infantino, A., in dry-harvested pea.
Porta-Puglia, A., Bouznad, Z., and Scott, E. S. 1999.
Ascochyta blight of chickpea in Australia: identification,
pathogenicity and mating type. Plant Pathology 48:230–234. Causal agent
Wallen, V. R. 1957. The identification and distribution of The cause of gray mold is the ascomycete fungus
physiologic races of Ascochyta pisi in Canada. Canadian
Botryotinia fuckeliana. However, this perfect stage is
Journal of Plant Science 37:337–341.
Wang, H., Hwang, S. F., Chang, K. F., Turnbull, G. D., and much less commonly seen than the anamorph, Botrytis
Howard, R. J. 2000. Characterization of Ascochyta isolates cinerea. Botrytis cinerea is characterized by its rapidly
and susceptibility of pea cultivars to the Ascochyta disease growing gray to white mycelium, gray-brown conidio-
complex in Alberta. Plant Pathology 49:540–545.
phores, and clusters of gray conidia. Conidia are
obovoid to ellipsoid and measure 8–14 x 6–9 μm. In
culture, some isolates sporulate very poorly if not
placed under ambient or incubation light.
Disease cycle
Botrytis is a common saprophyte that grows on plant
debris and has many plant hosts. Abundant conidia are
produced under optimal conditions of 16–21º C tem-
peratures and 100% relative humidity. Problems are
therefore usually associated with wet weather during
Botrytis cinerea (teleomorph = Botryotinia fuckeliana) and after flowering. Conidia, however, do not readily
GRAY MOLD infect healthy foliage and pod tissues. The presence of a
food source enables conidia to germinate, colonize the
Introduction and significance nutrient source, then spread onto and infect pods and
Gray mold is common in pea when there are wet or leaves. Therefore, petals and other floral parts provide
humid conditions during flowering. While there is some a nutrient supply for the conidia and facilitate infection.
yield loss due to damage to foliage, the greatest
economic damage is from infected and diseased pods.
354
Bleached spots often develop where fallen petals stick
to leaves, stems, or pods. Such spots can later turn into
gray to brown lesions. A more general infection of the
foliage occurs later in the season when the lower leaves
senesce. Senescing leaves are susceptible to infection and
develop brown lesions that support extensive gray
F UNGAL D ISEASES
sporulation when conditions are humid. Once estab-

lished in leaves or stipules, the pathogen can then spread
to stems, which wilt and die when lesions girdle the
stem. Botrytis commonly grows as a secondary invader
in downy mildew lesions, particularly on tendrils,
making diagnosis of the primary downy mildew 354 Gray mold on pea pods.
Control are produced singly or in chains of only two spores. The

Select sites that are well exposed to sun and winds, perfect stage forms on mature lesions and appears as
thereby allowing foliage to dry. Avoid over fertilizing so small, black, spherical fruiting bodies (cleistothecia).
that excessive, succulent foliage is not grown. Apply Cleistothecia measure 180 μm in diameter, have 10 to
fungicides in a timely manner during early flowering 30 unbranched appendages attached to the surface, and
and pod formation stages if weather conditions are contain three to ten asci. Each ascus holds two to eight
likely to favor the pathogen. A single spray is often used hyaline ascospores measuring 9–14 x 10–25 μm.
for vining pea, but two sprays may be required for dry Erysiphe pisi occurs in specialized forms that infect
harvested crops. Fungicide resistance in Botrytis has lucerne or alfalfa (Medicago sativa), vetch (Vicia spp.),
limited the effectiveness of dicarboximide fungicides chickpea (Cicer arietinum), pigeon pea (Cajanus cajan),
and possibly the newer strobilurin products. There are and lentils (Lens spp.). Isolates from pea infect only pea.
no resistant pea varieties.
Disease cycle
References Disease is favored by warm, dry days and cooler nights,
Ford, R. E. and Haglund, W. A. 1963. Botrytis cinerea blight of which lead to dew formation. The fungus overwinters
peas associated with senescent blossoms in northwestern on infected plant debris and may be seedborne. Conidia
Washington. Plant Disease Reporter 47:483–485.
are dispersed in the air, and spore release usually peaks
about midday. Conidia can germinate within an hour
and penetrate the leaf even at low humidity. The disease
cycle can be completed in less than 7 days under
optimal conditions. Disease severity usually is higher
Erysiphe pisi later in the summer season.
POWDERY MILDEW
Control
Introduction and significance Plant resistant cultivars or cultivars that are less severely
Powdery mildew has a worldwide distribution on pea affected by powdery mildew. Early planting and irri-
and the disease is capable of significantly reducing gating with overhead sprinklers can lower disease
yields. Powdery mildew is one of the more common severity. Apply sulfur and other fungicides when early
foliar problems of pea. stages of disease are observed.

Early symptoms are discrete, slightly discolored areas
on the upper surfaces of the oldest leaves with diffuse,
gray to white radiating fungal colonies. Mycelial 355
growth increases and colonies merge so that leaves and
eventually pods become covered in powdery white
growth (355). Advanced symptoms consist of yellow or
purple discoloration of leaf tissues beneath powdery
mildew colonies, early senescence of severely infected
leaves, and blight-like symptoms due to the drying out
of the foliage. Severe powdery mildew reduces seed
quality, may discolor seeds, and impairs flavor of the
F UNGAL D ISEASES
harvested product.
Causal agent
Powdery mildew is caused by the fungus Erysiphe pisi;
this obligate pathogen was previously known as
E. polygoni. Conidia typically measure 20 x 30 μm and 355 Sporulation of powdery mildew on pea.
FABACEAE 277
References formed and measure 10–11 μm in diameter. This

Cook, R. T. A. and Fox, R. T. V. 1992. Erysiphe pisi var. pisi on pathogen is both seedborne and soilborne and can
faba beans and other legumes in Britain. Plant Pathology survive for more than 10 years. Fusarium oxysporum
41:506–512.
f. sp. pisi has distinct races; differential host inoculations
Viljanen-Rollinson, S. L. H., Frampton, C. M. A., Gaunt, R .E.,
Falloon, R. E., and McNeil, D. L. 1998. Spatial and temporal are required to identify these.
spread of powdery mildew (Erysiphe pisi) on peas (Pisum Another legume, chickpea or garbanzo bean
sativum) varying in quantitative resistance. Plant Pathology
47:148–156.
(Cicer arietinum), is susceptible to its own Fusarium
wilt pathogen, F. oxysporum f. sp. ciceris. This
pathogen is found worldwide and has at least eight
distinct races.
Fusarium oxysporum f. sp. pisi
FUSARIUM WILT Disease cycle
The fungus infects pea roots and travels up the vascular
Introduction and significance tissue and into the stem and above-ground tissues.
Fusarium wilt has been recognized in North America Disease progresses rapidly when soil temperatures are
since the 1920s, and also is present in Europe and above 20º C. Under such conditions, wilt symptoms
Australia. There are two distinct forms of the disease, can be severe and plants may die at or before pod
called ‘wilt’ and ‘near wilt’ phases. The disease is of formation. In the UK, Fusarium wilt is also known as
limited importance in the UK because of the use of race St. John’s disease because symptoms are most apparent
1 resistant cultivars. Several other races are recognized around 24 June. ‘Near wilt’ refers to slower symptom
and these are capable of causing economic damage in development that occurs after flowering and is attrib-
other production areas. uted to race 2.
Symptoms and diagnostic features Control

Early symptoms include a downward curling of the Use resistant cultivars. Resistance to race 1 has been
leaves and stipules, stunted plant stature, and lack of stable and widely used for over 40 years. Resistance to
plant vigor. Plants later show progressive leaf yellowing other races is also available. Use seed that does not have
starting from the base of the plant and moving to the significant levels of the pathogen. Rotate crops away
shoot tip. The roots show no external symptoms. from pea, though such rotations do not eliminate soil
However, the vascular system in the main roots and inoculum. In some regions early planting may enable
lower stems will show a yellow, orange or light tan peas to mature before soil temperatures are optimal for
streaking or discoloration. wilt development.

Fusarium wilt is caused by the fungus Fusarium Haglund, W. A. and Kraft, J. M. 1979. Fusarium oxysporum f.
oxysporum f. sp. pisi. From infected vascular tissue in sp. pisi, race 6: Occurrence and distribution. Phytopathology
69:818–820.
stems, the pathogen can be isolated onto standard agar
Hubbeling, N. 1974. Testing for resistance to wilt and near-wilt
media such as potato dextrose agar. Isolates show con- of peas, caused by race 1 and race 2 of Fusarium oxysporum f.
siderable variation in mycelial growth, pigmentation, sp. pisi. Mededelingen van de Faculteit Landbouwweten-
schappen Rijksuniversiteit Gent 39:991–1000.
and spore production in culture. Pathogen morphology
Jimenez-Gasco, M. d. M., Perez-Artes, E., Jimenez-Diaz, R. M.
and colony characteristics are similar to other F. 2001. Identification of pathogenic races 0, 1B/C, 5, and 6 of
oxysporum fungi. The fungus forms one- or two- celled, Fusarium oxysporum f. sp. ciceris with random amplified
F UNGAL D ISEASES
oval to kidney-shaped microconidia on monophialides, polymorphic DNA (RAPD). European Journal of Plant
and four- to six-celled, fusiform, curved macroconidia. Roberts, D. D. and Kraft, J. M. 1973. Enumeration of Fusarium
Microconidia measure 6–15 x 2.5–4.0 μm, and macro- oxysporum f. sp. pisi race 5 propagules from soil.
conidia range from 27–60 x 3.5–5.5 μm. Macroconidia Phytopathology 63:765–768.
are usually produced in cushion-shaped structures
called sporodochia. Spherical chlamydospores are also
Mycosphaerella pinodes (= Ascochyta pinodes) Causal agent

ASCOCHYTA BLIGHT Ascochyta blight is caused by the ascomycete M.
pinodes. On senescent tissues, this fungus produces
Introduction and significance dark brown, spherical perithecia that measure 90–180
Three diseases of pea, each caused by different μm in diameter and contain bitunicate asci. Each ascus
Ascochyta fungi, were discovered in the late 1920s. The holds eight ascospores that measure 12–18 x 4–8 μm
pathogen names comprising the original Ascochyta and are two-celled. Mycosphaerella pinodes has an
complex have recently been changed. Ascochyta blight, asexual stage known as Ascochyta pinodes; A. pinodes
described here, is caused by Mycosphaerella pinodes produces spherical pycnidia that have hyaline, ellipsoid,
(the asexual stage is A. pinodes). Ascochyta pisi (page two-celled conidia measuring 8–18 x 3–5 μm. Conidia
274) causes leaf and pod spot. The foot rot pathogen are exuded out of pycnidia in yellowish (buff-colored)
A. pinodella is now classified as Phoma medicaginis var. masses. Phoma medicaginis var. pinodella also
pinodella (page 272). Because these three pathogens produces spherical pycnidia and hyaline conidia that
may occur together on pea crops, it can be difficult to resemble those of A. pinodes. However, conidia of P.
differentiate the various diseases. medicaginis var. pinodella are usually single-celled and
Ascochyta blight occurs widely on pea crops grown slightly smaller than those of M. pinodes. Different
in temperate regions, but is also known to cause races of M. pinodes have recently been identified.
damage in subtropical regions. Losses are due to foliage
damage and reduced productivity, and to direct infec- Disease cycle
tions on pods, making them unmarketable. Ascochyta Mycosphaerella pinodes produces survival structures
blight is considered the most serious of these three (sclerotia, chlamydospores) that enable this fungus to
diseases. overwinter on pea crop residues and survive in the soil.
Primary inoculum is by airborne ascospores that are
Symptoms and diagnostic features released from perithecia present on pea crop residues.
Mycosphaerella pinodes causes lesions on leaves, stems, Infection occurs within 1 to 2 days at 15–25º C, and
and pods (356, 357, 358). Lesions initially appear as after 4 days at 5º C. A minimum of 2 hours of leaf
small, pinpoint, irregularly shaped flecks that are dark wetness is need for germination. When environmental
brown in color. Lesions on leaves and pods enlarge, conditions favor disease development, symptoms can
generally are round to oval in shape, and contain con- appear 2 to 4 days after ascospore infection. Severe
centric rings of alternating shades of brown. Lesions on disease is associated with repeated pea cropping and
stems may become purple in color, and can enlarge and frequent wet weather after the lower leaves have started
girdle the stem. If conditions favor disease development, to senesce. Crops become more susceptible to disease
the lesions can coalesce and cause significant blighting with senescence, which has been attributed to the
of pea foliage (359). Foliar symptoms caused by M. reduction of the phytoalexin pisatin in senescent tissues.
pinodes are difficult to differentiate from those caused Disease progresses from lower foliage to the top leaves
by P. medicaginis var. pinodella. However, the leaf and by water-splashed conidia and airborne ascospores.
pod spot pathogen (A. pisi) causes spots that are tan to Mycosphaerella pinodes is a seedborne pathogen and
light brown, with darker brown to red-brown borders can infect other hosts such as Lathyrus, Phaseolus, and
(see page 274). Vicia.
Mycosphaerella pinodes can cause seedling
damping-off and lesions on hypocotyls and roots if seed Control
were infested. Therefore, the planting of infested seed Because the Ascochyta blight pathogen can persist in
F UNGAL D ISEASES
can result in poor stands. However, the foot rot the soil, avoid planting pea in fields known to be
pathogen (P. medicaginis var. pinodella) is known to infested with M. pinodes. Use seed that does not have
cause much more severe symptoms on below ground significant levels of the pathogen. Appropriate seed
parts of pea. treatments can also contribute to the management of
seedborne inoculum. Grow seed crops in dry areas to
enhance the production of clean seed. Avoid irrigating
FABACEAE 279
356 358
356 Early symptoms of Ascochyta blight of pea caused 358 Pea pods affected by Mycosphaerella pinodes.
by Mycosphaerella pinodes.
357 359
357 Aschochyta blight symptoms caused by 359 Heavily diseased pea foliage affected by
Mycosphaerella pinodes on senescent pea foliage. Mycosphaerella pinodes.
with overhead sprinklers. If sprinklers are used, time Biddle, A. J. 1994. Seed treatment usage on peas and beans in the
irrigations so that rapid drying of the foliage takes UK. In: Seed Treatment: Progress and Prospects.T. J. Martin
(ed.) BCPC Monograph No. 57:143–149. BCPC
place. Apply foliar fungicides during the flowering Publications, Farnham, UK.
period when foliar symptoms first occur on the lower Clulow, S .A., Lewis, B. G., and Matthews, P. 1992. Expression
senescent leaves and if wet weather is anticipated. of resistance to Mycosphaerella pinodes in Pisum sativum.
Disease forecast systems are being developed.
Kraft, J. M., Dunne, B., Goulden, D., and Armstrong, S. 1998. A
search for resistance in peas to Mycosphaerella pinodes. Plant
F UNGAL D ISEASES
References Disease 82:251–253.

Béasse, C., Ney, B., and Tivoli, B. 1999. Effects of pod infection Moussart, A., Tivoli, B., Lemarchand, E., Deneufbourg, F., Roi,
by Mycosphaerella pinodes on yield components of pea S., and Sicard, G. 1998. Role of seed infection by the
(Pisum sativum). Annals of Applied Biology 135:359–367. Ascochyta blight pathogen of dried pea (Mycosphaerella
pinodes) in seedling emergence, early disease development
Béasse, C., Ney, B., and Tivoli, B. 2000. A simple model of pea
and transmission of the disease to aerial plant parts.
(Pisum sativum) growth affected by Mycosphaerella pinodes.
Onfroy, C., Tivoli, B., Corbière, R., and Bouznad, Z .1999. Peronospora viciae
Cultural, molecular and pathogenic variability of
Mycosphaerella pinodes and Phoma medicaginis var. DOWNY MILDEW
pinodella isolates from dried pea (Pisum sativum) in France.
Roger, C. and Tivoli, B. 1996. Spatio-temporal development of
pycnidia and perithecia and dissemination of spores of Downy mildew can be a major problem in many pea-
Mycosphaerella pinodes on pea (Pisum sativum). Plant growing areas and is particularly a concern in northern
Pathology 45:518–528. Europe and irrigated seed growing areas of the western
Roger, C., Tivoli, B., and Huber, L. 1999. Effects of temperature
USA and Canada. The pathogen is adaptable, and new
and moisture on disease and fruit body development of
Mycosphaerella pinodes on pea (Pisum sativum). Plant races continue to emerge and grow on previously
Pathology 48:1–9. resistant cultivars. This is the same pathogen as the
Roger, C., Tivoli, B., and Huber, L. 1999. Effects of interrupted downy mildew that affects broad bean, though there
wet periods and different temperatures on the development of
Ascochyta blight caused by Mycosphaerella pinodes on pea may be physiological differences which limit cross
(Pisum sativum) seedlings. Plant Pathology 48:10–18. infection between pea and broad bean.
Thomas, J. E., Kenyon, D. M., Biddle, A. J., and Ward, R. L.
2000. Forecasting and control of leaf and pod spot
(Mycosphaerella pinodes) on field pea. Proceedings of the
BCPC Conference – Pests & Diseases 3:871–876. Seedlings infected at emergence are stunted and may die
Wang, H., Hwang, S. F., Chang, K. F., Turnbull, G. D., and (360). Local, non-systemic leaf lesions typically begin as
Howard, R. J. 2000. Characterization of Ascochyta isolates small, yellow, vein delimited blotches on the upper
and susceptibility of pea cultivars to the Ascochyta disease
complex in Alberta. Plant Pathology 49:540–545. surface of leaves (361). The undersides of these lesions
Wroth, J. M. 1998. Variation in pathogenicity among and within support sporulation that is gray to purple (362). As leaf
Mycosphaerella pinodes populations collected from field pea lesions age they become brown and dry. Systemically
in Australia. Canadian Journal of Botany 76, 1955–1966.
infected shoots are usually lighter in color than healthy
Xue, A. G., Warkentin, T. D., and Kenaschuk, E. O. 1997. Effects
of timing of inoculation with Mycosphaerella pinodes on foliage, have a silvery appearance, and also develop
yield and seed infection of field pea. Canadian Journal of gray to purple sporulation (363). Pods can be infected
Plant Science 78:685–689. and typically show large, yellow blotches on the pod
surface and white mycelial growth within the pod
(364). Pod lesions later turn brown and in some cases
become slightly distorted. Tendrils, particularly in semi-
leafless cultivars, can be severely affected and become
bleached and later colonized by Botrytis.
360 Pea seedling

360
Causal agent
infected with Downy mildew on pea and broad bean is caused by the
downy mildew. oomycete Peronospora viciae. In some reports the
pathogen is designated as a pathogen that is specific to
pea: Peronospora viciae f. sp. pisi. The pathogen
produces clusters of dichotomously branched sporan-
giophores that emerge through leaf stomata. Oval to
elliptic sporangia are borne on pointed branch tips and
measure 11–22 x 13–39 μm. The sexual structures, or
oospores, are produced in local foliar lesions and in
pods and can appear as early as 3 weeks after infection.
F UNGAL D ISEASES
Oospores are spherical, yellow to light brown, have

reticulate ridges, and measure 25–37 μm in diameter.
Isolates may be homothallic.
FABACEAE 281
361 363
361 Upper surface of pea leaf with downy mildew. 363 Pea shoots with systemic infection of downy
mildew.
362 364
362 Underside of pea leaf with downy mildew 364 Internal pea pod tissues showing downy mildew
sporulation. sporulation.

Though P. viciae is seedborne, infected seeds usually fail Practice good crop rotation with non-hosts to avoid
to germinate. Oospores in the soil are therefore the buildup of soilborne inoculum. Plant resistant cultivars.
most important source of initial inoculum and mostly However, when new races of the pathogen emerge, such
form at 10–15º C. In naturally infested soils, oospore resistance is overcome and new cultivars will need to be
numbers can range from 2 to 21 spores per gram of soil. developed. Use seed treatments to protect the seed and
Germinating seedlings infected by oospores develop emerging seedlings from infection during plant germi-
systemic symptoms and support abundant sporangia nation. Captan, thiram, and systemic phenylamide
that spread to other plants. Disease development is fungicides have provided some control as seed treat-
most rapid when temperatures are below 10º C and ments, and newer fungicides are being used in Europe.
leaves are wet. Sporangial production decreases rapidly Foliar fungicides have provided only limited control of
F UNGAL D ISEASES
if humidity is below 95%. Wind and rain disperse downy mildew.

sporangia, which penetrate the foliage by means of
germ tubes if there is at least 4 hours of leaf wetness.
Leaves become less susceptible to infection as they age.
Maximum infection requires 6 hours of leaf wetness at
8–20º C.
References With the exception of P. ultimum, these pathogens

Dickinson, C. H. and Singh, H. 1982. Colonization and usually produce zoospores that swim to and infect sus-
sporulation of Peronospora viciae on cultivars of Pisum ceptible tissues. Sexual structures, antheridia, oogonia,
sativum. Plant Pathology 31:333–341.
and oospores, are produced by all species. Pythium
Miller, M. W. and de Whalley, C. V. 1981. The use of metalaxyl
seed treatment to control pea downy mildew. Proceedings debaryanum and P. ultimum are favored when temper-
1981 British Crop Protection Conference – Insecticides and atures are below 20º C, while P. aphanidermatum is
Fungicides 1:341–348.
favored by temperatures above 20º C.
Pegg, G. F. and Mense, M. J. 1970. The biology of Peronospora
viciae on pea: laboratory experiments on the effect of
temperature, relative humidity and light on the production, Disease cycle
germination and infectivity of sporangia. Annals of Applied Pythium species survive in soil as mycelium, sporangia,
Biology 66:417–428.
Stegmark, R. 1994. Downy mildew on peas (Peronospora viciae
or oospores. The infective agent is the swimming
f. sp. pisi). Agronomie 14: 641–647. zoospore. The pathogen is stimulated to produce
Taylor, P. N., Lewis, B. G., and Mathews, P. 1990. Factors zoospores during seed imbibition and germination, and
affecting systemic infection of Pisum sativum by Peronospora seedling emergence, when seed and seedlings leak
viciae. Mycological Research 94:179–181.
Van der Gaag, D. J. and Frinking, H. D. 1997. Extraction of
nutrients into the soil. Infection is favored by high soil
oospores of Peronospora viciae from soil. Plant Pathology moisture. In northern Europe, problems are associated
46:675–679. with cold wet conditions that delay germination, while
Van der Gaag, D. J. and Frinking, H. D. 1997. Survival in parts of the USA the most severe attacks occur when
characteristics of oospore populations of Peronospora viciae
f. sp. pisi in soil. Plant Pathology 46: 978–988. temperatures are 18–24º C (above the optimum for ger-
mination of pea seeds). This latter condition is known
as Pythium wilt and often leads to death of plants.
Pythium spp.
PYTHIUM ROOT ROT, Control
DAMPING-OFF Rotate away from susceptible pea and legume crops,
though crop rotation is of limited value because of the
Introduction and significance soilborne nature of Pythium. Plant seed that has been
Damping-off and root rot in pea are commonly caused treated with fungicides such as thiram, captan, or dra-
by Pythium species, though several other soilborne zoxolon. Avoid using cultivars that are particularly
pathogens cause similar symptoms (see the pea section sensitive to this pathogen; for example, cultivars with
on foot rot complex in this chapter). If soil conditions wrinkled seeds are generally more severely affected than
favor Pythium activity, significant stand loss can result. those with round or dimpled seeds. Select sites and
manage fields so that soils drain well, soil compaction
Symptoms and diagnostic features is reduced, and low areas in the field are avoided.
With pre-emergence damping-off, pea seed and newly
germinated seedlings are attacked and rotted prior to References
the above-ground emergence of the seedling. Symptoms Kraft, J. M. 1974. The influence of seedling exudates on the
of post-emergence damping-off and root rot consist of resistance of peas to Fusarium and Pythium root rot.
stunted plants, yellowed lower leaves, general poor
Matthews, S. 1971. A study of seed lots of peas (Pisum sativum
growth, wilting, and eventual collapse and death of L.) differing in predisposition to pre-emergence mortality in
plants. Roots of infected plants appear water-soaked or soil. Annals of Applied Biology 68:177–183.
light brown in color. In severe cases, nearly all roots may Short, G. E. and Lacy, M. L. 1976. Carbohydrate exudation from
pea seeds: Effect of cultivar, seed age, seed color, and
be girdled or rotted off. temperature. Phytopathology 66:182–187.
F UNGAL D ISEASES
Causal agents
Damping-off and Pythium root rot are caused by the
oomycetes Pythium aphanidermatum, P. debaryanum,
and P. ultimum. All these species survive in the soil as
saprophytes and are favored by wet soil conditions.
FABACEAE 283
Sclerotinia minor, S. sclerotiorum, S. trifoliorum Bean leaf roll virus

WHITE MOLD, BEAN LEAF ROLL
SCLEROTINIA ROT
Introduction and significance Bean leaf roll virus (BLRV) is common in Europe, the
Sclerotinia has a wide host range and pea is included. Middle East, and the USA on both pea and broad bean.
Severe outbreaks occur sporadically in production areas
worldwide. For dry-harvested pea, the black sclerotia Symptoms and diagnostic features
of the pathogen can be found as a contaminant in Early infection of pea causes severe stunting, chlorosis,
harvested seed. and death of plants prior to flowering. If infected later
in the growth stage, pea shows chlorosis of apical
Symptoms and diagnostic features shoots and new leaves, upward rolling of leaves, and
Symptoms of white mold on pea are very similar to occasional brown leaf spots. Early infection of BLRV
white mold symptoms found on other legumes. See the on broad bean causes stunting and reduction in size of
phaseolus bean section on white mold (page 262). developing leaves. BLRV also causes thickening of the
leaf, leaf rolling, and interveinal yellowing (365, 366).
Causal agents The number of pods on affected plants is reduced.
White mold on pea is caused by Sclerotinia sclerotio-
rum and S. trifoliorum. See also the bean section on Causal agent and disease cycle
white mold in this chapter. BLRV is a luteovirus with isometric particles. The
pathogen is transmitted in a persistent manner by pea
Disease cycle (Acyrothosiphon pisum) and other (Aphis craccivora,
See the bean section on white mold in this chapter. Myzus persicae) aphids. BLRV is also known as Pea leaf
roll virus. In addition to pea and broad bean, BLRV
Control affects weed legumes, lucerne (alfalfa), and red and
For a description of control options, see the bean white clovers.
section on white mold in this chapter. Fungicides
applied at flowering can provide good control. Control
References (see Part 1).
Huang, H. C. and Kokko, E. G. 1992. Pod rot of dry peas due to
infection by ascospores of Sclerotinia sclerotiorum. Plant
Disease 76:597–600.
366 Apical
365 366
yellowing of broad
bean caused by
Bean leaf roll virus.
V IRAL D ISEASES
365 Rolled leaflets caused by Bean leaf roll virus.

Pea early browning virus 368 Orange 368

PEA EARLY BROWNING discoloration
inside pea stem
Introduction and significance infected with Pea
Pea early browning virus (PEBV) is thus far only found early browning
in Europe. virus.

Early symptoms on seedlings are chlorosis and death of
the shoot tips, resulting in formation of secondary
shoots (367). At this stage, the stem usually has a
distinctive orange-brown color (368). Older plants
develop purple-brown lesions on leaves, petioles, stems,
and pods (369, 370). Many of the lesions become pale
brown or bleached and can be confused with scorch
symptoms caused by herbicide or fertilizer applications.
Causal agent and disease cycle 369 Pea infected 369

PEBV belongs to the tobravirus group, has rod-shaped with Pea early
particles, and is transmitted by Paratrichodorus and browning virus,
Trichodorus nematodes. It is a seedborne virus. PEBV showing necrotic
is found particularly in the Netherlands and UK where leaf symptoms.
light sandy soils favor the nematode vector.
Control
Follow general suggestions in Part 1. Plant seed that is
free of the virus. Do not plant susceptible pea crops in
fields that have a history of this disease.
References
Hampton, R., Waterworth, H., Goodman, R. M., and Lee, R.
1982. Importance of seedborne viruses in crop germplasm.
367 370
V IRAL D ISEASES
367 Pea seedlings infected with Pea early browning 370 Pea pod with necrotic symptoms caused by Pea
virus. early browning virus.
FABACEAE 285
Pea enation mosaic virus Causal agent and disease cycle

PEA ENATION MOSAIC PEMV is the only member of the enamovirus group and
consists of two isometric particles measuring 25 nm and
Introduction and significance 28 nm. PEMV is transmitted in a persistent manner by
Pea enation mosaic virus (PEMV) is a common virus several aphid species and especially by the pea aphid
and was first reported in the USA in 1935. It is wide- (Acyrothosiphon pisum). Some strains are readily trans-
spread in north temperate areas and can cause losses up mitted mechanically.
to 50%. PEMV affects many of the major genera of
legumes worldwide, including pea, broad bean, Control
chickpea, and lentil. Follow general suggestions for managing virus diseases
(see Part 1).
Although early infections cause severe distortion of References
foliage and even death of plants, more typically there is Fargette, D., Jenniskens, M. J., and Peters, D. 1982. Acquisition
vein clearing and chlorotic or transluscent flecking of and transmission of pea enation mosaic virus by the
individual pea aphid. Phytopathology 72:1386–1390.
the leaves (371). Translucent areas may be produced
along the veins, together with leaf and pod distortion
and formation of enations. Enations are small tissue
proliferations or growths that usually form on the
undersides of leaves and on pods. Severe infection
causes leaf deformities and plant stunting.
371
V IRAL D ISEASES
371 Pea shoot tips infected with Pea enation mosaic virus, showing yellowing and mosaic symptoms.
Pea seedborne mosaic virus References

PEA SEEDBORNE MOSAIC Alconero, R., Provvidenti, R., and Gonsalves, D. 1986. Three
pea seedborne mosaic virus pathotypes from pea and lentil
germ plasm. Plant Disease 70:783–786.
Hampton, R. O., Kraft, J. M., and Muehlbauer, F. J. 1993.
Pea seedborne mosaic virus (PSbMV) was first reported Minimizing the threat of seedborne pathogens in crop germ
in the USA in 1968 but has now been disseminated plasm: elimination of pea seedborne mosaic virus from the
USDA-ARS germ plasm collection of Pisum sativum. Plant
worldwide due to its seedborne nature. Up to 90% seed Disease 77:220–224.
infection has been reported. Hampton, R., Waterworth, H., Goodman, R. M., and Lee, R.
1982. Importance of seedborne viruses in crop germ plasm.
Symptoms and diagnostic features Plant Disease 66:977–978.
Kohen, P. D., Doughterty, W. G., and Hampton, R. O. 1992.
Pea plants are stunted and can be distorted. Leaves roll Detection of pea seedborne potyvirus by sequence specific
downwards and develop chlorosis, mosaic, and other enzymatic amplification. Journal of Virological Methods
general virus-like foliar symptoms. Affected plants may 37:253–258.
fail to set pods or produce distorted pods or seed with Masmoudi, K., Suhas, M., Khetarpal, R. K., and Maury, Y. 1994.
Specific serological detection of the transmissible virus in pea
split seed coats. The disease delays plant maturity. Seed seed infected by pea seedborne mosaic virus. Phytopathology
infection occurs when plants are infected before 84:756–760.
flowering. Broad bean may show more severe rolling
and yellowing of the upper leaves.
Pea streak virus
Causal agent PEA STREAK

PSbMV is a potyvirus that is seedborne in pea, lentil
(Lens culinaris), and vetch. The particle shape is a Introduction and significance
flexuous rod. Chickpea is also a host but does not carry Pea streak virus (PeSV) is known mainly from the USA,
the virus in its seed. There are several strains of the virus though it has been identified in clover in Canada and
and many have a restricted host range. For example, a Germany.
lentil strain is unable to infect pea that carries the mo
gene for resistance to Bean yellow mosaic virus. Symptoms and diagnostic features
Early infection kills the plants of most pea cultivars,
Disease cycle while later infection results in purple or brown streaks
PSbMV is transmitted in a nonpersistent manner by on stems and petioles. Necrotic spots can develop on
aphids, particularly the pea aphid (Acyrothosiphon leaves. Pods show sunken, brown lesions, or may not
pisum), Myzus persicae, and Macrosiphum euphorbiae. develop fully if the plant is infected at an early stage.
The main source of infection is usually seed, and the
elimination of infected seed is the most important Causal agent and disease cycle
control measure; even a low level of seed infection can Researchers differ on whether or not PeSV is a carla-
lead to widespread disease. virus; it also shares characteristics with potexviruses.
Transmission is in a nonpersistent manner by the pea
Control aphid (Acyrothosiphon pisum). Problems often occur
Follow general suggestions for managing virus diseases close to alfalfa, which is a significant reservoir of the
(see Part 1). International regulations are used to pathogen.
prevent spread of this virus in seed. Resistance genes
have been identified for this virus. Control
Follow general suggestions in Part 1.
V IRAL D ISEASES
References
Hampton, R. O. and Webster, K. A. 1983. Pea streak and alfalfa
mosaic viruses in alfalfa: reservoir of viruses infectious to
Pisum peas. Plant Disease 67:308–310.
FABACEAE 287
VICIA FABA (BROAD BEAN)
Aphanomyces euteiches, Fusarium spp., Pythium spp., 373 Lower stem 373
Phytophthora megasperma, Rhizoctonia solani and root lesions
FUSARIUM AND OTHER and fungal growth
ROOT ROTS from Fusarium root
rot of broad bean.
There are a number of root rot diseases caused by
various pathogens on broad (or faba) bean. Five
different Fusarium species are particularly important.
One of them, F. solani f. sp. fabae, has been very
damaging in China, Japan, and Sudan, with losses of up
to 40%. Significant root rot problems are also caused
by species of Rhizoctonia, Pythium, and Phytophthora.
Three other pathogens, Thielaviopsis basicola, Macro-
phomina phaseoli, and Helicobasidium purpureum,
cause only occasional problems.

372
The pathogens cause various plant problems. Shortly
after planting, these soil inhabitants cause seed decay
and damping-off of emergent seedlings. Roots of both
young and mature plants develop rots that turn the root
water-soaked, then black. Mature plants show the
effects of below-ground infection by wilting and col-
lapsing of foliage (372). If Fusarium species are respon-
sible, then masses of white mycelium and pink or
orange spore clusters can be seen on the stem base and
roots (373). Fusarium infection may be associated with
insect damage if there is splitting of broad bean stem
tissues, which allows midge larvae (Resseliella species)
to become established.
Causal agents
Fusarium species affecting broad bean include
F. oxysporum, F. avenaceum, F. culmorum, F. gramin-
earum, and F. solani. Some Fusarium pathogens exhibit
host preferences or limitations and are designated with
the forma specialis (f. sp.) notation. An example of this
F UNGAL D ISEASES
is F. solani f. sp. fabae. The various Fusarium spp. are

identified by morphological features, characteristics
when grown in culture, and host ranges.
372 Wilting broad bean foliage caused by Fusarium

root rot.
A second group of root rot pathogens are in the Botrytis fabae,

oomycete category: Pythium spp., Phytophthora B. cinerea (teleomorph = Botryotinia fuckeliana)
megasperma, and Aphanomyces euteiches. Phytoph- CHOCOLATE SPOT
thora megasperma causes severe root rot and wilt in
spring planted broad bean in the UK, but isolates from Introduction and significance
broad bean were not pathogenic to pea, lupin, clover, This disease occurs in most production areas through-
sugar beet, or brassicas. Phytophthora erythroseptica out the world. Disease severity varies from year to year
var. pisi from pea is reported to infect broad bean. depending on environmental conditions. Severe attacks
Isolates of A. euteiches show considerable variation in may significantly reduce yields.
their host range and pathogenicity, and there may be
limited cross infection between various legumes. For Symptoms and diagnostic features
more details, see the pea section on Aphanomyces root The first symptoms are small, circular, red to brown leaf
rot in this chapter (page 270). spots measuring up to 5 mm in diameter. These spots
Rhizoctonia solani is another root pathogen of are visible on both sides of the leaf surface (374). These
broad bean. This fungus is a common pathogen of smaller, discrete lesions make up the ‘non-aggressive’
many other crops and survives for long periods in the phase of chocolate spot disease. The ‘aggressive’ phase
soil. The fungus has a basidiomycete perfect stage develops if there is suitable humid or wet weather and
(Thanatephorus cucumeris), though the role of this occurs when the small spots coalesce into large, irregu-
perfect stage in disease development is not clear. larly shaped gray to black leaf blotches that can result
in death of leaflets and premature defoliation (375,
Disease cycle 376). Aggressive lesions may have concentric lines
All pathogens considered here are soil inhabitants. within the diseased area, causing them to resemble
Therefore, initial inoculum is always from propagules leaf symptoms from other diseases. Stems develop
in field soils. These diseases are usually more severe elongated red, dark brown, or black lesions. Occasion-
where the field drains poorly, soil is compacted, seed ally, severe disease can kill overwintered plants before
beds are not properly prepared, and excess water is they reach flowering stage. Similar lesions also appear
applied during irrigation. on the flowers and pods. Diseased pods are usually
unmarketable.
Control
Practice crop rotation so that legume crops are not Causal agents
planted too frequently. A break of at least 4 years Chocolate spot is caused by the fungus Botrytis fabae.
between legume plantings is helpful. However, note that Overnight incubation of leaves with aggressive lesions
crop rotations will not eradicate soilborne pathogens will sometimes cause the fungus to sporulate; otherwise,
from fields. Manage the field soil to minimize soil com- standard isolations will be necessary to confirm this
paction and enhance good drainage. Irrigate properly pathogen. Botrytis fabae produces ellipsoidal to ovoid
so that plant stress is minimized but overwatering is conidia that measure 14–29 x 11–20 μm. In culture the
avoided. Seed treatments may provide partial control of pathogen forms profuse, small (1–3 mm), spherical to
seed rot and damping-off phases of root rot diseases. oblong, black sclerotia. In addition to B. fabae,
B. cinerea is thought to contribute to chocolate-spot
References disease by either initiating and forming its own leaf
Salt, G.A. 1983. Root diseases of Vicia faba L. In: The Faba Bean spots, or by co-infecting spots along with B. fabae.
(Vicia faba L.): A Basis for Improvement. (Ed. By P.D. Botyrtis cinerea conidia are significantly smaller (6–18
Hebblethwaite) pp.393–419. Butterworths, London.
F UNGAL D ISEASES
x 4–11μm) than conidia of B. fabae. Botryotinia fucke-

liana, the teleomorph stage of B. cinerea, is rarely
observed on this host.
FABACEAE 289
374 374 Foliar 375

symptoms of
chocolate spot of
broad bean.
375 Broad bean with aggressive and non-aggressive

symptoms on leaflets.
Disease cycle 376

While B. fabae can be seedborne, this aspect is probably
of little importance. Disease is initiated when sclerotia
on infected debris produce conidia. Conidia move via
wind currents and land on susceptible broad bean
tissues. Overwintered and volunteer broad bean plants
that support established infections allow the pathogen
to survive and infect new crops in the spring. Frost and
other damage to the foliage during the winter or early
spring also allow early build up of inoculum. Optimum
temperatures for disease development are 15–20º C,
but activity occurs over the range of 4–30º C. Infection
does not require the presence of free water and occurs
when relative humidity is between 85–100%. The
disease can develop rapidly, with leaf infection able to
take place in less than 12 hours and new lesions
appearing in less than 48 hours. Under optimum con-
ditions, leaves can collapse within 4 days. The pathogen
is favored by high humidity, with little lesion develop-
ment below 70% relative humidity. After initial
infection, conidia are produced when the relative
humidity is high (80–90%); these spores move in the air
and further spread the disease.
Control
F UNGAL D ISEASES
Implement cultural practices to enhance broad bean

growth; stressed plants suffering from nutritional defi-
ciencies, poor drainage, and other factors are more sus-
ceptible. Avoid low-lying or sheltered sites. To improve
drying of plant foliage and decrease humidity, select
sites that have good exposure to wind and sun, increase 376 Broad bean field affected with chocolate spot.
row spacing between plants, and orient crop rows Didymella fabae (anamorph = Ascochyta fabae)
parallel with prevailing winds. For overwintered crops, LEAF AND POD SPOT
adjust the planting date so that vigorous shoot growth
prior to winter is reduced. For the UK, planting should Introduction and significance
be from late October onwards. Fungicides are only This important seedborne disease is present in all the
partially successful in controlling severe chocolate spot. major production areas. Seed tests and pathogen
Foliar sprays are usually initiated at early to mid- thresholds are applied to seed stocks, and Ascochyta is
flowering when non-aggressive spots start to increase a major cause of rejection for seed lots. Distinct strains
on the lower leaves. Triazole or strobilurin fungicides may differentially infect vetch (Vicia sativa), soybean
are often applied with chlorothalonil products. (Glycine max), and bean.

Creighton, N. F., Bainbridge, A., and Fitt, B. D. L. 1985. Symptoms can occur first on the initial leaves of
Epidemiology and control of chocolate spot (Botrytis fabae) seedlings growing from infected seed. Symptoms are
on winter field beans (Vicia faba). Crop Protection
4:235–243. slightly sunken, gray to black leaf spots that measure
Gladders, P., Ellerton, D. R., and Bowerman, P. 1991. Optimising 1–2 cm in diameter and have distinct dark brown or
the control of chocolate spot. Aspects of Applied Biology 27, black margins (377). Leaf spots usually contain small
Production and Protection of Legumes, pp. 105–110.
but visible dark brown fruiting bodies called pycnidia.
Harrison, J.G. 1980. Effects of environmental factors on growth
of lesions on field bean leaves infested by Botrytis fabae. Pycnidia are conspicuous in the gray-colored lesions
Annals of Applied Biology 95:53–61. and may be produced in concentric rings, while these
Harrison, J.G. 1984. Effect of humidity on infection of field bean structures are more difficult to see in darker, black leaf
leaves by Botrytis fabae and on germination of conidia.
spots. Therefore, the black leaf spots may resemble
Harrison, J.G. 1984. The biology of Botrytis spp. on Vicia beans chocolate spot lesions. On stems and pods, lesions are
and chocolate spot disease – a review. Plant Pathology usually sunken and penetrate deeply (378). Stem lesions
37:168–201. can cause wilting of the foliage and stem collapse.
Koike, S. T. 1998. Severe outbreak of chocolate spot of fava
bean, caused by Botrytis fabae, in California. Plant Disease
Infected pods may drop from the plant; seed inside
82:831. diseased pods become dark brown and stained.
Lane, A. and Gladders, P. 2000. Pests and Diseases of Oilseeds,
Brassica seed crops and Field beans. Chapter 3, BCPC Pest
and Disease Management Handbook (ed. D V Alford) pp.
52–83. Blackwell Science, Oxford.
377 378
F UNGAL D ISEASES
377 Close-up of leaf and pod spot lesions of broad 378 Broad bean pods with pink spore ooze from the
bean. leaf and pod spot pathogen.
FABACEAE 291
Causal agent Peronospora viciae

Leaf and pod spot is caused by Didymella fabae. This is DOWNY MILDEW
an ascomycete fungus and produces subglobose, dark
brown pseudothecia and ascospores that are hyaline, Introduction and significance
two-celled, and measure 15–18 x 10–14 μm. The upper Damaging attacks of downy mildew occur regularly on
cell is wider than the lower cell and there is a constric- broad bean. This is the same downy mildew that affects
tion at the septum. In diseased tissues, pycnidia of the pea, though there may be physiological differences that
Ascochyta fabae imperfect stage are dark brown, limit cross infection between broad bean and pea.
spherical, and produce asexual conidia. Conidia are
guttulate, straight or slightly curved, measure 16–24 x Symptoms and diagnostic features
3.5–6 μm, and have from one to three septa. The Foliar symptoms consist of various sized blotches and
pathogen is seedborne. lesions that first are chlorotic, later turn red-brown, and
can reach up to 2–3 cm in diameter (379, 380). The
Disease cycle pathogen produces purple-brown sporulation on the
The fungus can remain viable in seed for up to 3 years, undersides of lesions. Systemic symptoms are
but survival on soil-incorporated crop residues is only a sometimes found and appear as a general chlorosis in
few months. Perithecia release ascospores that can
function as primary inoculum and be blown long
distances by winds. However, secondary spread via 379
conidia from pycnidia depends on splashing water and
will therefore only travel as far as the rain and sprinklers
disperse the conidia. The disease cycle takes 12 to 18
days and is favored by wet and cool conditions.
Control
pathogen. For broad bean, thresholds for infested seed
are 0 positive seed per 600 seeds tested. Fungicide seed
treatments are usually only partially effective. Foliar
fungicides applied for controlling other diseases may
have some efficacy against Ascochyta. There are few 379 Downy mildew lesion on the upper leaf surface of
products specifically registered for leaf and pod spot. broad bean.
Use resistant cultivars if available.
380
References
Bond, D. A. and Pope, M. 1980. Ascochyta fabae on winter
beans (Vicia faba): pathogen spread and variation in host
resistance. Plant Pathology 29:59–65.
Hewett, P. D. 1973. The field behaviour of seed-borne Ascochta
fabae and disease control in field beans. Annals of Applied
Biology 74:287–295.
Gaunt, R. E. 1983. Shoot diseases caused by fungal pathogens.
In: The Faba Bean (Vicia faba L.): A Basis for Improvement.
(Ed. By P.D. Hebblethwaite) pp.463–492. Butterworths,
F UNGAL D ISEASES
London.
Jellis, G. J. and Punithalingam, E. 1991. Discovery of Didymella
fabae sp. nov., teleomorph of Ascochyta fabae, on faba bean
straw. Plant Pathology 40:150–157.
Madeira, A. D., Fyrett, K. P., Rossall, S., and Clarke, J. A. 1993.
Interactions between Ascochyta fabae and Botrytis fabae.
Mycological Research 97:1217–1222. 380 Underside of downy mildew lesion of broad bean.
the upper leaves, accompanied by profuse sporulation Sclerotinia minor, S. sclerotiorum, S. trifoliorum
on the leaf underside. Old downy mildew lesions WHITE MOLD,
become dry, brown to black in color, and can be SCLEROTINIA ROT
colonized by Botrytis fungi.
381
Causal agent
Downy mildew is caused by the oomycete Peronospora
viciae. For a description of this pathogen see the pea
section on downy mildew in this chapter (page 280).
Disease cycle
Primary inoculum is mainly soilborne oospores, and
secondary spread is by airborne sporangia. This disease
is favored by cool, moist conditions. For more details,
see the pea section on downy mildew in this chapter.
Control
Use resistant cultivars. Rotate broad bean and other 381 Broad bean, like field bean pictured here, can be
legume crops with non-hosts so that soil inoculum does severely affected by Sclerotinia.
not build up to high levels; crop rotations, however, will
not prevent disease because of the far ranging aerial 382
sporangia. Some seed treatments can help prevent
seedling infection from soilborne oospores. Apply foliar
fungicides to reduce secondary spread.
References
Biddle, A. J., Thomas, J., Kenyon, D., Hardwick, N. V., and
Taylor, M. C. 2003. The effect of downy mildew
(Peronospora viciae) on the yield of spring sown field beans
(Vicia faba) and its control. Proceedings of the BCPC
International Congress – Crop Science & Technology 2003
2:947–952.
Glasscock, H. H. 1963. Downy mildew of broad bean. Plant
Van der Gaag, D. J., Frinking, H. D., and Geerrds, C. F. 1993.
Production of oospores by Peronospora viciae f. sp. fabae. 382 Young broad bean plants dying from Sclerotinia
Netherlands Journal of Plant Pathology 99, Supplement trifoliorum infections.
3:83–91.

Sclerotinia diseases are important on many legume
crops, including broad bean. Crops in coastal regions of
North Africa, Asia, North America, and Western
Europe can experience significant problems with
F UNGAL D ISEASES
Sclerotinia pathogens. Three species of Sclerotinia occur

on broad bean. Sclerotinia sclerotiorum is the most
commonly found species on this crop. In the UK,
S. trifoliorum is the important species on overwintered
FABACEAE 293
crops; severe disease is often associated with previous Uromyces vicia-fabae

red clover (Trifolium pratense) plantings. Sclerotinia RUST
minor affects broad bean but is less of a problem.
Interestingly, in California broad bean appears to be Introduction and significance
immune to S. minor. This common and widely occurring rust disease affects
broad bean, pea, lentil, and other plants in the
Symptoms and diagnostic features Fabaceae. There is some specialization of races, which
Symptoms of white mold on broad bean, caused by all vary in their host ranges. Rust is capable of reducing
three species of Sclerotinia, are very similar to white yields and is particularly severe in North Africa, the
mold symptoms found on other legumes (381). For Mediterranean region, and the Middle East. More
symptom descriptions, see the phaseolus bean section typically, however, rust epidemics develop after
on white mold in this chapter (page 262). flowering, especially on autumn-planted crops, and its
effects on yield and quality are limited.
Causal agents
White mold on broad bean can be caused by any of the Symptoms and diagnostic features
three Sclerotinia species: S. sclerotiorum, S. trifoliorum, Initial rust symptoms are small, chlorotic leaf spots that
(382), and S. minor. For descriptions of these pathogens first develop on leaves lower in the plant canopy.
see the bean section on white mold in this chapter. Typical orange-brown, raised pustules, called uredinia,
develop from these yellow spots (383). The pustules are
Disease cycle usually bordered with a chlorotic halo and later break
For a description of the disease cycle, see the bean open, releasing the dusty orange-brown spores. As rust
section on white mold in this chapter (page 262). develops, the number of spots and pustules increases
and leads to drying and death of entire leaves. A general
Control epidemic causes an overall bronzed appearance and
For a description of control options, see the bean extensive defoliation. Rust also has an aecia stage that
section on white mold in this chapter.
References
Jellis, G. J., Davies, J. M. L., and Scott, E. S. 1984. Sclerotinia on
oilseed rape: implications for crop rotation. Proceedings of
the British Crop Protection Conference – Pests & Diseases
1984 2:709–716. 383
Jellis, G. J., Smith, D. B., and Scott, E. S. 1990. Identification of
Sclerotinia spp. on Vicia faba. Mycological Research
94:407–409.
Willets, H. J. and Wong, J. A-L. 1980. The biology of Sclerotinia
sclerotiorum, S. trifoliorum, and S. minor with emphasis on
specific nomenclature. Botanical Review 46: 101–165.
Williams, G. H. and Western, J. H. 1965. The biology of
Sclerotinia trifoliorum Erikss. and other species of sclerotium-
forming fungi. I Apothecium formation from sclerotia.
F UNGAL D ISEASES
Williams, G. H. and Western, J. H. 1965. The biology of

Sclerotinia trifoliorum Erikss. and other species of sclerotium-
forming fungi. II The survival of sclerotia in soil. Annals of
383 Rust uredinia on broad bean.
384 386
384 Rust aecia on upper leaf surfaces of broad bean.
385
385 Rust aecia on lower leaf surfaces of broad bean. 386 Telial stage of rust of broad bean.
causes yellow spots on leaves (384, 385). The conspic- reported to overwinter in Mediterranean climates but
uous dark brown teliospore stage forms on plant tissues are unable to survive severe winters. In the UK, aecidia
in late summer when crops are maturing (386). on V. faba have been reported only occasionally in late
autumn or at the end of winter. The previous name for
Causal agent this pathogen was Uromyces fabae.
Rust of broad bean is caused by the fungus Uromyces
vicia-fabae. This pathogen is a macrocyclic, autoecious Disease cycle
rust that produces sub-globoid to ovoid, pale brown The type of initial inoculum appears to depend on the
urediniospores. Urediniospores are echinulate, have nature of the winter season in various regions. If winters
three to four pores, and measure 18–28 x 18–22 μm. are relatively mild, then urediniospores from volunteer
Teliospores, a second spore type, are similar in shape to plants are the initial inoculum. In regions having more
F UNGAL D ISEASES
the urediniospores but are smooth walled and darker severe winters, teliospores from crop residues germinate
brown. Teliospores are also larger, measuring 24–35 x and result in aecidia on the spring planted broad beans.
18–25 μm, and are attached to brown stalks (pedicels) Teliospores may remain viable for up to 2 years. There
that can be up to 100 μm long. A third spore type, are reports that seeds may harbor this pathogen. High
aecidiospores, are yellow, polygonoid–globoid in shape, humidity and warm temperatures favor development of
and measure 18–36 x 16–24 μm. Aecidiospores are this disease.
FABACEAE 295
Control Broad bean stain virus, Broad bean true mosaic virus
Destroy volunteer plants and bury crop residues so that BROAD BEAN STAIN,
they decompose. Apply fungicides prior to or at an early BROAD BEAN TRUE MOSAIC
stage of rust development. Effective products are dithio-
carbamates, strobilurins, and chlorothalonil, which are Introduction and significance
protectants, and triazoles and morpholines, which have Some viruses of interest that infect broad bean are the
some eradicative activity. Sources of rust resistance have following: Bean yellow mosaic virus, Bean leaf roll
been identified but may not be completely satisfactory. virus, Broad bean stain virus, Broad bean true mosaic
Plant resistant cultivars as they become available. virus. In this chapter, Bean yellow mosaic virus is
discussed in the virus section for bean, and Bean leaf roll
References virus is discussed in the virus section for pea. Broad
Conner, R. L. and Bernier, C. C. 1982. Host range of Uromyces bean stain virus (BBSV), in nature, infects only broad
viciae-fabae. Phytopathology 72:687–689. bean and occurs in Europe, the Mediterranean area,
Conner, R. L. and Bernier, C. C. 1982. Race identification of
and Australia.
Uromyces viciae-fabae. Plant Pathology 4:157–160.
Murray, D. C. and Walters, D. R. 1992. Increased photosynthesis
and resistance to rust infection in upper, uninfected leaves of Symptoms and diagnostic features
rusted broad beans (Vicia faba L.). New Phytologist BBSV causes severe mosaic symptoms on leaves,
120:235–242.
though symptom expression can vary between succes-
Rashid, K. Y. and Bernier, C. C. 1986. Selection for slow rusting
in faba bean to Uromyces viciae–fabae. Crop Protection sive leaves. Plants are stunted and produce deformed
5:218–224. pods. BBSV induces a brown necrosis or stain around
Rubiales, D. and Sillero, J. C. 2003. Uromyces viciae-fabae the periphery of infected seed (387) in cultivars such as
haustorium formation in susceptible and resistant faba bean
lines. European Journal of Plant Pathology 109:71–73. Aquadulce; however, other cultivars such as Triple
Sache, I., and Zadoks, J. C. 1995. Life-table analysis of faba bean White show no such effect. Yield loss may be as high as
rust. European Journal of Plant Pathology 101:431-439. 30 to 40%.
Sillero, J. C., Moreno, M. T., and Rubiales, D. 2000.
Characterization of new sources of resistance to Uromyces
viciae-fabae in a germplasm collection of Vicia faba. Plant Causal agents and disease cycle
Pathology 49: 389–395. BBSV has isometric particles that measure 28 nm in
Williams, P. F. 1978. Growth of broad beans infected by diameter and belongs to the comovirus group. Infected
Uromyces viciae-fabae. Annals of Applied Biology
24: 329–334.
seed is an important source of BBSV as transmission
rates to seedlings may approach 40%. BBSV can be
detected in seed by immuno-scanning electron micro-
scopy (ISEM). In the field, BBSV is vectored by weevils,
particularly Apion vorax and Sitona lineatus.
Broad bean true mosaic virus (BBTMV) is also a
387
comovirus that has particle shape, symptoms, biology,
epidemiology, and vectors very similar to BBSV.
Serological tests, however, show that BBTMV and
BBSV are distinct from each other. BBTMV is
commonly seedborne and affected seedlings are stunted
and produce few pods. There is some evidence of
cultivar resistance for BBTMV.
V IRAL D ISEASES
Control
(see Part 1).
387 Broad bean seed coat showing necrosis due to
Broad bean stain virus.
Lactuca sativa Lettuce
LETTUCE (Lactuca sativa) is in the Asteraceae (aster family) and is the only
commercially grown Lactuca species. Lettuce is perhaps the most popular fresh salad
vegetable in the world and is almost exclusively used as a fresh product. (Some lettuce is used
in stir-fried dishes in Asian cuisine, and lettuce is cooked in a few dishes in western countries.)
Lettuce most likely originated in the Mediterranean area. It has a long history of use for
human consumption and today is grown throughout the world. Several lettuce types are
grown commercially. Head-forming types are crisphead or iceberg, and butterhead or bibb
lettuce. Loose, non-head-forming types are romaine or cos, and leaf or loose-leaved
(mostly red and green leaf) cultivars.
Aster yellows phytoplasma of the phytoplasma, age of the plant when infected, and
ASTER YELLOWS other factors. Plants are generally stunted and yellowed
(388). Leaves can be malformed in various ways, and
Introduction and significance often remain small and thickened (389). When the plant
Aster yellows is periodically important on lettuce crops is sliced lengthwise, the arrangement of the stems
throughout the world. Disease incidence is usually low, sometimes shows a twisted, spiral configuration (390).
so this problem is considered a minor disease. Characteristic, diagnostic pink to orange-tan latex
oozes to leaf and petiole surfaces and results in oblong
Symptoms and diagnostic features to circular deposits in the interior parts of lettuce heads
Symptoms and disease severity of aster yellows on (391). Plants infected early in their development will not
lettuce can be highly variable, depending on the strain form heads.
388 389
388 Chlorotic and stunted lettuce infected by aster 389 Deformed lettuce infected by aster yellows.
yellows.
L ACTUCA S ATIVA 297
390
leafhopper vector. The distribution of aster yellows
follows the pattern of leafhopper migration from
foothills, pastures, and weedy areas. The aster yellows
phytoplasma has an extremely broad host range and
can infect hundreds of different plant species.
Phytoplasmas have not yet been cultured. Nucleic acid
preparations or serological methods are necessary to
confirm the presence of this pathogen. Sieve elements
from plant vascular tissue may contain particulate
material generated by the pathogen that can be stained
with Azure A and viewed with a light microscope.
390 Lettuce infected with aster yellows can develop a
twisting of the petioles. Control
Do not plant lettuce or other sensitive crops in fields or
391 Aster yellows areas having a history of the disease. Such locations are
391
causes pink latex frequented by the vector or have in the vicinity a natural
deposits to form in reservoir of the pathogen; therefore, lettuce planted here
lettuce. will be exposed to the problem.
References
Deely, J., Stevens, W. A., and Fox, R. T. V. 1979. Use of Dienes’
stain to detect plant diseases induced by mycoplasmalike
organisms. Phytopathology 69:1169–1171.
Deng, S. and Hiruki, C. 1991. Genetic relatedness between two
nonculturable mycoplasmalike organisms revealed by nucleic
acid hybridization and polymerase chain reaction.
Lee, I.-M., Davis. R. E., Chen, T.-A., Chiykowski, L. N., Fletcher,
J., Hiruki, C., and Schaff, D. A. 1992. A genotype-based
system for identification and classification of mycoplasmalike
organisms (MLOs) in the aster yellows MLO strain cluster.
Lee, I.-M., Davis. R. E., and Hsu, H.-T. 1993. Differentiation of
strains in the aster yellows mycoplasma-like organism strain
Causal agent cluster by serological assay with monoclonal antibodies.
Aster yellows disease is caused by the aster yellows
Severin, H. H. P. and Frazier, N. W. 1945. California aster
phytoplasma. Phytoplasmas, like typical bacteria, are yellows on vegetable and seed crops. Hilgardia 16:573–596.
prokaryotes but are placed in a distinct category called Zhang, J., Hogenhout, S. A., Nault, L. R., Hoy, C. W., and Miller,
mollicutes. Mollicutes are single-celled organisms that S. A. 2004. Molecular and symptom analyses of phytoplasma
strains from lettuce reveal a diverse population.
lack a cell wall, appear in various shapes (called pleo- Phytopathology 94:842–849.
morphism), and have very small genomes. Phyto- Zhou, X., Hoy, C. W., Miller, S. A., and Nault, L. R. 2002.
plasmas inhabit the phloem tissue of their host plants. Spacially explicit simulation of aster yellows epidemics and
This pathogen affects a very wide host range of culti- control on lettuce. Ecological Modeling 151:293–307.
vated and wild plants.

Disease cycle
The aster yellows phytoplasma is vectored by adult
leafhoppers, especially the aster leafhopper (Macro-
steles quadrilineatus). The phytoplasma overwinters in
perennial or biennial host plants and in the body of the
Pseudomonas cichorii
392
VARNISH SPOT

Varnish spot is a disease that is associated with con-
taminated water sources, and therefore tends to be
limited to certain production areas. The disease is of
periodic importance in California and also occurs in
most lettuce producing areas elsewhere in the world.

The disease affects only the inner leaves of lettuce
varieties that form an enclosed head; hence this disease
will not usually be found on romaine or leaf lettuce
varieties that have an open architecture. To see the 392 Lesions of varnish spot on lettuce.
symptoms, remove the outer wrapper leaves of the
headed plant. Varnish spot appears as dark brown, 393
shiny, firm, necrotic lesions on these inner leaves (392,
393). The disease initially results in small lesions
(1–3 mm diameter) that can later expand and coalesce
into extensive necrotic sections encompassing entire
leaves. Lesion borders are usually not delimited by
veins. A notable feature is that lesions caused by this
pathogen remain intact; the lesions are not soft, mushy,
or broken down. This firmness is in contrast to
secondary bacterial soft rots and slime of lettuce in
which tissues are disintegrated (394). The disease is
particularly challenging because the symptoms cannot
be observed without cutting into the lettuce heads.
Therefore, even if the disease is detected in a few field 393 Close-up of lesions of varnish spot on lettuce.
samples, the likely incidence of the disease remains
unknown. Growers and harvesters must speculate on 394
the advisability of harvesting such fields.
Causal agent
Varnish spot is caused by the bacterium Pseudomonas
cichorii. Pseudomonas cichorii is a fluorescent, Gram -
negative rod in the Group I pseudomonad group. The
pathogen can be isolated on standard microbiological
media. Colonies are cream to light yellow in color,
smooth, and produce a fluorescent pigment on King’s
medium B. While P. cichorii is known to infect other

vegetable crops, little information is available on
whether lettuce strains can infect other plants or vice
versa. On lettuce, P. cichorii has also been reported to
cause leaf spot and stem rot diseases, which are distinct
from varnish spot. 394 In contrast to varnish spot, bacterial slime
infections are soft and watery.
Disease cycle 395 395 Initial root

Varnish spot occurs when water contaminated with lesions of corky
P. cichorii is used to sprinkle irrigate head-forming root of lettuce.
lettuce crops that are at the rosette stage of develop-
ment. There is some evidence that P. cichorii also
survives for brief periods in the soil and could be
splashed up onto plants via sprinkler irrigation or rain.
As infested lettuce heads begin to grow and become
enclosed, the bacteria are trapped within the head,
infect the leaves, and initiate disease.
Control
Alter the irrigation system so that overhead sprinklers
are not used. If sprinklers must be used, do not plant
cultivars that form a totally enclosed head. Do not plant
consecutive lettuce crops because infested crop residues
also harbor the pathogen. Rotate with non-host crops
so that soilborne inoculum levels are reduced. Treat
the irrigation water with chemicals such as copper
compounds, which perhaps provide some control.
References
Dhanvantari, B. N. 1990. Occurrence of bacterial stem rot
caused by Pseudomonas cichorii in greenhouse-grown lettuce
in Ontario. Plant Disease 74:394.
Grogan, R. G., Misaghi, I. J., Kimble, K. A., Greathead, A. S.,
Ririe, D., and Bardin, R. 1977. Varnish spot, destructive 396
disease of lettuce in California caused by Pseudomonas
cichorii. Phytopathology 67:957–960.
Rhizomonas suberifaciens
CORKY ROOT

In some lettuce producing areas, corky root is a limiting
factor in lettuce production. In parts of California the
disease is widespread and affects large areas of the crop.

Early symptoms consist of yellow bands and patches on
taproots of lettuce seedlings (395). These yellow areas
gradually expand, taking on a green-brown color and

developing cracks and rough areas on the root surface.
As disease severity increases, the entire taproot may
become brown, severely cracked, brittle, and nonfunc-
tional; the feeder root system can also be reduced and
damaged (396). As the disease continues to progress,
the taproot may be reduced to a short (3–6 cm long) 396 Severe root lesions of corky root of lettuce.
397 Disease cycle

As a soil inhabitant, the pathogen survives in the soil for
a long period of time. Corky root disease is typically
more of a problem when soil temperatures are relative-
ly warmer, with severity steadily increasing as tempera-
tures rise from 10 to 31° C. High rates of nitrogen
fertilizers, especially nitrates, also enhance disease
severity.
Control
Plant corky root resistant cultivars, though some strains
have been isolated that can overcome such resistance.
397 Stubbed-off taproot of lettuce affected by corky Avoid planting consecutive lettuce crops and rotate
root. with non-host plants. Reduce the amount of nitrogen
fertilizers used on the lettuce crop; slow-release fertiliz-
ers may be useful in this regard. Use drip irrigation as
this can lessen corky root severity. For fields with heavy
stump and the plant forced to survive via adventitious disease pressure, use lettuce transplants instead of direct
roots that develop from this stump (397). The disease seeding. Corky root is much less severe on the fibrous
may cause some internal discoloration and hollowing root systems of transplants compared with the central
of the root pith, though root symptoms are mostly on taproot system of direct seeded plants.
the exterior root surfaces. When the root is severely
diseased, above-ground symptoms consist of wilting References
during warm weather, stunting of plants, and general Koike, S. T. and Schulbach, K. F. 1994. Evaluation of lettuce
poor, uneven, and delayed growth. cultivars for resistance to corky root disease. Biological and
Cultural Tests 9:29.
Mou, B. and Bull, C. 2004. Screening lettuce germplasm for new
Causal agent sources of resistance to corky root. Journal of the American
Corky root disease is caused by the bacterium Society for Horticultural Science 129:712–716.
Rhizomonas suberifaciens. Rhizomonas suberifaciens O’Brien, R. D. and van Bruggen, A. H. C. 1991. Populations of
Rhizomonas suberifaciens on roots of host and nonhost
is a soilborne, Gram-negative bacterium. The bacterium plants. Phytopathology 81:1034–1038.
is an oligotrophic organism that grows only on media van Bruggen, A. H. C., Brown, P. R., and Jochimsen, K. N. 1990.
with low carbon content and has a very slow growth Host range of Rhizomonas suberifaciens, the causal agent of
corky root of lettuce. Plant Disease 74:581–584.
rate. For these reasons, R. suberifaciens is difficult to
van Bruggen, A. H. C., Brown, P. R., Shennan, C., and
isolate and grow in culture. Attempt isolations by using Greathead, A. S. 1990. The effect of cover crops and
the semi-selective S-medium. Colonies are cream to off- fertilization with ammonium nitrate on corky root of lettuce.
white in color, wrinkled, and after one week have Plant Disease 74:584–589.
van Bruggen, A. H. C., Grogan, R. G., Bogdanoff, C. P., and
attained a colony diameter of only 1 mm (incubated at Waters, C. M. 1988. Corky root of lettuce in California
28° C). Rhizomonas suberifaciens causes disease on caused by a Gram negative bacterium. Phytopathology
lettuce, endive, and sowthistle (Sonchus oleraceus) and 78:1139–1145.
prickly lettuce (Lactuca serriola) weeds. The bacterium van Bruggen, A. H. C., Jochimsen, K. N., and Brown, P. R. 1990.
Rhizomonas suberifaciens gen. nov., sp. nov., the causal agent
can also live as a rhizosphere organism, and it has been of corky root of lettuce. International Journal of Systematic
recovered from the roots of barley and other non-hosts. Bacteriology 40:175–188.
Xanthomonas campestris pv. vitians mucoid, slow-growing colonies typical of most xan-
BACTERIAL LEAF SPOT thomonads. However, X. campestris pv. vitians weakly
Introduction and significance such as SX and MXP media are not diagnostic for
Bacterial leaf spot was previously considered a minor isolating and identifying this pathogen. Tween medium
disease of lettuce. However, in recent years the disease is useful because this bacterium forms characteristic
has become more important and can at times cause sig- white calcium salt crystals when growing on it. Early
nificant economic damage. The disease is prevalent in research indicated that X. campestris pv. vitians was a
both the USA and in Europe. pathogen of both lettuce and ornamental aroid plants.
Based on fatty acid analyses and reactions to mono-
Symptoms and diagnostic features clonal antibodies, it is now known that this lettuce
Early symptoms of bacterial leaf spot are small pathogen is distinct from X. campestris strains isolated
(2–5 mm), water-soaked leaf spots on the older leaves from aroids. Xanthomonas campestris pv. vitians is
of the plant. These lesions are typically bordered by leaf mostly limited to lettuce hosts. Recent research
veins and are angular in shape. Lesions quickly turn indicates that X. campestris pv. vitians is composed of
black – this is a diagnostic character of the disease homogeneous strains, and that genetically distinct
(398). If disease is severe, numerous lesions may strains are not yet found.
coalesce, resulting in the collapse of the leaf. Older
lesions dry up and become papery in texture, but retain Disease cycle
the black color. Lesions rarely occur on newly develop- The pathogen is highly dependent on wet, cool condi-
ing leaves. If diseased heads are packed in cartons, tions for infection and disease development. Splashing
secondary decay organisms can colonize the lesions and water from overhead irrigation and rain disperses the
result in postharvest problems. Bacterial leaf spot pathogen in the field. The pathogen can be seedborne.
occurs on the leaves of both leaf and head lettuce If infested seed is used to grow lettuce transplants in a
varieties as well as on flower bracts of lettuce seed crops greenhouse, the pathogen may become established on
(399). these plants because of favorable conditions in the
greenhouse. The bacterium can survive for several
Causal agent months in the soil and be splashed onto subsequent
Bacterial leaf spot is caused by Xanthomonas lettuce crops. The bacterium has also been found
campestris pv. vitians. The pathogen can be isolated on growing epiphytically on weed plants, but the signifi-
standard microbiological media and produces yellow, cance of this factor in disease development is not
398 399
398 Black spots of bacterial leaf spot on lettuce. 399 Lettuce flower bracts infected with bacterial
leaf spot.
known. Research indicates that X. campestris pv. Bremia lactucae

vitians can move systemically in lettuce vascular tissue. DOWNY MILDEW
Control Introduction and significance

Research in California indicates that commercial lettuce Downy mildew is probably the most important foliar
seed is infrequently infested with this pathogen. In disease of lettuce worldwide and can attack all lettuce
addition, infestation thresholds have not been estab- types. Losses are experienced when severe downy
lished for seedborne inoculum of this disease. However, mildew causes lowered yield and quality and when
if seedborne inoculum becomes important, use seed diseased leaves need to be trimmed from the harvested
that does not have significant levels of the pathogen. produce.
Examine lettuce transplants and remove symptomatic
plants. Reduce or eliminate overhead sprinkler irriga- Symptoms and diagnostic features
tion in the production field. Some resistant cultivars are Downy mildew results in light green to yellow angular
available. Do not plant consecutive lettuce crops, and spots on the upper surfaces of leaves (400). White fluffy
use crop rotations having non-host plants so that growth of the pathogen develops primarily on the
soilborne inoculum levels can decline. Copper based undersides of these spots (401). With time, the lesions
fungicides appear to provide only marginal control. turn brown and dry up. Older leaves are usually
References attacked first; such leaves that have lesions and are in
Barak, J. D. and Gilbertson, R. L. 2003. Genetic diversity of contact with the soil can become soft and rotted due to
Xanthomonas campestris pv. vitians, the causal agent of secondary decay organisms, such as Botrytis cinerea.
bacterial leafspot of lettuce. Phytopathology 93:596–603.
On occasion the pathogen can cause systemic infections
Barak, J. D., Koike, S. T., and Gilbertson, R. L. 2001. Role of
crop debris and weeds in the epidemiology of bacterial leaf that result in dark discoloration and streaking of
spot of lettuce in California. Plant Disease 85:169–178. internal vascular and pith tissues. If downy mildew
Barak, J. D., Koike, S. T., and Gilbertson, R. L. 2002. Movement infects the cotyledons of young seedlings, the plants can
of Xanthomonas campestris pv. vitians in the stems of lettuce
and seed contamination. Plant Pathology 51:506–512. die. Greenhouse-grown lettuce transplants can also be
Carisse, O., Ouimet, A., Toussaint, V., and Philion, V. 2000. infected. Cultivated lettuce is the main host, though
Evaluation of the effect of seed treatments, bactericides, and B. lactucae infects wild Lactuca species, artichoke, and
cultivars on bacterial leaf spot of lettuce caused by
Xanthomonas campestris pv. vitians. Plant Disease
other plants in the Asteraceae.
84:295–299.
McGuire, R. G., Jones, J. B., and Sasser, M. 1986. Tween media Causal agent
for semiselective isolation of Xanthomonas campestris pv. Downy mildew is caused by the obligate parasite
vesicatoria from soil and plant material. Plant Disease
70:887–891. Bremia lactucae, which belongs in the oomycete group
Pernezny, K., Raid, R. N., Stall, R. E., Hodge, N. C., and Collins, of organisms. Bremia lactucae conidiophores emerge
J. 1995. An outbreak of bacterial spot of lettuce in Florida from leaf stomates, branch dichotomously, and have
caused by Xanthomonas campestris pv. vitians. Plant Disease
79:359–360.
distinctively flared tips on which sterigmata are formed.
Sahin, F. and Miller, S. A. 1997. Identification of the bacterial leaf Conidia are hyaline, ovoid, measure 12–30 x
spot pathogen of lettuce, Xanthomonas campestris pv. 11–28 μm, and have apical papilla. Bremia lactucae is
vitians, in Ohio, and assessment of cultivar resistance and heterothallic and requires B1 and B2 mating types to be
seed treatment. Plant Disease 81:1443–1446.
present for the production of the sexual oospore.
Oospores are spherical, thick walled, and measure
20–31 μm. However, in some lettuce production areas
oospores are not observed even if both mating types
F UNGAL D ISEASES
have been found.

Bremia lactucae is a complex pathogen and consists
of multiple races (pathotypes). Pathotypes are identified
by testing their virulence on differential sets of lettuce
cultivars having various resistance genes. The world-
wide nomenclature of these pathotypes is confusing
because different countries use their own numbering 401 401 Sporulation
system (e.g. NL1, NL2, etc. in the Netherlands; IL1, of downy mildew
IL2, etc. in Israel; CA V, CA VI, etc. in California). on lettuce leaf
Standardization is improving and BL (for B. lactucae) underside.
numbers are now widely used in Europe.
Lettuce is subject to a second downy mildew disease
caused by Plasmopara lactucae-radicis. This pathogen
is apparently restricted to the roots of lettuce and causes
tan to brown necrotic lesions. Profuse sporulation can
be observed on infected root surfaces, and oospores
develop in the root cortex. This downy mildew disease
has only been detected on lettuce grown in hydroponic
systems.
Disease cycle
Humid, cool conditions are required for B. lactucae to
sporulate and to infect lettuce. Initial inoculum consists
of conidia from surrounding plants (weeds, other
lettuce fields) and, in some regions, oospores. The are continually challenged and overcome by B. lactucae
conidia are produced on lesions at night, and are then isolates. Apply fungicides prior to the development of
released into the air in the early morning if relative the disease. Isolates from several countries have
humidity is high. The spores are dispersed by winds but developed insensitivity to the phenylamide fungicide
are short-lived. Infection takes place in only 3 or 4 hours metalaxyl, and in California B. lactucae isolates were
if free moisture is on the leaves or near saturation con- found to be resistant to fosetyl-Al. Resistance manage-
ditions are present and temperatures are optimal ment strategies dictate that different fungicides be used
(10–22° C). in rotation to slow down the development of insensi-
tivity. Research has been conducted on disease predic-
Control tion models for B. lactucae. Such systems potentially
Plant resistant cultivars. However, because there are can help farmers reduce the number of fungicide appli-
a number of different pathotypes and also diverse cations made to lettuce; however, a consistently reliable
isolates of uncharacterized genetics, resistant cultivars and commercially available model is not yet available.
Culturally, use irrigation systems that reduce leaf
wetness and humidity, such as drip irrigation.
400 Greenhouse-grown transplants should especially be
protected so that downy mildew is not brought to the
field on these plants.
References
Brown, S., Koike, S. T., Ochoa, O. E., Laemmlen, F., and
Michelmore, R. W. 2003. Insensitivity to the fungicide
fosetyl-Aluminium in California isolates of the lettuce downy
mildew pathogen, Bremia lactucae. Plant Disease
87:502–508.
F UNGAL D ISEASES
Cobelli, L., Collina, M., and Brunelli, A. 1998. Occurrence in

Italy and characteristics of lettuce downy mildew (Bremia
lactucae) resistant to phenylamide fungicides. European
Journal of Plant Pathology 104:449–455.
Crute, I. R. 1987. Occurrence, characteristics, distribution,
400 Chlorotic and angular lesions of downy mildew on genetics, and control of a metalaxyl-resistant pathotype of
Bremia lactucae in the United Kingdom. Plant Disease
lettuce. 71:763–767.
Davies, J. M.Ll. 1994. Integrated control of downy mildew in Botrytis cinerea (teleomorph = Botryotinia fuckeliana)
crisp lettuce. Proceedings of the Brighton Crop Protection
Conference - Pests and Diseases 2: 817–822. GRAY MOLD
Garibaldi, A., Minuto, A., Gilardi, G., and Gullino, M. L. 2003.
First report of Bremia lactucae causing downy mildew on Introduction and significance
Helichrysum bracteatum in Italy. Plant Disease 87:315.
Gray mold is a common but usually minor lettuce
Ilott, T. W., Hulbert, S. H., and Michelmore. R. W. 1989. Genetic
analysis of the gene-for-gene interaction between lettuce disease. However, if environmental conditions are
(Lactuca sativa) and Bremia lactucae. Phytopathology favorable for the pathogen, gray mold can cause signif-
79:888–897.
icant crop loss in greenhouse-grown lettuce as well as in
Lebeda, A. and Reinink, K. 1991. Variation in the early
development of Bremia lactucae on lettuce cultivars with the field. Lettuce that is transplanted into the field can
different levels of field resistance. Plant Pathology at times be severely affected.
40:232–237.
Lebeda, A. and Schwinn, F. J. 1994. The downy mildews – an
overview of recent research progress. Journal of Plant Disease
and Protection 101:225–254. The initial symptom of gray mold is a water-soaked,
Lebeda, A. and Zinkernagel, V. 2003. Evolution and distribution brown-gray to brown-orange, mushy rot that occurs on
of virulence in the German population of Bremia lactucae. the oldest leaves and at the base of damaged or
senescent leaves and stems. Injured tissues that are wet
Norwood, J. M. and Crute, I. R. 1985. Further characterization
of field resistance in lettuce to Bremia lactucae (downy or in contact with the soil are especially susceptible.
mildew). Plant Pathology 34:481–486. Such leaves need to be trimmed off the plant at harvest.
O’Neill, T. M., Gladders, P., and Ann, D. M. 1997. Prospects for The pathogen uses this compromised tissue as a food
integrated control of lettuce diseases. Proceedings of the
BCPC/ANPP Conference, University of Canterbury, Kent, base and later progresses into the healthy parts of the
UK: Crop Protection and Food Quality: Meeting Customer lettuce crown, causing a similar decay of the main stem
Needs, pp. 485–490. and attached leaves (402). The characteristic gray fuzzy
Scherm, H., Koike, S. T., Laemmlen, F. F., and van Bruggen, A. H.
C. 1995. Field evaluation of fungicide spray advisories against
growth of the fungus can usually be readily seen on
lettuce downy mildew (Bremia lactucae) based on measured diseased areas. Black sclerotia may form on these
or forecast morning leaf wetness. Plant Disease 79:511–516. diseased tissues, although some isolates produce few or
Scherm, H. and van Bruggen, A. H. C. 1994. Weather variables no sclerotia. In advanced stages of the disease, a severely
associated with infection of lettuce by downy mildew (Bremia
lactucae) in coastal California. Phytopathology 84:860–-865. infected plant is girdled at the crown, wilts, and
Schettini, T. M., Legg, E. J., and Michelmore, R. W. 1991. collapses, resulting in symptoms that closely resemble
Insensitivity to metalaxyl in California populations of Bremia lettuce drop or Phoma basal rot. Young seedlings and
lactucae and resistance in California lettuce cultivars to
downy mildew. Phytopathology 81:64–70.
transplants can also die from gray mold (403). In
Stanghellini, M. E., Adaskaveg, J. E., and Rasmussen, S. L. 1990. California, early spring plantings of transplanted
Pathogenesis of Plasmopara lactucae-radicis, a systemic root romaine cultivars are particularly susceptible and gray
pathogen of cultivated lettuce. Plant Disease 74:173–178. mold can result in significant stand reduction.
Stanghellini, M. E., and Gilbertson, R. L. 1988. Plasmopara
lactucae-radicis, a new species on roots of hydroponically
Gray mold can also develop on upper lettuce leaves
grown lettuce. Mycotaxon 31:395–400. if such tissues are damaged. For example, if young,
Su, H., van Bruggen, A. H. C., Subbarao, K. V., and Sherm, H. inner leaf tips of romaine cultivars have tipburn
2004. Sporulation of Bremia lactucae affected by symptoms, Botrytis cinerea conidia can land on such
temperature, relative humidity, and wind in controlled
conditions. Phytopathology 94:396–401. tissue, colonize the necrotic tissue, and proceed to rot
the rest of the leaf.
Causal agent
The causal agent of gray mold is Botrytis cinerea. The
F UNGAL D ISEASES
perfect stage, Botryotinia fuckeliana, apparently is not

found on lettuce. Conidiophores of B. cinerea are long
(1–2 mm), become gray-brown with maturity, and
branch irregularly near the apex. Conidia are clustered
at the branch tips and are single-celled, pale brown,
ellipsoid to obovoid, and measure 6–18 x 4–11 μm.
402 403
402 Crown decay of lettuce caused by gray mold. 403 Lettuce transplants infected with gray mold.
The pathogen can be isolated on standard microbio- pathogens and pests. Reduce leaf wetness by avoiding
logical media. Some isolates sporulate poorly in culture or reducing sprinkler irrigation. Schedule crop residue
unless incubated under lights (12 h light/12 h dark). If incorporation and soil preparation so that excessive
formed, sclerotia are black, oblong or dome-shaped, plant residues at planting are minimized. Plant trans-
and measure 4–10 mm. The fungus grows best at plants in a timely manner so that the plants are not too
18–23° C but is inhibited at warm temperatures above large and overly mature; old transplants are subject to
32° C. On host tissue the fungus produces characteris- additional leaf breakage and damage during planting,
tically profuse sporulation that is dense, velvety, and and hence are more susceptible to gray mold infection.
grayish brown in color. Because romaine transplants are especially prone to
gray mold disease, plant this lettuce type by using direct
Disease cycle seeding when possible. To reduce overall humidity, ade-
Botrytis cinerea survives in and around fields as a sapro- quately ventilate or heat greenhouses. Apply fungicides
phyte on crop debris, as a pathogen on numerous crops to protect plants from gray mold. However, B. cinerea
and weed plants, and as sclerotia in the soil. Conidia strains resistant to dicarboximide fungicides are already
develop from these sources and become windborne. widespread in some geographic areas. Use diverse
When conidia land on senescent or damaged lettuce fungicide products with different modes of action to
tissue, they will germinate if free moisture is available reduce the risk of pathogen insensitivity.
and rapidly colonize this food base. Once established,
the pathogen will grow into adjacent healthy stems and References
leaves, resulting in disease symptoms and the produc- Delon, R., Kiffer, E., and Mangenot, F. 1977. Ultrastructural
tion of additional conidia. Cool temperatures, free study of host-parasite interactions: II. Decay of lettuce caused
by Botrytis cinerea and phyllosphere bacteria. Canadian
moisture, and high humidity favor the development of Journal of Botany 55:2463–2470.
the disease. Lettuce tissues are predisposed to infection O’Neill, T. M., Gladders, P., and Ann, D. M. 1997. Prospects for
by frost or heat damage, physiological problems such as integrated control of lettuce diseases. Proceedings of the
BCPC/ANPP Conference, University of Canterbury, Kent,
tipburn, or the activity of other pathogens such as UK: Crop Protection and Food Quality: Meeting Customer
Bremia lactucae, Phoma exigua, Rhizoctonia solani, Needs, pp. 485–490.
F UNGAL D ISEASES
and Sclerotinia species. Wang, Z.-N., Coley-Smith, J. R., and Wareing, P. W. 1986.
Dicarboximide resistance in Botrytis cinerea in protected
lettuce. Plant Pathology 35:427–433.
Control Wareing, P. W., Wang, Z.-N., Coley-Smith, J. R., and Jeves, T. M.
Because B. cinerea initiates infection on damaged 1986. Fungal pathogens in rotted basal leaves of lettuce in
tissues, minimize damage to lettuce that is caused by Humberside and Lancashire with particular reference to
Rhizoctonia solani. Plant Pathology 35:390–395.
cultural practices, environmental extremes, or other
Fusarium oxysporum f. sp. lactucae

404
FUSARIUM WILT

The first report indicating that lettuce was susceptible
to Fusarium wilt was made in 1960 in Asia (Japan). The
disease was later found in the USA in the early 1990s
(California) and late 1990s (Arizona), and most
recently was reported in Europe (Italy) in 2002. This
disease is becoming a serious concern in certain areas in
the southwest USA.

Fusarium wilt causes infected seedlings to wilt and
possibly die. Vascular stem and taproot tissues of
affected seedlings are red or brown. In older plants,
leaves turn yellow, wilt, and become necrotic. Internally,
the stem vascular system is red-brown to dark brown
and a red-brown discoloration develops in the cortex of
the crown and taproot (404). The taproot may develop
a hollow cavity. Plants are usually stunted and may fail
to form heads (405). Fusarium wilt symptoms resemble 404 Vascular discoloration of Fusarium wilt of
those caused by ammonium toxicity and Verticillium lettuce.
wilt.
405
Causal agent
The cause of Fusarium wilt of lettuce is Fusarium
oxysporum f. sp. lactucae. The pathogen morphology
and colony characteristics are similar to other F.
oxysporum fungi. The fungus forms one- or two-celled,
oval to kidney shaped microconidia on monophialides,
and three- to five-celled, fusiform, curved macroconi-
dia. Macroconidia are usually produced in cushion-
shaped structures called sporodochia. Chlamydospores
are also formed. The pathogen is usually readily
isolated from symptomatic vascular tissue. Semi-
selective media like Komada’s medium can help isolate 405 Stunted, declining lettuce plants with Fusarium
the pathogen if secondary rot organisms are present in wilt.
the sample. Inoculation experiments indicate that the
fungus appears to be host specific to lettuce, and that Disease cycle
lettuce is not susceptible to other forma speciales of the Like other Fusarium wilt pathogens, F. oxysporum f. sp.
F. oxysporum group. Currently, 3 races (1, 2, and 3) of lactucae is a soil inhabitant that can survive in the soil
F UNGAL D ISEASES
this pathogen are known to exist. for indefinite periods of time due to the production of
resilient chlamydospores. The disease tends to be more
severe on lettuce planted in the warmer months of the
season. Seedborne inoculum of F. oxysporum f. sp.
lactucae has been hypothesized, but has not yet been
documented.
Control Golovinomyces cichoracearum

Avoid planting lettuce in fields known to be infested, or ( = Erysiphe cichoracearum)
plant lettuce in these locations only in the spring or early POWDERY MILDEW
summer when symptoms are likely to be less severe.
Plant tolerant or less susceptible cultivars if available. Introduction and significance
Romaine lettuce appears to be more tolerant than other Powdery mildew is generally considered a minor
types. Minimize the movement of contaminated, disease of lettuce and is primarily reported in North
infested soil to clean fields. America and Europe. However, in some regions and
under certain conditions, powdery mildew can cause
References significant reductions in crop quality.
Fujinaga, M., Ogiso, H., Tsuchiya, N., and Saito, H. 2001.
Physiological specialization of Fusarium oxysporum f. sp. Symptoms and diagnostic features
lactucae, a causal organism of Fusarium root rot of crisp head
lettuce in Japan. Journal of General Plant Pathology This powdery mildew fungus grows ectophytically and
67:205–206. appears as a white, powdery growth on both upper and
Fujinaga, M., Ogiso, H., Tsuchiya, N., Saito, H., Yamanaka, S., lower sides of lettuce leaves (406). Older leaves are
Nozue, M., and Kojima, M. 2003. Race 3, a new race of
Fusarium oxysporum f. sp. lactucae determined by a
always infected first and most severely. Such infections
differential system with commercial cultivars. Journal of may cause chlorosis and deformity and buckling of the
General Plant Pathology 69:23–28. leaves. In advanced stages, leaves may begin to dry out
Garibaldi, G., Gilardi, G., and Gullino, M. 2002. First report of and turn brown. On occasion, the sexual phase will
Fusarium oxysporum on lettuce in Europe. Plant Disease
86:1052. occur and small, brown cleistothecia may be seen on the
Hubbard, J. C. and Gerik, J. S. 1993. A new wilt disease of leaves. All lettuce types are susceptible.
lettuce incited by Fusarium oxysporum f. sp. lactucum forma
specialis nov. Plant Disease 77:750–754.
Causal agent
Komada, H. 1975. Development of a selective medium for
quantitative isolation of Fusarium oxysporum from natural The causal agent, Golovinomyces cichoracearum (pre-
soil. Review of Plant Protection Research. 8:114–124. viously named Erysiphe cichoracearum), produces
Matheron, M. E. and Koike, S. T. 2003. First report of Fusarium epiphytic mycelium that grows superficially on host
wilt of lettuce caused by Fusarium oxysporum f. sp. lactucae
in Arizona. Plant Disease 87:1265.
surfaces. Conidiophores are borne on this surface
Matuo, T. and Motohashi, S. 1967. On Fusarium oxysporum f. mycelium. Conidia are produced in long chains, are
sp. lactucae n. f. causing root rot of lettuce. Transactions of hyaline, ellipsoid to barrel-shaped, and measure 25–45
the Mycological Society of Japan 8:13–15. x 14–25 μm. Globose cleistothecia have numerous
Pasquali, M., Dematheis, F., Gilardi, G., Gullino, M. L., and
Garibaldi, A. 2005. Vegetative compatibility groups of
hypha-like appendages and contain up to 10–25 asci.
Fusarium oxysporum f. sp. lactucae from lettuce. Plant Asci contain two ascospores that are ovoid to ellipsoid.
Disease 89:237–240.
Yamauchi, N., Horiuchi, S., and Satou, M. 2001. Pathogenicity
groups in Fusarium oxysporum f. sp. lactucae on
horticultural types of lettuce cultivars. Journal of General
406 F UNGAL D ISEASES
406 Powdery mildew sporulation on lettuce leaf.

Golovinomyces cichoracearum is listed in the literature Microdochium panattonianum

as infecting over 150 plant species. However, there is ANTHRACNOSE, RING SPOT
evidence that distinct strains, or physiological races,
exist within G. cichoracearum populations. Under Introduction and significance
experimental conditions, powdery mildew from lettuce Anthracnose disease is also called shot hole, ring spot,
could infect the following plants: vegetables – artichoke, or rust and is found in most lettuce producing areas of
cantaloupe, chicory, cucumber, endive; ornamentals – the world. If weather conditions favor disease develop-
calendula, dahlia, delphinium, florist’s cineraria, ment, this problem can cause widespread crop loss.
sunflower, and zinnia; weeds – prickly or wild lettuce
(Lactuca serriola) and milk thistle (Silybum marianum). Symptoms and diagnostic features
G. cichoracearum isolates from calendula, zinnia, and Initial symptoms are small (2–3 mm), water-soaked
wild lettuce, however, failed to infect lettuce. spots occurring on outer leaves. Spots enlarge, turn
yellow, and are usually angular in shape. Under cool,
Disease cycle moist conditions, white to pink spore masses of the
Initial inoculum can be either airborne conidia from fungus will be visible in the centers of the tan-colored
diseased host plants or ascospores emerging from cleis- lesions (407). If disease is severe, the lesions will
tothecia. Optimum temperatures for fungal growth and coalesce and cause significant dieback of the leaf, and in
development are 18–20° C. Maximum spore germina- some cases will result in significant stunting of the plant
tion requires high humidity, but free moisture may (408). As spots age, the affected tissue will dry up and
actually inhibit germination. become papery in texture. Eventually the centers of
these spots can fall out, resulting in a shot hole appear-
Control ance and hence the use of that name. Anthracnose
Plant resistant cultivars or apply fungicides such as lesions are often clustered along the midribs of lower
sulfur compounds. leaves.
References
Crute, I. R. and Burns, I. G. 1983. New or unusual records: 407
407 Leaf spots of
Powdery mildew of lettuce (Lactuca sativa). Plant Pathology anthracnose on
32: 455–457.
lettuce.
Lebada, A., Mieslerova, B., Dolezalova, I., and Kristkova, E.
2002. Occurrence of powdery mildew on Lactuca viminea
subsp. chondrilliflora in south France. Mycotaxon 84:83–87.
Schnathorst, W. C. 1959. Spread and life cycle of the lettuce
powdery mildew fungus. Phytopathology 49:464–468.
Schnathorst, W. C. 1960. Effects of temperature and moisture
stress on the lettuce powdery mildew fungus. Phytopathology
50:304–308.
Schnathorst, W. C., Grogan, R. G., and Bardin, R. 1958.
Distribution, host range, and origin of lettuce powdery
mildew. Phytopathology 48:538–543.
Turini, T. A. and Koike, S. T. 2002. Comparison of fungicides for
control of powdery mildew on iceberg lettuce, 2001.
Fungicide and Nematicide Reports. Vol. 57:V042.
F UNGAL D ISEASES
Causal agent 408

The pathogen is Microdochium panattonianum. Older
literature lists the pathogen as Marssonina panattoni-
ana. The pathogen can be isolated on standard micro-
biological media, though confirmation of anthracnose
might be better accomplished by microscopic examina-
tion of leaf spot tissue that has been collected from the
field. The fungus is very slow growing and on agar
media will form small, raised, slimy appearing colonies
of white to pink mycelium after several days (10 mm
colony diameter, 7 days, 24° C). Though sometimes
difficult to observe, conidiophores are solitary or
grouped in sporodochia. Conidia are hyaline, smooth,
fusiform, slightly curved, with one septum. The lower
cell is slightly smaller and tapers towards the base. 408 Severe stunting of lettuce affected with
Dimensions of the conidia are 3–4 x 13–16 μm. anthracnose.
Microsclerotia consist of groups of multicellular, thick-
walled cells that measure 60–100 μm and may be
observed in infected tissue. M. panattonianum infects References
lettuce and other Lactuca species and has also been Couch, H. B. and Grogan, R. G. 1955. Etiology of lettuce
reported on chicory and endive. At least five different anthracnose and host range of the pathogen. Phytopathology
45:375–380.
races of the pathogen have been identified.
Galea, V. J., Price, T. V., and Sutton, B. C. 1986. Taxonomy and
biology of lettuce anthracnose fungus. Transactions of the
Disease cycle British Mycological Society 86:619–628.
The fungus can survive for up to 4 years as microscle- Moline, H. E. and Pollack, F. G. 1976. Conidiogenesis of
Marssonina panattoniana and its potential as a serious
rotia in soil. The anthracnose pathogen requires cool, postharvest pathogen of lettuce. Phytopathology
wet conditions for infection and symptom development 66:669–674.
and hence is associated with rainy weather. Splashing Ochoa, O., Delp, B., and Michelmore, R. W. 1987. Resistance in
Lactuca spp. to Microdochium panattonianum (lettuce
water moves microsclerotia and conidia from soil onto anthracnose). Euphytica 36:609–614.
leaves, resulting in infection. Optimum temperatures Parman, T. and Price, T. V. 1991. Production of microsclerotia by
for disease development are approximately 18–20° C Microdochium panattonianum. Australasian Plant Pathology
and symptoms can appear 4 to 8 days after infection. 20:41–46.
Patterson, C. L. and Grogan, R. G. 1985. Source and survival of
While all lettuce types are susceptible, romaine cultivars primary inoculum of Marssonina panattoniana, causal agent
are particularly sensitive. of lettuce anthracnose. Phytopathology 75:13–19.
Patterson, C. L. and Grogan, R. G. 1991. Role of microsclerotia
Control as primary inoculum of Microdochium panattonianum,
incitant of lettuce anthracnose. Plant Disease 75:134–138.
Avoid planting lettuce in fields having a history of the Wicks, T. J., Hall, B., and Pezzaniti, P. 1994. Fungicidal control of
disease. Rotate with non-host plants to help reduce soil anthracnose (Microdochium panattonianum) on lettuce.
inoculum levels, though such rotations will not Australian Journal of Experimental Agriculture 34: 277–283.
eliminate the pathogen unless hosts are not planted for
over 4 years. Use irrigation systems (furrow or drip irri-
gation) that reduce or eliminate leaf wetting. Plant
F UNGAL D ISEASES
resistant cultivars if they are available. Apply protectant

fungicides, such as strobilurins, which are effective for
controlling this disease.
Phoma exigua 410 Transverse 410

PHOMA BASAL ROT section of lettuce
showing sunken
Introduction and significance crown cavity of
Phoma basal rot was reported as a problem in green- Phoma basal rot.
house lettuce production in the United Kingdom in the
early 1990s. More recently, this disease has caused
significant losses on romaine grown in the USA
(California).

Above ground symptoms are similar to those caused by
lettuce drop and gray mold diseases and consist of
wilting and yellowing of lower leaves, one-sided growth
of plants, overall stunting, and eventual plant collapse
(409). However, in contrast to these other crown rots,
there is no visible fungal growth at the crowns of
infected plants. Rather, Phoma basal rot causes distinct,
dark brown to black, sunken cavities to develop at the 411
crown and upper taproot tissues (410, 411, 412).
Lesions are notably dry and firm. Lesions can extend
deep into the crowns and roots, resulting in extensive
weakening of the plant structure; such plants can easily
be broken off at the ground level. Secondary fungi,
especially Botrytis cinerea, can colonize these stem
lesions. In greenhouse grown lettuce in Europe this
disease also results in circular, dark gray to black leaf
spots that can expand up to 3 cm in diameter. With time
the inner leaf spot tissue dries out, cracks, and falls out,
resulting in a shot hole effect. The fruiting bodies of the
pathogen can be observed in leaf spot tissues. 411 Black crown cavity of Phoma basal rot of lettuce.
409 412
F UNGAL D ISEASES
409 Collapsed lettuce plants infected with Phoma 412 Cross section showing lettuce crown infection
basal rot. from Phoma basal rot.
Causal agent Rhizoctonia solani

The causal agent of Phoma basal rot is Phoma exigua, (teleomorph = Thanatephorus cucumis)
a soilborne fungus. The fungus produces dark, ostiolate BOTTOM ROT
pycnidia that bear hyaline, straight or slightly curved,
ellipsoid or cylindrical conidia that measure 5–10 x Introduction and significance
2–4 μm. Conidia are mostly single-celled but can Bottom rot is generally a minor disease problem. The
become one septate. Pycnidia can be found in leaf spots pathogen is found worldwide and can cause some
of this disease, but rarely in the crown rot phase. Most limited damage to lettuce. In some regions, greenhouse-
lettuce types show some susceptibility, though romaine grown lettuce may develop significant bottom rot.
cultivars appear to be the most sensitive to damage.
Disease cycle Bottom rot typically infects lettuce plants as the heads
The epidemiology of this disease has not yet been doc- begin to form, though the responsible pathogen can at
umented. For greenhouse grown lettuce in the UK, the times cause damping-off of seedlings. Brown, sunken
disease can be more common during the winter lesions form on leaf midribs that are in contact with the
months. soil (413, 414). If conditions are favorable, the lesions
Control
Apply fungicides to the base of young lettuce plants. 413
Avoid keeping soils overly wet, as the disease is some-
times associated with wet conditions. If possible, plant
susceptible romaine in fields that do not have a history
of the disease.
References
Koike, S. T. 2001. Investigation of a new crown rot disease of
lettuce. California Lettuce Research Board Annual Report.
Koike, S. T., Subbarao, K. V., Verkley, G. J. M., O’Neill, T., and
Fogle, D. 2003. Phoma basal rot of lettuce caused by P. exigua
in California. Phytopathology 93:S47.
O’Neill, T. M. and McPherson, G. M. 1991. Rots, spots, and
blotches—new disease problems affecting protected lettuce. 413 Infected petiole bases of lettuce with bottom rot
Grower, June 6 issue, pp. 11–18.
disease.
414
F UNGAL D ISEASES
414 Decayed crown of lettuce affected by bottom rot.

can enlarge rapidly and rot the lower leaves. Tan to Control
brown mycelium and amber-colored drops of liquid Bottom rot is controlled in some cases by the use of
may be evident in the rotted areas. The fungus can fungicides; apply chemicals to the base of the plant.
sometimes penetrate and infect leaves inside the head, Rotate crops with non-hosts to help reduce soil
resulting in a rot of the entire plant. Symptoms are most inoculum. Do not plant back into fields having unde-
evident on plants that are near or at maturity. The composed plant residue from a previous crop. Plant in
activity of secondary decay organisms can result in a well-draining soil and avoid over irrigation so that the
very soft, slimy decay of the base of infected plants and bed tops can be kept dry. Select appropriate cultivars, as
contribute to collapse of the head. lettuce varieties that have upright growth habits expe-
rience less disease severity and incidence.
Causal agent
Bottom rot is caused by the basidiomycete fungus References
Rhizoctonia solani, which is a soilborne fungus with a Grosch, R., Schneider, J. H. M., and Kofoet, A. 2004.
very broad host range. Rhizoctonia solani has no Characterisation of Rhizoctonia solani anastomosis groups
causing bottom rot in field-grown lettuce in Germany.
asexual fruiting structures or spores, but produces char- European Journal of Plant Pathology 110:53–62.
acteristically coarse, brown, approximately right-angle Herr, L. J. 1992. Characteristics of Rhizoctonia isolates
branching hyphae. The hyphae are distinctly constricted associated with bottom rot of lettuce in organic soils in Ohio.
at branch points, and cross walls with dolipore septa
Herr, L. J. 1993. Host sources, virulence, and overwinter survival
are deposited just after the branching. Hyphal cells are of Rhizoctonia solani anastomosis groups isolated from field
multi-nucleate. Small, tan to brown loosely aggregated lettuce with bottom rot symptoms. Crop Protection
clumps of mycelia function as sclerotia. The teleomorph 12:521–526.
Koike, S. T. and Martin, F. N. 2005. Evaluation of fungicides for
Thanatephorus cucumis is not commonly observed on controlling bottom rot of iceberg lettuce, 2001 and 2002.
symptomatic lettuce, but when it occurs it is a whitish, Fungicide and Nematicide Tests (online). Report 60:V150.
thin, delicate, flat hymenial layer present on plant DOI: 10.1094/FN60. American Phytopathological Society,
St. Paul, MN.
surfaces near the soil surface. Basidia and basidiospores
Kuramae, E. E., Buzeto, A. L., Ciampi, M. B., and Souza, N. L.
(measuring 7–13 x 4–7 μm) are produced in this layer. 2003. Identification of Rhizoctonia solani AG 1-IB in lettuce,
The role of the perfect stage in disease development is AG 4 HG-I in tomato and melon, and AG 4 HG-III in
not known. Rhizoctonia solani isolates are divided up broccoli and spinach, in Brazil. European Journal of Plant
into a series of distinct groups, called anastomosis Mahr, S. E. R., Stevenson, W. R., and Sequeira, L. 1986. Control
groups (AGs), which have differing virulence levels and of bottom rot of head lettuce with iprodione. Plant Disease
in some cases preferred host ranges. AG 4 isolates have 70:506–509.
been associated with bottom rot of lettuce. Pieczarka, D. J. and Lorbeer, J. W. 1975. Microorganisms
associated with bottom rot of lettuce grown on organic soil in
New York state. Phytopathology 65:16–21.
Disease cycle Wareing, P. W., Wang, Z.-N., Coley-Smith, J. R., and Jeves, T. M.
Rhizoctonia solani is a soil inhabitant that survives as 1986. Fungal pathogens in rotted basal leaves of lettuce in
Humberside and Lancashire with particular reference to
sclerotia or as mycelium in and on crop residue and soil Rhizoctonia solani. Plant Pathology 35:390–395.
organic matter. Disease develops when lower portions
of developing lettuce leaves come in contact with
infested soil. Warm (25–27° C), moist soil conditions
are conducive to infection and disease development.
This disease can also occur under cool, moist conditions
in over-wintered greenhouse crops where lettuce has
F UNGAL D ISEASES
been regularly grown.


416
LETTUCE DROP

Lettuce drop is an economically important problem in
North America, Europe, Australia, and New Zealand,
and the pathogens are found throughout the world. In
some lettuce producing regions, such as California, this
disease is generally considered the most important
soilborne problem of the crop. If severe, 75% or more
of a particular planting may be lost to this disease. In
Europe, lettuce drop has increased in importance since
the introduction of crisphead types which have longer
growing periods than butterhead cultivars. On crops 416 Collapsed lettuce plant infected by Sclerotinia
other than lettuce, this disease is called white mold. minor.

Lettuce drop disease is caused by two species of
Sclerotinia. Sclerotinia minor only infects lettuce stems
and leaves that are in contact with the soil. Once
infection takes place, the fungus causes a brown, soft,
watery decay of the lower leaves and crown (415). The
outer leaves then wilt and the entire plant can collapse,
usually when lettuce is near maturity (416). White
mycelium and small (3–5 mm), black, irregularly
shaped sclerotia form on the decayed crown, on upper
taproot tissues, and on leaves attached to decaying
crowns (417). The overall above-ground symptoms
resemble those of gray mold and Phoma basal rot.
Sclerotinia sclerotiorum can also infect lower leaves
and stems, causing symptoms similar to those of 417 Sclerotia and mycelium of Sclerotinia minor on
S. minor (418). In addition, S. sclerotiorum produces lettuce.
415 418
F UNGAL D ISEASES
415 Rotted lettuce crown infected by Sclerotinia minor. 418 Rotted lettuce crown caused by Sclerotinia
sclerotiorum.
aerial spores that can infect the upper parts of plants. 419
Dispersed by winds, these spores usually infect
damaged or senescing tissue. Both crown and upper leaf
infections likewise result in a brown, soft, watery rot
that is accompanied by white mycelium and black,
oblong or dome-shaped sclerotia that are 5–10 mm
long. Plant collapse also tends to occur near harvest.
Causal agents
White mold is caused by two species of Sclerotinia,
S. minor and S. sclerotiorum. The two pathogens are
distinguished primarily by the size of sclerotia.
Sclerotinia minor sclerotia typically are significantly
smaller than those of S. sclerotiorum (419). In addition, 419 Comparison of sclerotia from the two Sclerotinia
S. sclerotiorum produces apothecia (420), while species that infect lettuce: S. sclerotiorum (left); S. minor
S. minor does not generally do so in the field. For (right).
detailed descriptions of these pathogens, see the bean
white mold section in the chapter on legume diseases 420
(page 262).
Disease cycle
For detailed descriptions of the disease cycles, see the
bean white mold section in the chapter on legume
diseases. Recent studies on lettuce indicated that asco-
spores of S. sclerotiorum may be able to survive several
weeks on leaves. Such survival means that lettuce can
become infected some time after the arrival of the
inoculum.
Control
For an integrated approach to Sclerotinia control, see 420 Apothecia of Sclerotinia sclerotiorum forming from
the bean white mold section in the chapter on legume one sclerotium.
diseases. Because S. minor completes its life cycle in the
soil, control this lettuce drop pathogen by applying
fungicides to lettuce after plants have been thinned,
rotating to non-host crops, and deep plowing soils to References
bury sclerotia below the root zone. Note that the Bell, A. A., Liu, L., Reidy, B., Davis, R. M., and Subbarao, K. V.
planting of some cover crops can significantly increase 1998. Mechanisms of subsurface drip-mediated suppression
of lettuce drop caused by Sclerotinia minor. Phytopathology
S. minor inoculum. Crop residues from broccoli 88:252–259.
plantings show suppressive effects against S. minor. Clarkson, J. P., Phelps, K., Whipps, J. M., Young, C. S., Smith, J.
Control of lettuce drop caused by S. sclerotiorum is A., and Watling, M. 2004. Forecasting Sclerotinia disease on
lettuce: towards developing a prediction model for carpogenic
more difficult because inoculum usually consists of germination of sclerotia. Phytopathology 94:268–279.
F UNGAL D ISEASES
aerial ascospores that enter lettuce fields at unpre- Clarkson, J. P., Staveley, J., Phelps, K., Young, C. S., and Whipps,
dictable intervals. Apply fungicides at rosette stage to J. M. 2003. Ascospore release and survival in Sclerotinia
provide some protection. Biological control with com- sclerotiorum. Mycological Research 107:213–222.
Dillard, H. R., and Grogan, R. G. 1985. Relationship between
mercial formulations of the mycoparasite Conio- sclerotial spatial pattern and density of Sclerotinia minor and
thyrium minitans has shown some promise against the incidence of lettuce drop. Phytopathology 75:90–94.
S. sclerotiorum, but not for S. minor.
Grube, R., and Ryder, E. 2004. Identification of lettuce (Lactuca Verticillium dahliae
sativa) germplasm with genetic resistance to drop caused by
Sclerotinia minor. Journal of the American Society for VERTICILLIUM WILT
Hao, J. J., Subbarao, K. V., and Duniway, J. M. 2003. Introduction and significance
Germination of Sclerotinia minor and S. sclerotiorum
sclerotia under various soil moisture and temperature This disease is not yet widespread in the world. It has
combinations. Phytopathology 93:443–450. been reported from Greece and the USA (California). In
Hao, J. J., Subbarao, K. V., and Koike, S. T. 2003. Effects of some lettuce producing areas in California the pathogen
can cause significant damage.
Disease 87:159–166.
Hawthorne, B. T. 1975. Observations on the development of Symptoms and diagnostic features
apothecia of Sclerotinia minor Jagg. in the field. New Zealand Initial symptoms appear at rosette stage when the lower
Journal of Agricultural Research 19:383–386.
leaves wilt. Those leaves closest to the lettuce head can
Hubbard, J. C., Subbarao, K. V., and Koike, S. T. 1997.
Development and significance of dicarboximide resistance in yellow, die, and remain closely appressed to the head.
Sclerotinia minor isolates from commercial lettuce fields in Discolored streaks occur in the vascular tissues of the
California. Plant Disease 81:148-153.
taproot and crown, and can be a combination of green,
Imolehin, E. D., and Grogan, R. G. 1980. Factors affecting
survival of sclerotia, and effects of inoculum density, relative brown, or black (421). As disease develops, the plant’s
position, and distance of sclerotia from the host on infection
of lettuce by Sclerotinia minor. Phytopathology
70:1162–1167.
Imolehin, E. D., Grogan, R. G., and Duniway, J. M. 1980. Effect
of temperature and moisture tension on growth, sclerotial
production, germination, and infection by Sclerotinia minor.
Jones, E. E., and Whipps, J. M. 2002. Effect of inoculum rates
and sources of Coniothyrium minitans on control of 421
Sclerotinia sclerotiorum disease in glasshouse lettuce.
Meltzer, M. S., Smith, E. A., and Boand, G. J. 1997. Index of
plant hosts of Sclerotinia minor. Canadian Journal of Plant
Patterson, C. L., and Grogan, R. G. 1985. Differences in
epidemiology and control of lettuce drop caused by
Sclerotinia minor and Sclerotinia sclerotiorum. Plant Disease
69:766–770.
Subbarao, K. V. 1998. Progress towards integrated management
of lettuce drop. Plant Disease 82:1068–1078.
Subbarao, K. V., Hubbard, J. C., and Schulbach, K. F. 1997.
Comparison of lettuce diseases and yield under subsurface
drip and furrow irrigation. Phytopathology 87:877–883.
Subbarao, K. V., Koike, S. T., and Hubbard, J. C. 1996. Effects of
deep plowing on the distribution and density of Sclerotinia
minor sclerotia and lettuce drop incidence. Plant Disease
80:28–33.
Wu, B. M., and Subbarao, K. V. 2003. Effects of irrigation and
tillage on temporal and spatial dynamics of Sclerotinia minor
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sclerotia and lettuce drop incidence. Phytopathology

93:1572–1580.
Young, C. S., Clarkson, J. P., Smith, J. A., Watling, M., Phelps, K.,
and Whipps, J. M. 2004. Environmental conditions
influencing Sclerotinia sclerotiorum infection and disease
development in lettuce. Plant Pathology 53:387–397.
421 Vascular discoloration of Verticillium wilt of
lettuce.
422
Disease cycle
Researchers are still investigating the relationship of
lettuce V. dahliae isolates to isolates from other plants.
For example, V. dahliae from lettuce infects artichoke,
cotton, eggplant, pepper (chile type), potato, strawberry
(variable response), tomato, and watermelon. However,
the lettuce isolates could not readily infect alfalfa,
cabbage, cauliflower, or pepper (bell type) which are
hosts of V. dahliae. Another potentially important
aspect to lettuce Verticillium wilt is the confirmation
that several weeds found in and around lettuce fields are
hosts to V. dahliae: shepherd’s purse (Capsella bursa-
pastoris), hairy nightshade (Solanum sarrachoides),
sowthistle (Sonchus oleraceus), and groundsel (Senecio
vulgaris). Some of these isolates from weed hosts are
more strongly virulent on lettuce than lettuce isolates.
Control
Plant resistant or tolerant cultivars as they become
available. Pre-plant treatment of soil with effective
fumigants will give short-term control, though the use
422 Collapsed plants of Verticillium wilt of lettuce. of such materials is not usually economically feasible for
lettuce production. Rotate crops so that lettuce is not
planted in fields having a history of the problem.
outer whorl of leaves turns yellow, wilts, and dies (422). Minimize spread of infested soil to other, uninfested
Both wilting and vascular discoloration symptoms may areas. Be aware that infested lettuce seed and possibly
appear that are similar to those caused by Fusarium wilt weeds and weed seeds are sources of the pathogen.
or ammonium toxicity.
References
Causal agent Ligoxigakis, E. K. and Vakalounakis, D. J. 2000. Hosts of
The causal pathogen is Verticillium dahliae. It can be Verticillium dahliae race 2 in Greece. In: Tjamos, E. C., Rowe,
R. C., Heale, J. B., and Fravel, D. R. Advances in Verticillium:
isolated on standard microbiological media, though Research and Disease Management. American
semi-selective media such as NP-10 can also be used. Phytopathological Society Press.
On general purpose media, the pathogen forms the Sorensen, L. H., Schneider, A. T., and Davis., J. R. 1991.
Influence of sodium polygalacturonate sources and improved
characteristic hyaline, verticillate conidiophores bearing recovery of Verticillium species from soil. (Abstract)
3–4 phialides at each node, and hyaline, single-celled, Phytopathology 81:1347.
ellipsoidal conidia that measure 2–8 x 1–3 μm. Older Subbarao, K. V. 2000. Biology and epidemiology of Verticillium
cultures form dark brown to black torulose microscle- wilt of lettuce. California Lettuce Research Board Annual
Report pp. 96–103.
rotia that consist of groups of swollen cells formed by Vallad, G. E., Bhat, R. G., Koike, S. T., Ryder, E. J., and
repeated budding. Microsclerotia size varies greatly and Subbarao, K. V. 2005. Weedborne reservoirs and seed
is in the range of 15–100 μm diameter. Microsclerotia transmission of Verticillium dahliae in lettuce. Plant Disease
89:317–324.
enable the pathogen to survive in the soil for extended
periods of time (up to 8 to 10 years). In infested lettuce
F UNGAL D ISEASES
fields in California, inoculum levels are extremely high

and can reach levels as high as 400–600 micro-
sclerotia/gram of soil. An important discovery is that
this lettuce pathogen can be seedborne in lettuce.
Therefore, infested lettuce seed could be a means of
spreading the pathogen to previously uninfested fields.

423

Beet western yellows is an occasional virus problem of
lettuce in North America and Europe. Diagnosis of this
disease may be complicated because symptoms caused
by this virus can closely resemble those of nutrient
deficiencies

Symptoms usually do not develop until plants reach
rosette stage or later. At this point in crop development, 423 Leaf chlorosis of beet western yellows of lettuce.
the leaves develop chlorotic blotches in interveinal
tissue. This yellowing continues until the oldest, lower
leaves are bright yellow to sometimes almost white in 424
color, with the main leaf veins remaining green (423,
424). Yellowed leaves often have a thick, brittle texture.
Yellowing can progress until the wrapper leaves
adjacent to the head also turn yellow, and head color
may be unacceptably light green. In most lettuce
varieties, significant stunting or reduction in plant size
does not occur. Overall symptoms of this yellows
disease may resemble iron chlorosis.

The pathogen is the Beet western yellows virus
(BWYV), which is a polerovirus. BWYV has isometric
particles with diameters of 25 nm and single-stranded,
linear RNA genomes. BWYV may be found in
numerous crop and weed plants, and the host list is 424 Close-up of leaf chlorosis of beet western yellows
extensive, including over 150 documented plant of lettuce, showing characteristic green veins.
species. Some isolates or strains of this virus have
different abilities to infect certain plants; thus, not all
strains of BWYV may be able to infect all known hosts, References
greatly complicating the etiology of this disease for Falk, B. W. and Guzman, V. I. 1981. A virus as the causal agent of
lettuce. BWYV is vectored by several aphid vectors, spring yellows of lettuce and escarole. Proceedings of the
Florida State Horticultural Society 94:149–152.
especially the green peach aphid (Myzus persicae), in a
Pink, D. A. C., Walkey, D. G. A., and McClement, S. J. 1991.
persistent manner. Genetics of resistance to beet western yellows virus in lettuce.
Control Walkey, D. G. A. and Pink, D. A. C. 1990. Studies on resistance
to beet western yellows virus in lettuce (Lactuca sativa) and
Follow general suggestions for managing virus diseases the occurrence of field sources of the virus. Plant Pathology
(see Part 1). Plant tolerant cultivars. Remove weed hosts 39:141–155.
V IRAL D ISEASES
and keep aphid populations low. Zink, F. W. and Duffus, J. E. 1972. Association of beet western
yellows and lettuce mosaic viruses with internal rib necrosis
of lettuce. Phytopathology 62:1141–1144.
Lettuce mosaic virus Causal agent

LETTUCE MOSAIC Lettuce mosaic is caused by Lettuce mosaic virus
(LMV). LMV is a potyvirus and consists of filamentous
Introduction and significance rods measuring approximately 750 x 15 nm and single-
Lettuce mosaic is one of the most important virus stranded RNA genomes. Throughout the world, LMV
diseases of lettuce. This disease occurs in all lettuce- isolates are divided into four distinct groups, or patho-
producing areas in the world. Integrated disease man- types (I, II, III, IV), based upon the ability of the isolate
agement programs help limit the impact of this virus. to infect various differential cultivars having mo and g
However, outbreaks still occur and can possibly cause resistance genes. LMV is vectored in a nonpersistent
crop loss. manner by many different aphids and can also be sap
transmitted. LMV is the only economically important
Symptoms and diagnostic features lettuce virus that is seedborne. In addition to lettuce, the
Symptoms can vary greatly depending on the particular virus can infect numerous other plants. However, in
type or cultivar of lettuce infected, age of infected plant, commercial settings it appears that LMV primarily
virus strain, and environmental conditions. Plants that infects plants in the Asteraceae. Ornamentals such as
are infected at a young stage are stunted, deformed, and Gazania species and weeds like bristly oxtongue (Picris
(in some varieties) show a mosaic or mottling pattern echioides) can be important reservoir hosts in
(425, 426). Such plants rarely grow to full size. Plants California.
that are infected later in the growth cycle will show a
different set of symptoms. These plants may reach full Disease cycle
size, but the older outer leaves will be yellow, twisted, or Initial inoculum of the virus comes from infected seed
otherwise deformed. On head lettuce the wrapper or diseased lettuce and alternate hosts. Aphids carry the
leaves will often curve back away from the head (427). virus from the diseased hosts to uninfected, new lettuce.
Developing heads may be deformed. In some cases If aphid activity is extensive, the virus can be rapidly
brown, necrotic flecks occur on the wrapper leaves and spread throughout a field and result in a high incidence
leaf margins may be more serrated than normal. of lettuce mosaic disease. An important aphid vector in
California is the green peach aphid (Myzus persicae).
However, the lettuce aphid (Nasonovia ribis-nigri) does
not vector the virus.
425 426
V IRAL D ISEASES
425 Stunting and chlorosis of lettuce caused by lettuce 426 Mosaic symptom on leaf lettuce caused by lettuce
mosaic. mosaic.
427
References
Dinant, S. and Lot, H. 1992. Lettuce mosaic virus: a review. Plant
Falk, B. W and Purcifull, D. E. 1983. Development and
application of ELISA test to index lettuce seeds for lettuce
mosaic virus in Florida. Plant Disease 67:413–416.
Grogan, R. G. 1980. Control of lettuce mosaic with virus-free
seed. Plant Disease 64:446–449.
Grogan, R. G. 1983. Lettuce mosaic virus control by the use of
virus-indexed seed. Seed Science and Technology
11:1043–1049.
Krause-Sakate, R., Le Gall, O., Fakhfakh, H., Peypelut, M.,
Marrakchi, M., Varveri, C., Pavan, M. A., Souche, S. Lot, H.,
Zerbini, F. M., and Candresse, T. 2002. Molecular and
biological characterization of Lettuce mosaic virus (LMV)
isolates reveals a distinct and widespread type of resistance-
breaking isolate: LMV-Most. Phytopathology 92:563–572.
Nebreda, M., Moreno, A., Perez, N., Palacios, I., Seco-
427 Lettuce leaf curling symptom of lettuce mosaic.
Fernandez, V., and Fereres, A. 2004. Activity of aphids
associated with lettuce and broccoli in Spain and their
efficiency as vectors of Lettuce mosaic virus. Virus Research
100:83–88.
Control
Pink, D. A. C., Kostova, D., and Walkey, D. G. A. 1992.
Use seed that does not have significant levels of the Differentiation of pathotypes of lettuce mosaic virus. Plant
pathogen. Infection thresholds differ according to Pathology 41:5–12.
the epidemiological features of a particular area. Van Vuurde, J. W. L. and Maat, D. Z. 1983. Routine application
of ELISA for the detection of lettuce mosaic virus in lettuce
Researchers found that a zero in 30,000 seed infection seeds. Seed Science and Technology 11:505–513.
threshold is required for LMV control in California’s Zerbini, F. M., Koike, S. T., and Gilbertson, R. L. 1995.
Salinas Valley. However, in parts of Europe the seed Biological and molecular characterization of lettuce mosaic
infection threshold is zero in 2,000 seed. Control weeds potyvirus isolates from the Salinas Valley of California.
in and around the lettuce production areas, because Zerbini, F. M., Koike, S. T., and Gilbertson, R. L. 1997. Gazania
weeds can be a significant reservoir of the virus and the spp.: A new host of lettuce mosaic potyvirus, and a potential
source from which aphids obtain the virus. Plow down, inoculum source for recent lettuce mosaic outbreaks in the
Salinas Valley of California. Plant Disease 81:641–646.
in a timely manner, old lettuce plantings because
infected lettuce plants, like weeds, are a source of virus.
A 2-week lettuce-free period in California helps prevent
continuous, year-to-year buildup of LMV and helps
reduce the amount of virus that would ‘bridge’ over
from one season to the next. Plant resistant lettuce
cultivars if available. While controlling aphids does not
prevent the transmission of LMV, managing these
vectors is helpful in slowing LMV spread.
V IRAL D ISEASES
Lettuce necrotic stunt virus

428
LETTUCE DIEBACK

Romaine cultivars consistently show the most pro-
nounced and serious symptoms of lettuce dieback,
though several leaf lettuce and butterhead cultivars are
also susceptible. This is a new disease that has been doc-
umented only since the late 1990s.

Infected lettuce can be severely stunted with mature,
diseased plants failing to develop past the eight to ten
leaf stage. Extensive chlorosis is present on the
outermost leaves (428). The younger, inner leaves often
remain dark green in color, but become rough and 428 Lettuce infected with lettuce dieback showing
leathery in texture. The chlorotic outer leaves usually brown necrotic lesions.
develop necrotic spotting that can turn into extensive
areas of brown, dead tissue (429). Affected redleaf 429
lettuce takes on an orange color (430). The roots of
severely affected plants can be necrotic and rotted,
although it is not clear if such symptoms are caused
directly by the pathogen or by secondary decay factors.
Currently used iceberg cultivars are immune to this
problem.
Causal agent
The causal agent is Lettuce necrotic stunt virus (LNSV).
LNSV is a tombusvirus and consists of isometric
particles measuring up to 30 nm in diameter and
double-stranded RNA genomes. Strains of this lettuce 429 Stunted and chlorotic lettuce infected with lettuce
pathogen form a new, highly significant cluster within dieback disease.
the group and have 3’-terminal genomic nucleotide
sequences that are distinct from previously described 430
Tomato bushy stunt virus (TBSV) sequences. Based on
this sequence information, this lettuce pathogen
appears to be a new tombusvirus that is closely related
to TBSV. Presently, diagnosis directly from lettuce tissue
is not reliable, even using sensitive methods such as
Western blot analysis, reverse transcriptase-PCR, and
immunocapture-PCR. Instead, symptomatic lettuce
tissues are used to mechanically inoculate indicator
plants (Chenopodium quinoa, Nicotiana benthamiana,
V IRAL D ISEASES
N. clevelandii); serological or molecular methods are

then employed to test local lesions or plant sap from the
indicator species.
430 Red leaf lettuce cultivar infected with lettuce
dieback disease.
Disease cycle Mirafiori lettuce virus

LNSV has no known invertebrate or fungal vector. LETTUCE BIG VEIN
Rather, the virus resides in soil and water and is spread
in river water, irrigation runoff, flood waters, and Introduction and significance
infested soil and mud. Research is needed to determine Big vein disease is generally a minor disease, though
the exact host range of LNSV, but preliminary infor- severe symptoms can reduce the quality of the
mation indicates that the LNSV and TBSV host ranges commodity. This disease occurs in the USA, Brazil,
are probably very similar. Europe, and Japan.

Plant resistant romaine and leaf lettuce cultivars as they Lettuce big vein disease causes veins in leaves to become
become available. Recently released romaine cultivars greatly enlarged and clear (431). Such deformities are
have good resistance. Iceberg lettuce can be planted in easily seen if the leaf is examined with a light source
infested fields, as these cultivars do not develop disease. behind it. The enlarged veins cause the rest of the leaf to
Preliminary experiments indicated that the disease was be ruffled, buckled, and malformed (432). If infected
not controlled by the application of soil fumigants. If early in the growth cycle, lettuce plants can be stunted.
susceptible romaine must be used, select fields that do
not have a history of the problem. Avoid spreading
infested soil and mud to clean fields. 431 431 Enlarged
veins of big vein of
References lettuce.
Gerik, J. S., Duffus, J. E., Perry, R., Stenger, D. C., and Van
Maren, A. F. 1990. Etiology of tomato plant decline in the
California desert. Phytopathology 80:1352–1356.
Grube, R. C. and Ryder, E. J. 2003. Romaine lettuce breeding
lines with resistance to lettuce dieback caused by
tombusviruses. HortScience 38:627–628.
Liu, H.-Y., Sears, J. L., Obermeier, C., Wisler, G. C., Ryder, E. J.,
Duffus, J. E., and Koike, S. T. 1999. First report of tomato
bushy stunt virus isolated from lettuce. Plant Disease 83:301.
Obermeier, C., Sears, J. L., Liu, H. Y., Schlueter, K. O., Ryder, E.
J., Duffus, J. E., Koike, S. T., and Wisler, G. C. 2001.
Differentiation of tombusvirus strains that cause diseases of
lettuce and tomato in the southwestern U.S. Phytopathology
91:797–806.
Tomlinson, J. A. and Faithfull, E. M. 1984. Studies on the
occurrence of tomato bushy stunt virus in English rivers.
432
V IRAL D ISEASES
432 Lettuce plant on left is infected with big vein.

Plant on the right is healthy.
Severely affected plants can be so deformed as to be Control

unmarketable, and head lettuce varieties may fail to Use resistant cultivars. In badly infested fields with
form a head or be delayed in development. histories of severe disease, delay planting lettuce until
the warmer time of the year. Crop rotations with non-
Causal agent hosts will not prevent the disease, but will help reduce
The causal agent of lettuce big vein disease eluded iden- disease severity for subsequent lettuce crops. When
tification for many years. Researchers believed that the producing lettuce transplants, do not allow the plants
pathogen was a virus, and had confirmed that this agent and trays to come into contact with infested soil.
could be graft-transmitted and vectored by a soil
microorganism, Olpidium brassicae. Only recently has References
the pathogen, Mirafiori lettuce virus (MiLV), been iden- Campbell, R. N. 1965. Weeds as reservoir hosts of the lettuce big
tified. MiLV is an ophiovirus with particles that are vein virus. Canadian Journal of Botany 43:1141–1149.
Campbell, R. N. and Grogan, R. G. 1963. Big vein of lettuce and
highly kinked filaments. These particles are difficult to
its transmission by Olpidium brassicae. Phytopathology
see with an electron microscope because they have low 53:252–259.
contrast and greatly vary in size and shape. Confirming Colariccio, A., Chaves, A. L. R., Eiras, M., Chagas, C. M., Lenzi,
the etiology of lettuce big vein disease was complicated R., and Roggero, P. 2003. Presence of lettuce big-vein disease
and associated viruses in a subtropical area of Brazil. Plant
by the presence of other non-pathogenic viruses in the Pathology 52:792.
O. brassicae vector. One such virus, Lettuce big vein Lot, H., Campbell, R. N., Souche, S., Milne, R. G., and Roggero,
virus, is now known to be non-pathogenic to lettuce. P. 2002. Transmission by Olpidium brassicae of Mirafiori
lettuce virus and lettuce big vein virus, and their roles in
The genome of MiLV consists of four RNA segments. lettuce big vein etiology. Phytopathology 92:288–293.
Navarro, J. A., Botella, F., Maruhenda, A., Sastre, A., Sanchez-
Disease cycle Pina, M. A., and Pallas, V. 2004. Comparative infection
MiLV is a soilborne virus and is introduced into lettuce progress analysis of lettuce big vein virus and Mirafiori lettuce
virus in lettuce crops by developed molecular diagnosis
plants by a soil chytrid fungus, Olpidium brassicae. techniques. Phytopathology 94:470–477.
This vector survives in the soil for long periods of time Roggero, P., Lot, H., Souche, S., Lenzi, R., and Milne, R. G.
and produces swimming zoospores that move about in 2003. Occurrence of mirafiori lettuce virus and lettuce big-
vein virus in relation to development of big-vein symptoms in
soil water and attach themselves to lettuce roots. When lettuce crops. European Journal of Plant Pathology
zoospores infect and colonize the epidermal cells of the 109:261–267.
roots, they themselves do not cause disease but transmit van der Wilk, F., Dullemans, A. M., Verbeek, M., and van den
MiLV into the plant. The lettuce big vein disease does Heuvel, J. F. J. M. 2002. Nucleotide sequence and genomic
organization of an ophiovirus associated with lettuce big vein
not occur in nature if O. brassicae is absent; however, disease. Journal of General Virology 83:2869–2877.
not all O. brassicae isolates contain MiLV. The disease White, J. G. 1980. Control of lettuce big-vein disease by soil
is spread by the movement of infested soil and water sterilisation. Plant Pathology 29:124–130.
that contain viruliferous O. brassicae. Seedlings can be
infected within 8 days of planting, and symptoms can
appear 18 days after infection. Disease symptoms
develop most extensively if air temperatures are rela-
tively cool (below 16-20° C). Temperatures above
22° C will generally prevent symptom development.
Olpidium brassicae can persist in the soil as resilient
resting sporangia, thereby ensuring that the virus will
also be present for many years, even in the absence of its
lettuce host.
V IRAL D ISEASES
Tomato spotted wilt virus

433
TOMATO SPOTTED WILT

Tomato spotted wilt is an important, though sporadic,
problem that can cause significant losses in some lettuce
areas, such as the USA (Hawaii) and Tasmania. The
virus is found worldwide on many different hosts.

Symptoms tend to develop on one side of a plant and
include yellowing of leaves, brown to dark brown
necrotic spots on leaves and petioles, and a twisting of 433 Early symptoms of tomato spotted wilt of
the plant foliage (433, 434). Margins of leaves can wilt. lettuce.
Young foliage may especially show many brown
necrotic spots. Plants infected early may die. 434
Causal agent
Tomato spotted wilt disease is caused by the Tomato
spotted wilt virus (TSWV). TSWV is a tospovirus and
has isometric particles, measuring approximately
80–110 nm, which are surrounded with membranes.
TSWV has a genome consisting of three linear single-
stranded RNAs and is vectored by several species of
thrips; at least 8 species are found to be vectors. The
western flower thrips (Frankliniella occidentalis) is
probably the most important vector, though Thrips
tabaci has been implicated as the main vector in 434 Advanced symptoms of tomato spotted wilt of
Tasmania. TSWV has one of the most extensive host lettuce.
ranges of any known plant virus and can infect over
900 different cultivated and weedy plant species.
References
Disease cycle Cho, J. J., Mau, R. F. L., German, T. L., Hartmann, R. W., Yudin,
Only thrips in their larval stage can acquire the virus via L. S., Gonsalves, D., and Provvidenti, R. 1989. A
multidisciplinary approach to management of tomato spotted
feeding on infected plants. The larvae can transmit wilt virus in Hawaii. Plant Disease 73:375–383.
TSWV after a 4–12 day incubation period. Viruliferous Cho, J. J., Mitchell, W. C., Mau, R. F. L., and Sakimura, K. 1987.
larvae then pupate and the emerging adults move away Epidemiology of tomato spotted wilt virus disease on
crisphead lettuce in Hawaii. Plant Disease 71:505–508.
and spread the virus. Thrips transmit the virus in the cir-
Groves, R. L., Walgenbach, J. F., Moyer, J. W., and Kennedy, G.
culative propagative manner. Weed hosts are an G. 2002. The role of weed hosts and tobacco thrips,
important reservoir of the virus and source of the thrips. Frankliniella fusca, in the epidemiology of tomato spotted
wilt virus. Plant Disease 86:573–582.
Mumford, R. A., Barker, I., and Wood, K. R. 1996. The biology
Control of tospoviruses. Annals of Applied Biology 128:159–183
Controlling TSWV is difficult. Use non-host plants in Wilson, C. R. 1998. Incidence of weed reservoirs and vectors of
V IRAL D ISEASES
crop rotations to help limit inoculum. Control weeds tomato spotted wilt tospovirus on southern Tasmania. Plant
adjacent to and near lettuce fields. Insecticide applica- Pathology 47:171–176.
Yudin, L. S., Tabashnik, B. E., Cho, J.J., and Mitchell, W. C.
tions to manage thrips will not prevent the disease from 1990. Disease-prediction and economic models for managing
occurring but might help limit major tomato spotted tomato spotted wilt virus disease in lettuce. Plant Disease
wilt outbreaks. 74:211–216.
Turnip mosaic virus

435
TURNIP MOSAIC

Turnip mosaic is an occasional virus problem that
affects lettuce.

Early symptoms include numerous, small, light green to
yellow, circular and irregular spots on leaves (435).
Later symptoms include curvature of the midrib and
distortion of the leaf blade. Infected young lettuce may
remain stunted and small with deformed, ruffled foliage
(436).
435 Eye spot symptom of turnip mosaic of lettuce.
Turnip mosaic is caused by Turnip mosaic virus
(TuMV). TuMV is a potyvirus and has filamentous 436
particles measuring approximately 720 nm in length
and is vectored by several aphids in a nonpersistent
manner. TuMV has a very wide host range.
Control
Plant resistant cultivars and avoid susceptible ones. For
example, crisphead cultivars with downy mildew resist-
ance derived from P. I. 91532 are very susceptible to
TuMV. Remove weed hosts. Keep aphid populations
under control, though the direct effect of such steps on
disease incidence is questionable.
References
Duffus, J. E. and Zink, F. W. 1969. A diagnostic host reaction for
the identification of turnip mosaic virus. Plant Disease
Zink, F. W. and Duffus, J. E. 1970. Linkage of turnip mosaic
virus susceptibility and downy mildew, Bremia lactucae, 436 Stunting and deformity of turnip mosaic of lettuce.
resistance in lettuce. Journal of the American Society for
V IRAL D ISEASES
AMMONIUM TOXICITY 437

If conditions favor development of this abiotic disorder,
significant loss of plant stands can occur. In general, this
disorder is of low to moderate concern.

Lettuce roots are sensitive to high levels of ammonium
in the soil. The central core of the root first turns yellow
to light brown, then becomes dark brown to red in
color, though typically a brick red discoloration is seen
(437, 438). In severe cases, the root xylem collapses and
a central cavity forms throughout the length of the root
and even into the lower crown of the plant. Lateral 437 Discolored lettuce vascular tissue caused by
roots may be short, with blackened tips. In some situa- ammonium toxicity.
tions the external surface of the root turns yellow or
light brown and develops cracks, which mimic corky 438
root symptoms. Above ground symptoms indicate that
plants have damaged root systems and consist of poor
growth, stunting, yellowing of older foliage, and
wilting. Plants damaged by excess ammonium have
symptoms in the vascular tissue that resemble those
caused by Fusarium and Verticillium wilts. In general,
the hollow root cavity symptom is more characteristic
of ammonium toxicity, while Verticillium wilt tends to
have black, not red, vascular discoloration.
Causal factor
This problem results from the buildup of ammonium in
the root zone of lettuce plants. Ammonium toxicity
occurs when soils are cool, compacted, and water-
logged. Sealing of the soil surface from sprinkler irriga-
tion or rain can also contribute to this problem. Such
conditions result in slow nitrification rates in the soil.
Low soil pH and excessive fertilization also contribute
to this problem. Ammonium toxicity tends to occur
most often in direct seeded lettuce.
Control
Few management steps are practical for correcting 438 Discolored lettuce vascular tissue caused by
A BIOTIC D ISORDERS
ammonium toxicity problems. To help prevent ammonium toxicity.

ammonium toxicity development, prepare soils so that
they are not compacted or sealed.
References
Marlatt, R. B. 1967. Nonpathogenic diseases of lettuce: their
identification and control. Bulletin 721. University of Florida.
TIPBURN 439

Tipburn is a physiological disorder of lettuce. If envi-
ronmental conditions favor development of this abiotic
disorder, significant quality loss can take place.

All lettuce types can develop tipburn, though lettuces
that form an entirely enclosed head, such as iceberg and
butterhead, develop this disorder more frequently and
severely. Symptoms mostly occur on the margins of
developing leaf tips and consist of light to dark brown 439 Tipburn symptoms on butterhead lettuce.
speckling, lesions, and necrosis (439, 440). In severe
cases tipburn can result in extensive damage. Secondary
440
decay can result in soft bacterial rot or ‘slime.’ The gray
mold pathogen, Botrytis cinerea, can colonize the
necrotic areas, progress into adjacent healthy leaf tissue,
and cause brown, soft decay. Symptomatic leaves are
usually found within the inner whorls of open-head
cultivars and underneath the enclosing wrapper leaves
of closed-head types. The disease causes significant
concerns for harvesters because enclosed head varieties
do not show external symptoms, and tipburn can only
be detected after the lettuce is cut open.
440 Tipburn symptoms on iceberg lettuce.
Causal factor
Tipburn develops when the plant cannot provide itself
with sufficient calcium. Conditions that interfere with
calcium uptake or that favor rapid plant growth may Barta, D. J. and Tibbitts, T. W. 2000. Calcium localization and
trigger tipburn. These include warm temperatures tipburn development in lettuce leaves during early
enlargement. Journal of the American Society for
combined with high fertilization rates and dry root- Horticultural Science 125:294–298.
zone soil. The disorder is similar to blackheart of celery, Collier, G. F. and Tibbitts, T. W. 1984. Effects of relative humidity
and to tipburn of spinach and other leafy vegetables. and root temperature on calcium concentration and tipburn
development in lettuce. Journal of the American Society for
Control Frantz, J. M., Ritchie, G., Cometti, N. N., Robinson, J., and
Plant resistant cultivars. Avoid applying excessive Bugbee, B. 2004. Exploring the limits of crop productivity:
amounts of fertilizer, and irrigate with drip irrigation beyond the limits of tipburn in lettuce. Journal of the
systems. Foliar calcium supplements may have some Misaghi, I. J. and Grogan, R. G. 1978. Effect of temperature on
benefit on open-head lettuce cultivars. tipburn development in head lettuce. Phytopathology
68:1738–1743.
Misaghi, I. J. and Grogan, R. G. 1978. Physiological basis for
A BIOTIC D ISORDERS
References
tipburn development in head lettuce. Phytopathology
Ashkar, S. A. and Ries, S. K. 1971. Lettuce tipburn as related to 68:1744–1753.
nutrient imbalance and nitrogen composition. Journal of the Misaghi, I. J., Grogan, R. G., and Westerlund, F. V. 1981. A
American Society for Horticultural Science 96:448–452. laboratory method to evaluate lettuce cultivars for tipburn
Barta, D. J. and Tibbetts, T. W. 1991. Calcium localization in tolerance. Plant Disease 65:342–344.
lettuce leaves with and without tipburn: comparison of Misaghi, I. J., Matyac, C. A., and Grogan, R. G. 1981. Soil and
controlled-environment and field-grown plants. Journal of foliar applications of CaCl2 and Ca(NO3)2 to control tipburn
the American Society for Horticultural Science 116:870–875. of head lettuce. Plant Disease 65:821–822.
327
Solanum lycopersicum Tomato
TOMATO (Solanum lycopersicum) is one of the most widely produced plants in the Solanaceae
(nightshade family). Fruit is valued for its high nutrition, and the crop is grown throughout the
world. Tomato originated in South America. Field-grown tomatoes are widely grown in warm
temperate and tropical climates, and glasshouse tomatoes are produced in many additional
regions. There is little commercial, outdoor production in northern Europe, although tomatoes
are grown outdoors in gardens. A wide diversity of fruit types is available, including large red
beefsteak, small cherry, yellow pear, and others. Tomatoes are grown for fresh market produce
as well as a range of processed products such as tomato juice, canned peeled tomatoes, tomato
purée and sauce, ketchup, soups, and sun-dried tomatoes.
Clavibacter michiganensis subsp. michiganensis collapse. Stems can split and result in the formation of
BACTERIAL CANKER open breaks, or cankers. Stems break off easily at
branch nodes.
Introduction and significance In addition to the symptoms caused by primary
Bacterial canker was first noted in 1909 and today is infections, secondary infections and their resulting
still an important tomato disease found throughout the symptoms occur when bacteria are splashed onto the
world. Periodic outbreaks can cause significant damage surfaces of foliage, stems, and fruit. Leaves and stems
to tomato crops in numerous geographic regions. can develop white to cream-colored, raised, blister-like
spots. Such spots on young stems may turn tan in color.
Initial symptoms are the result of primary, systemic
infections. These symptoms usually affect the lower
foliage first and consist of curling of leaves, wilting of 441 Vascular 441
leaves and branches, chlorosis of leaves, and brown streaking caused
necrosis and shriveling of leaf tissue. These leaf by bacterial canker
symptoms sometimes develop on only one side of the of tomato.
leaf, with the other leaf side appearing normal. Internal
vascular tissue begins to turn light yellow to tan in color.
As disease develops the vascular tissue turns darker
brown to red-brown (441; also 451, page 333). The
central pith tissue of the stem becomes discolored,
turning yellow and sometimes brown. The pith tissue
also becomes damaged, resulting in a mealy texture,

separation of the pith from the adjacent vascular tissue,
and hollowing of the stem center. In advanced stages the
pathogen becomes systemic in plant phloem tissues and
causes the overall plant to grow poorly, wilt, and
possibly die. Foliage throughout the canopy will
continue to wilt, turn yellow then brown, and finally
442
Disease cycle
Primary inoculum can come from many sources and
includes infested plant debris in soil, infected volunteer
tomato plants, infected weed hosts, contaminated
wood stakes, diseased transplants, and infested seed.
Depending on weather conditions, infested tomato
leaves and stems that are not buried below ground
allow the pathogen to survive for long periods of time;
such crop residues can be sources of initial inoculum for
new tomato plantings.
Infested seed is a particularly important inoculum
source because bacteria can spread and disease can
develop when plants are grown under greenhouse con-
ditions. A 1% seed transmission rate is sufficient to give
442 Fruit lesions caused by bacterial canker of tomato. 100% disease. The practices of clipping or mowing
transplants and using overhead sprinkler irrigation can
significantly spread the pathogen, though young,
diseased transplants may show few or no symptoms of
bacterial canker until later in their growth. During
Secondary fruit symptoms are very characteristic and transplanting, the diseased or contaminated plants
are a useful diagnostic feature. Spots occur on green result in bacterial spread to equipment, workers’ hands,
fruit and are at first small, round, and white or yellow. and previously clean transplants.
Such spots enlarge slightly (up to 3–4 mm in diameter) Once bacterial canker is established on plants in the
and develop raised, brown centers that remain encircled field, the pathogen can be spread plant-to-plant via
by the white to cream-colored spot (442; also 451, page splashing water (rain, sprinkler irrigation), contami-
333). They are commonly called ‘bird’s eye spots.’ nated tools and implements, and workers’ hands.
Bacteria enter the tomato host via stomates, small
Causal agent wounds, and broken trichomes. After entering through
The pathogen is Clavibacter michiganensis subsp. these openings, the pathogen can become systemic and
michiganensis. This organism is an aerobic, non-spore- will colonize and move through the xylem tissue.
forming, Gram-positive bacterium. This pathogen can Disease development is favored by warm conditions
be isolated on standard microbiological media and (24–32° C) and factors that create succulent growth of
produces yellow colonies on nutrient agar; colonies the tomato.
reach 3–4 mm in diameter after 5 days incubation.
Specialized media such as SCM medium are very useful Control
for recovering this pathogen. Bacterial cells can be pleo- Monitor tomato seed fields regularly so that bacterial
morphic in culture, but are rod shaped when isolated canker problems can be detected at an early stage and
from plants. Optimum growth occurs at 24–27° C. The managed appropriately. Obtain and plant high-quality
pathogen is not a true soilborne pathogen, but it can seed that does not have detectable, economically
survive in soil for long periods in dried tomato plant important levels of C. michiganensis subsp. michiga-
residues. In older references the pathogen is listed as nensis. Use a hot water seed treatment or treat seed with
Corynebacterium michiganense. Clavibacter michiga- hydrochloric acid, calcium hypochlorite, or other rec-
nensis subsp. michiganensis is most important as a ommended materials. Hot water treatments can reduce
pathogen on tomato. However, the pathogen can infect seed viability and germination percentages. Seed health
other solanaceous plants such as pepper, aubergine testing and certification programs help regulate the
(eggplant), Nicotiana glutinosa, and the weeds black availability and cleanliness of such seed. Such seed tests
nightshade (Solanum nigrum), perennial nightshade (S. usually involve the washing of a 10,000 seed sample
douglasii), and cutleaf nightshade (S. triflorum). and subsequent plating of the liquid onto semi-selective
S OLANUM LYCOPERSICUM 329
medium. Discard heavily infested seed. Use resistant References

cultivars if such are available. Chang, R. J., Ries, S. M., and Pataky, J. K. 1992. Effects of
Though young transplants may not exhibit bacterial temperature, plant age, inoculum concentration, and cultivar
on the incubation period and severity of bacterial canker of
canker symptoms, inspect transplants and remove tomato. Plant Disease 76:1150–1155.
suspect plants and surrounding transplant trays. Chang, R. J., Ries, S. M., and Pataky, J. K. 1991. Dissemination
Sanitize benches that hold transplants, transplant trays, of Clavibacter michiganensis subsp. michiganensis by
practices used to produce tomato transplants.
and equipment that comes into contact with plants. Phytopathology 81:1276–1281.
Roguing of affected plants may be worthwhile if disease Chang, R. J., Ries, S. M., and Pataky, J. K. 1992. Local sources of
incidence is low. Lower the water pressure in irrigation Clavibacter michiganensis ssp. michiganensis in the
equipment to reduce damage to leaves. Consider development of bacterial canker on tomatoes.
applying preventative fungicides (copper-based Fatmi, M. and Schaad, N. W. 1988. Semiselective agar medium
materials) for protecting transplants. Realize that the for isolation of Clavibacter michiganense subsp.
practice of mowing transplants to regulate transplant michiganense from tomato seed. Phytopathology
78:121–126.
height can readily spread the pathogen. Instead,
Fatmi, M., Schaad, N. W., and Bolkan, H. A. 1991. Seed
implement growing practices that involve air movement treatments for eradicating Clavibacter michiganensis subsp.
or differential temperature management. michiganensis from naturally infected tomato seeds. Plant
Minimize damage to plants during transplanting, Disease 75:383–385.
Forster, R. L. and Echandi, E. 1973. Relation of age of plants,
transplant only when foliage is dry, and periodically temperature, and inoculation concentration to bacterial
sanitize transplanting equipment. Avoid using overhead canker development in resistant and susceptible Lycopersicon
sprinkler irrigation in the field. In the field, use new spp. Phytopathology 63:773–777.
wooden stakes or stakes that have been steamed or Gitaitis, R., McCarter, S., and Jones, J. 1992. Disease control of
tomato transplants produced in Georgia and Florida. Plant
treated with chlorine. With an appropriate disinfectant, Disease 76:651–656.
periodically and regularly sanitize tools such as clippers Gitaitis, R. D., Beaver, R. W., and Voloudakis, A. E. 1991.
and pruning shears. Do not allow equipment or Detection of Clavibacter michiganensis subsp. michiganensis
in symptomless tomato transplants. Plant Disease
workers to pass through fields when foliage is wet. 75:834–838.
Copper sprays may provide some disease control. Once Gleason, M. L., Gitaitis, R. D., and Ricker, M. D. 1993. Recent
the tomato crop is finished, incorporate the crop progress in understanding and controlling bacterial canker of
tomato in Eastern North America. Plant Disease
residues to enhance plant decomposition and the dissi-
77:1069–1076.
pation of bacteria. Rotate to a non-host crop before Gleason, M. L., Braun, E. J., Carlton, W. M., and Peterson, R. H.
returning to tomato and do not allow volunteer tomato 1991. Survival and dissemination of Clavibacter
or weed hosts to survive. michiganensis subsp. michiganensis in tomatoes.
Hausbeck, M. K., Bell, J., Medina-Mora, C., Podolsky, R., and
Fulbright, D. W. 2000. Effect of bactericides on population
sizes and spread of Clavibacter michiganensis subsp.
michiganensis on tomatoes in the greenhouse and on disease
development and crop yield in the field. Phytopathology
90:38–44.
Thompson, E., Leary, J. V., and Chun, W. W. C. 1989. Specific
detection of Clavibacter michiganensis subsp. michiganensis
by homologous DNA probe. Phytopathology 79:311–314.
Fatmia, M., and Schaad, N. W. 2002. Survival of Clavibacter
michiganensis ssp. michiganensis in infected tomato stems
under natural field conditions in California, Ohio and
Morocco. Plant Pathology 51:149–154.
Pseudomonas syringae pv. tomato pathogen can be isolated on standard microbiological

BACTERIAL SPECK media and produces cream-colored colonies typical of
most pseudomonads. When cultured on Kings medium
Introduction and significance B, it produces a diffusible pigment that fluoresces blue
Bacterial speck is a relatively minor disease of tomato under ultraviolet light. Strains of this pathogen can be
that can cause economic damage if environmental con- host specific to tomato, while other strains can infect
ditions favor severe infections. The disease occurs both tomato and pepper. This pathogen is seedborne,
worldwide. which results in infection of tomato seedlings. Two
distinct races (races 0 and 1) have been documented.
Foliar symptoms are dark brown to black spots on Disease cycle
leaves and stems (443). Leaf spots can be circular to Primary inoculum can come from infested seed,
angular in shape, and individual spots are generally soilborne plant debris, or reservoir plant hosts. Infested
smaller than 5 mm in diameter. Spots are visible from seed is a particularly important inoculum source
both top and bottom sides of the infected leaf and are because bacteria can spread and disease can develop
often surrounded by a yellow halo. Leaf spots can when plants are grown under greenhouse conditions.
coalesce and result in the necrosis of large areas of the The practice of using overhead sprinkler irrigation can
leaf. Stems and petioles also develop dark brown to significantly spread the pathogen. Once diseased trans-
black spots that are irregular in shape but tend to be plants are in the field, the pathogen can spread plant-to-
slightly elongated along the axis of the stem (444, 445). plant via splashing water (rain, sprinkler irrigation),
In severe cases, bacterial speck can result in stunted contaminated tools and implements, and workers’
growth, delayed crop maturity, and reduced yields. hands. Disease development is favored by high
Symptoms on green fruit consist of small (less than humidity (greater than 80% relative humidity), free
3 mm in diameter), slightly raised, superficial black moisture, and cool temperatures (18–24° C). Seedlings
lesions or specks (446 also 451, page 333). Such specks are particularly susceptible. The pathogen is not a
usually are not surrounded by halos. soilborne organism, but it can survive in the soil on
infested plant residues for up to 30 weeks. The
Causal agent pathogen can overwinter on volunteer tomato plants;
Bacterial speck is caused by the aerobic, Gram-negative weeds can also support pathogen populations on root
bacterium Pseudomonas syringae pv. tomato. The and leaf surfaces.
443 443 Leaf spots 444

444 Stem lesions
caused by bacterial on field-grown
speck of tomato. tomato caused by
bacterial speck.
445 446
445 Stem lesions on tomato transplants caused by 446 Fruit lesions caused by bacterial speck of tomato.
bacterial speck.
Control References
Regularly monitor tomato seed fields so that early Bashan, Y. 1986. Field dispersal of Pseudomonas syringae pv.
outbreaks can be controlled. Obtain and plant high- tomato, Xanthomonas campestris pv. vesicatoria, and
Alternaria macrospora by animals, people, birds, insects,
quality seed that does not have detectable, economical- mites, agricultural tools, aircraft, soil particles, and water
ly important levels of P. syringae pv. tomato. Use a hot sources. Canadian Journal of Botany 64:276–281.
water seed treatment or treat seed with hydrochloric Bashan, Y., Okon, Y., and Henis, Y. 1982. Long-term survival of
Pseudomonas syringae pv. tomato and Xanthomonas
acid, calcium hypochlorite, or other recommended campestris pv. vesicatoria in tomato and pepper seeds.
materials. Hot water treatments can reduce seed Phytopathology 72:1143–1144.
viability and germination percentages. Seed health Cuppels, D. A. and Elmhirst, J. 1999. Disease development and
testing and certification programs help regulate the changes in the natural Pseudomonas syringae pv. tomato
population on field tomato plants. Plant Disease 83:759–764.
availability and cleanliness of such seed. Such seed tests Gitaitis, R., McCarter, S., and Jones, J. 1992. Disease control of
usually involve the washing of a 10,000 seed sample tomato transplants produced in Georgia and Florida.
and subsequent plating of the liquid onto semi-selective Plant Disease 76:651–656.
medium. Discard heavily infested seed. Use resistant Goode, M. J. and Sasser, M. 1980. Prevention – the key to
controlling bacterial spot and bacterial speck of tomato.
cultivars if such become available. Plant Disease 64:831–834.
Inspect transplants and remove symptomatic plants McCarter, S. M., Jones, J. B., Gitaitis, R. D., and Smitley, D. R.
and surrounding transplant trays. Sanitize benches that 1983. Survival of Pseudomonas syringae pv. tomato in
association with tomato seed, soil, host tissue, and epiphytic
hold transplants, transplant trays, and equipment that weed hosts in Georgia. Phytopathology 73:1393–1398.
comes into contact with plants. Consider applying pre- Smitley, D. R. and McCarter, S. M. 1982. Spread of
ventative spray applications (copper-based materials Pseudomonas syringae pv. tomato and role of epiphytic
combined with maneb fungicides, newer chemistry populations and environmental conditions in disease
development. Plant Disease 66:713–717.
such as acibenzolar-S-methyl) for protecting trans- Voloudakis, A. E., Gitaitis, R. D., Westbrook, J. K., Phatak, S. C.,
plants. Avoid using overhead sprinkler irrigation in the and McCarter, S. M. 1991. Epiphytic survival of
field. With an appropriate disinfectant, periodically and Pseudomonas syringae pv. syringae and Pseudomonas
syringae pv. tomato on tomato transplants in Southern
regularly sanitize tools such as clippers and pruning Georgia. Plant Disease 75:672–675.
shears. Do not allow equipment or workers to pass

through fields when foliage is wet. Copper+mancozeb
sprays provide some control. Once the tomato crop is
finished, incorporate the crop residues to enhance plant
decomposition and the dissipation of bacteria. Rotate
to a non-host crop before returning to tomato, and do
not allow volunteer tomato or weed hosts to survive.
Xanthomonas campestris pv. vesicatoria

447
BACTERIAL SPOT

While bacterial spot occurs throughout the world, this
disease is most serious in tropical and sub-tropical
tomato growing areas, such as the southeastern USA
and Brazil, where both high humidity and rainfall are
present.

Initial foliar symptoms consist of circular to irregularly
shaped, water-soaked spots on leaves (447). These spots
later turn dark brown and usually remain smaller than 447 Leaf spots due to bacterial spot on tomato
5 mm in diameter. As disease progresses, the spots may transplants.
coalesce and result in leaves having significant necrotic
areas (448). Severely infected seedlings can become 448
defoliated. While infected leaves may show some
chlorosis, the individual spots usually are not sur-
rounded by yellow halos. Dark streaks may develop on
petioles and stems. In severe cases, bacterial spot can
result in stunted growth, a scorched appearance to the
foliage, defoliation, and reduced yields. Early symptoms
on green fruit consist of small (less than 3 mm in
diameter), raised blisters (449, 450, 451). These
diseased spots enlarge into brown, rough scabs that
measure 5–8 mm in diameter.
Causal agent
Bacterial spot is caused by the aerobic, Gram-negative
bacterium Xanthomonas campestris pv. vesicatoria. 448 Leaf spots of bacterial spot on mature tomato
The pathogen can be isolated on standard microbio- leaves.
logical media and produces yellow, mucoid, slow-
growing colonies typical of most xanthomonads. 449
However, X. campestris pv. vesicatoria only weakly
such as SX and MXP media are not diagnostic for
isolating and identifying this pathogen. Tween medium
is useful, because this bacterium forms characteristic
white calcium salt crystals when growing on it. This
pathogen is seedborne, which results in infection of
tomato seedlings.
Xanthomonad pathogens from tomato and pepper
hosts are a complex group of organisms. At least three
tomato strains of this pathogen are host specific to
tomato and are designated as T1, T2, and T3. Other
strains are host specific to pepper. Finally, other strains 449 Fruit lesions of bacterial spot of tomato.
are pathogenic on both of these hosts; these pepper– Control

tomato strains are designated as PT strains. Researchers Use seed that does not have detectable, economically
further find that xanthomonad pathogens from tomato important levels of the pathogen. Regularly monitor
and pepper can be divided into various groups (A, B, C, tomato seed fields so that early outbreaks can be con-
and D) based on genetic and biochemical parameters. trolled. Use a hot water seed treatment or treat seed
The assignment of these groups to various species and with hydrochloric acid, calcium hypochlorite, or other
pathovars is still being debated. recommended materials. Hot water treatments can
reduce seed viability and germination percentages. Seed
Disease cycle health testing and certification programs help regulate
Primary inoculum can come from infested seed, the availability and cleanliness of such seed. Such seed
soilborne plant debris, or reservoir plant hosts. Infested tests usually involve the washing of a 10,000 seed
seed is a particularly important inoculum source sample and subsequent plating of the liquid onto semi-
because bacteria can spread and disease can develop selective medium. Discard heavily infested seed.
when plants are grown under greenhouse conditions. Inspect transplants and remove symptomatic plants
The practice of using overhead sprinkler irrigation can and surrounding transplant trays. Sanitize benches that
significantly spread the pathogen. Once diseased trans- hold transplants, transplant trays, and equipment that
plants are in the field, the pathogen can be spread plant- comes into contact with plants. Consider applying
to-plant via splashing water (rain, sprinkler irrigation), preventative fungicide applications (copper-based
contaminated tools and implements, and workers’ materials combined with maneb fungicides) for pro-
hands. Disease development is favored by high tecting transplants. Avoid using overhead sprinkler
humidity and warm temperatures in the 24–30° C irrigation in the field. With an appropriate disinfectant,
range. The pathogen is not a soilborne organism, but it periodically and regularly sanitize tools such as clippers
can survive in the soil on infested plant residues. The and pruning shears. Do not allow equipment or
pathogen can also overwinter on volunteer tomato workers to pass through fields when foliage is wet.
plants and on weeds such as black nightshade (Solanum Copper+mancozeb sprays provide some disease
nigrum) and ground cherry (Physalis minima). control. Once the tomato crop is finished, incorporate
the crop residues to enhance plant decomposition and
the dissipation of bacteria. Rotate to a non-host crop
before returning to tomato and do not allow volunteer
tomato or weed hosts to survive.
450 451
450 Bacterial spot lesions on tomato fruit. 451 Comparison of bacterial spot (right), speck (top),
and canker (left) symptoms on tomato fruit.
References Pseudomonas corrugata

Bashan, Y., Okon, Y., and Henis, Y. 1982. Long-term survival of TOMATO PITH NECROSIS
Pseudomonas syringae pv. tomato and Xanthomonas
campestris pv. vesicatoria in tomato and pepper seeds.
Phytopathology 72:1143–1144. Introduction and significance
Bouzar, H., Jones, J. B., Stall, R. E., Hodge, N. C., Minsavage, G. Tomato pith necrosis has been reported in the USA, UK,
V., Benedict, A. A., and Alvarez, A. M. 1994. Physiological, and other countries. This disease is widespread in parts
chemical, serological, and pathogenic analyses of a
worldwide collection of Xanthomonas campestris pv.
of South America. Pith necrosis affects older plants and
vesicatoria strains. Phytopathology 84:663–671. symptoms usually do not show until fruit begin to
Gitaitis, R., McCarter, S., and Jones, J. 1992. Disease control of develop.
tomato transplants produced in Georgia and Florida. Plant
Disease 76:651–656.
Goode, M. J. and Sasser, M. 1980. Prevention – the key to
Symptoms and diagnostic feature
controlling bacterial spot and bacterial speck of tomato. Plant Early symptoms include wilting of young foliage and
Disease 64:831–834. chlorosis and wilting of older leaves. Affected leaves can
Jones, J. B., Bouzar, H., Somodi, G. C., Stall, R. E., Pernezny, K., curl up and turn brown on their edges. Dark brown to
El-Morsy, G., and Scott, J. W. 1998. Evidence for the
preemptive nature of tomato race 3 of Xanthomonas black lesions develop on the surfaces of lower stems.
campestris pv. vesciatoria in Florida. Phytopathology 88:33–38. Internally, such stems have pith tissue that contains
Jones, J. B., Pohronezny, K. L., Stall, R. E., and Jones, J. P. 1986. cavities, is darkly discolored, and can become hollow
Survival of Xanthomonas campestris pv. vesicatoria in
Florida on tomato crop residue, weeds, seeds, and volunteer
(452, 453). Adventitious roots may grow profusely
tomato plants. Phytopathology 76:430–434. from these symptomatic stems. Vascular tissue may be
Jones, J. B., Stall, R. E., and Bouzar, H. 1998. Diversity among brown. In advanced stages the internal pith symptom
Xanthomonads pathogenic on pepper and tomato. Annual may progress high up into the plant, and severely
Review of Phytopathology 36:41–58.
Jones, J. B., Stall, R. E., Scott, J. W., Somodi, G. C., Bouzar, H.,
affected plants may collapse and die. Overall, tomato
and Hodge, N. C. 1995. A third tomato race of pith necrosis symptoms may resemble those of bacterial
Xanthomonas campestris pv. vesicatoria. Plant Disease canker.
79:395–398.
McGuire, R. G., Jones, J. B., and Sasser, M. 1986. Tween media
for semiselective isolation of Xanthomonas campestris pv. Causal agents
vesicatoria from soil and plant material. Plant Disease Tomato pith necrosis is caused by Pseudomonas
70:887–891.
corrugata. The pathogen is an aerobic, Gram-negative
McGuire, R. G., Jones, J. B., Stanley, C. D., and Csizinszky, A. A.
1991. Epiphytic populations of Xanthomonas campestris pv. bacterium that can be isolated on standard microbio-
vesicatoria and bacterial spot of tomato as influenced by logical media and produces buff-colored, raised,
nitrogen and potassium fertilizer. Phytopathology wrinkled colonies, with or without green centers, on
81:656–660.
nutrient dextrose agar. On King’s medium B, this
Obradovic, A., Mavridis, A., Rudolph, K., Janse, J. D.,
Arsenijevic, M., Jones, J. B., Minsavage, G. V., Wang, J.-F. bacterium produces a yellow-green, nonfluorescent, dif-
2004. Characterization and PCR-based typing of fusible pigment. Though considered mostly a pathogen
Xanthomonas campestris pv. vesicatoria from peppers and
tomatoes in Serbia. European Journal of Plant Pathology
of tomato, P. corrugata can cause small brown lesions
110:285–292. on alfalfa.
Scott, J. W. and Jones, J. B. 1986. Sources of resistance to Recent discoveries show that pith necrosis can also
bacterial spot in tomato. HortScience 21:304–306. be caused by other species such as P. viridiflava,
Sijam, K., Chang, C. J., and Gitaitis, R. D. 1992. A medium for
differentiating tomato and pepper strains of Xanthomonas
P. fluorescens biotype I, and Erwinia carotovora
campestris pv. vesicatoria. Canadian Journal of Plant pathogens. This indicates that the cause or etiology of
Pathology 14:182–184. pith necrosis may be complex. Pseudomonas corrugata
Stahl, R. E., Beaulieu, C., Egel, D., Hodge, N. C., Leite, R. P., is reported to cause pith necrosis on pepper, as well.
Minsavage, G. V., Bouzar, H., Jones, J. B., Alvarez, A. M., and
Benedict, A. A. 1994. Two genetically diverse groups of
strains are included in Xanthomonas campestris pv.
vesicatoria. International Journal of Systematic Bacteriology
44:47–53.
452 453
452 Discolored central pith tissue of stem affected by 453 Pith necrosis of tomato showing laddering of
Pseudomonas corrugata. central pith in stems.

Tomato pith necrosis appears to develop when there are Alippi, A. M., Dal Bo, E., Ronco, L. B., López, M. V., López, A.
low night temperatures, high nitrogen levels, and high C., and Aguilar, O. M. 2003. Pseudomonas populations
causing pith necrosis of tomato and pepper in Argentina are
humidity. Disease is expressed when the first fruit set is highly diverse. Plant Pathology 52:287–302.
near the mature green stage. Inoculum is possibly Jones, J. B., Jones, J. P., Stall, R. E., and Miller, J. W. 1983.
seedborne, but disease epidemiology is poorly Occurrence of stem necrosis on field-grown tomatoes incited
by Pseudomonas corrugata in Florida. Plant Disease
understood. 67:425–426.
Lai, M., Opgenorth, D. C., and White, J. B. 1983. Occurrence of
Control Pseudomonas corrugata on tomato in California. Plant
Few control recommendations have been established. Disease 67:110–112.
Lukezic, F. L. 1979. Pseudomonas corrugata, a pathogen of
Avoid using excessively high nitrogen fertilizer rates. Do tomato, isolated from symptomless alfalfa roots.
not use overhead sprinkler irrigation in the field. With Phytopathology 69:27–31.
an appropriate disinfectant, periodically and regularly Scarlett, C. M., Fletcher, J. T., Roberts, P., and Lelliott, R. A.
sanitize tools such as clippers and pruning shears. Do 1978. Tomato pith necrosis caused by Pseudomonas
corrugata n. sp. Annals of Applied Biology 88:105–114.
not allow equipment or workers to pass through fields
when foliage is wet. Once the tomato crop is finished,
incorporate the crop residues to enhance plant decom-
position and the dissipation of bacteria. Rotate to a
non-host crop before returning to tomato and do not
allow volunteer tomato or weed hosts to survive.
Alternaria alternata
454
BLACK MOLD

Black mold disease affects only ripe tomato fruit.
Significant fruit losses can occur if environmental con-
ditions favor disease development.

On ripe tomato fruit the initial symptoms consist of
irregularly shaped flecks and stains on the cuticle. The
affected areas are small and tan to brown. With suitable
environmental conditions, the small infected areas
expand into large, sunken, circular to oval-shaped
lesions that can extend deep into the fruit (454). The 454 Fruit lesions caused by black mold of tomato in
black, velvety growth of the pathogen covers the surface the field.
of the lesions (455). Lesions break down and the fruit
will rot. The large infected areas can also support the 455
growth of other decay fungi such as Stemphylium
species, which are considered by some researchers to be
weak tomato fruit pathogens, and Cladosporium and
Aspergillus species, which are saprobes. Postharvest
spread of the disease can occur if infected fruit are
stored for long periods.
Causal agent
Black mold is caused by the fungus Alternaria alternata.
logical media. On potato dextrose agar, colonies are
usually dark green to black and have limited aerial
mycelium. Conidia are obclavate, ovoid, or ellipsoidal
in shape and often have a short, conical beak that does 455 Fruit lesions caused by black mold of tomato.
not exceed one-third of the length of the spore. Conidia
are pale to gold brown, smooth or verruculose, measure
20–63 x 9–18 μm, and have three to five cross septa and
occasional longitudinal septa. Conidia are produced in
long chains that sometimes branch. In contrast to fruit are damaged or wet from dew, rains, and irriga-
A. alternata f. sp. lycopersici, the causal agent of tions, conidia germinate and infect the fruit. Fruit
Alternaria stem canker, the black mold A. alternata is damaged by sunburn or blossom end rot (a calcium
not host specific to tomato. This pathogen is an active deficiency) are particularly susceptible to colonization
saprobe and can colonize damaged tissues of other by A. alternata. Disease development is most rapid at
plants and readily grows on dead organic matter. 24–28° C.
F UNGAL D ISEASES

Alternaria alternata is commonly found on decaying Harvest fruit in a timely manner so that ripe fruit are
plant material in and around fields, including senescent not left in the field longer than necessary. Do not irrigate
and dead tomato leaves of the current crop. Conidia are with overhead sprinklers. Apply protectant fungicides
blown onto ripe fruit via winds and splashing water. If 4 to 6 weeks before harvest.
References 456 Stem cankers 456

Bartz, J. A. 1971. Studies on the causal agent of black fungal on tomato caused
lesions on stored tomato fruit. Proceedings of the Florida by Alternaria
State Horticultural Society 84:117–119.
alternata f. sp.
Davis, R. M., Miyao, E. M., Mullen, R. J., Valencia, J., May, D.
M., and Gwynne, B. J. 1997. Benefits of applications of lycopersici.
chlorothalonil for the control of black mold of tomato. Plant
Disease 81:601–603.
Morris, P. F., Connolly, M. S., and St. Clair, D. A. 2000. Genetic
diversity of Alternaria alternata isolated from tomato in
California assessed using RAPDs. Mycological Research
104:286–292.
Pearson, R. C. and Hall, D. H. 1975. Factors affecting the
occurrence and severity of blackmold of ripe tomato fruit
caused by Alternaria alternata. Phytopathology
65:1352–1359.
Simmons, E. G. 1999. Alternaria themes and variations
(236–243): host specific toxin producers. Mycotaxon
70:325–369.
Simmons, E. G. 2000. Alternaria themes and variations
(244–286) species on Solanaceae. Mycotaxon 75:1–115.
Alternaria alternata f. sp. lycopersici Causal agent

ALTERNARIA STEM CANKER The causal agent is Alternaria alternata f. sp. lycopersici.
Introduction and significance logical media. On potato dextrose agar, colonies are
Alternaria stem canker is primarily a problem on initially whitish and cottony. With age, colonies darken
tomatoes grown in coastal regions in California. The and become gray to almost black and show appressed
disease is of limited distribution. growth. Conidia are light olive-brown to dark brown
and are dictyospores having three to five cross septa,
Symptoms and diagnostic features occasional longitudinal septa, and short-beaked apical
Large, irregularly shaped, dark brown to almost black
cankers form on stems. Cankers characteristically
contain light and dark concentric zonation within their 457
borders. Cankers continue to enlarge as the plant
develops, resulting in girdled stems (456) and the death
of the stems and even the entire plant. Vascular and pith
tissue beneath the cankers can show brown streaking
and become dry and cracked. Infected leaves develop
irregularly shaped, dark brown to black areas that are
primarily interveinal. Affected plants may be stunted.
Fruit symptoms always begin on green, unripe fruit and
F UNGAL D ISEASES
appear as brown, circular to oval, sunken lesions that

also have concentric rings in them (457). This green
fruit disease is distinct from blackmold disease which is
caused by a different Alternaria pathogen that affects
only ripe fruit.
457 Fruit lesions of Alternaria stem canker of tomato.
cells on the terminal ends. Conidia are produced in Alternaria solani ( = Alternaria tomatophila)
chains of three to five and measure 18–50 x 7–18 μm. EARLY BLIGHT
The fungus is pathogenic on tomato only and produces
a host-specific toxin (AAL-toxin, analogs TA and TB) Introduction and significance
that moves systemically from stem cankers to leaves, Early blight occurs on tomato throughout the world
causing the interveinal necrotic lesions. and can be an important disease.

The pathogen can survive in the soil for up to a year on The disease begins as small, brown to black, circular
infested tomato residue. Infection takes place when lesions on mature leaves (458). Such lesions may be sur-
plants come in contact with infested residue or when rounded by chlorotic tissue. As disease develops, the
conidia are spread, via winds, to host tomato plants. spots enlarge and can be 8–10 mm or larger in diameter.
Cankers also occur around wounds such as pruning At this later stage the leaf spots contain characteristic
cuts on pole tomato. Spore germination and infection concentric rings. With severe infections, plants can
requires free moisture on the host tissue. Optimum tem- become defoliated and the exposed fruit are subject to
perature for disease development is 25° C. sunburn damage. Infections on stems initially consist of
small, brown, sunken lesions. Stem lesions expand and
Control become elongated or oval lesions with concentric rings.
Plant resistant cultivars, as this will virtually eliminate Stem lesions can eventually girdle the stem and result in
serious disease outbreaks. Resistance to this pathogen stem or plant death. Seedlings can show stem lesions at
is achieved by a single gene (Asc) with two alleles, which the soil level when they are less than 3 weeks old. Fruit
confers complete protection against this pathogen. If infections, at either the green or ripe stage, consist of
using susceptible cultivars, avoid irrigating with sunken, dark brown to black, circular spots that also
overhead sprinklers. Rotate crops so that tomato does contain concentric rings. Early blight green fruit and
not immediately follow a previous tomato crop. Use stem symptoms may resemble fruit and stem infections
effective fungicides if available. caused by the Alternaria stem canker pathogen.
References
Akamatsu, H., Itoh, Y., Kodama, M., Otani, H., and Kohmoto,
K. 1997. AAL-toxin-deficient mutants of Alternaria alternata
tomato pathotype by restriction enzyme-mediated
integration. Phytopathology 87:967–972.
Clouse, S. D. and Gilchrist, D. G. 1987. Interaction of the asc
locus in F8 paired lines of tomato with Alternaria alternata f.
sp. lycopersici and AAL-toxin. Phytopathology 77:80–82. 458
Fuson, G. B. and Pratt, D. 1988. Effects of the host-selective
toxins of Alternaria alternata f. sp. lycopersici on suspension-
cultured tomato cells. Phytopathology 78:1641–1648.
Gilchrist, D. G. and Grogan, R. G. 1976. Production and nature
of a host-specific toxin from Alternaria alternata f. sp.
lycopersici. Phytopathology 66:165–171.
Grogan, R. G., Kimble, K. A., and Misaghi, I. 1975. A stem
canker disease of tomato caused by Alternaria alternata f. sp.
lycopersici. Phytopathology 65:880–886.
F UNGAL D ISEASES
458 Leaf spots of early blight of tomato.


Early blight is caused by the fungus Alternaria solani. Select and plant resistant cultivars as available. Use seed
The pathogen can be isolated on standard microbio- that does not have significant levels of the pathogen.
logical media. Cultures appear gray-brown in color and Treat infested seed lots with hot water or fungicides.
usually produce a yellow or red diffusable pigment. Inspect and discard infected, symptomatic transplants.
Sporulation in culture is enhanced by exposing colonies Multiple applications of fungicides are usually required
to light. Conidia are olivaceous brown to dark brown to control this disease. Some forecasting programs, such
and are obclavate to obpyriform, having seven to eight as TOMCAST, are used to assist with fungicide timing
cross septa, and occasional longitudinal septa. Conidia for early blight control. Practice crop rotation so that
usually have long-beaked apical cells that can be the the selected field did not have tomato in the previous
same as or exceed the length of the spore body. Conidia year. Remove volunteer tomato and host weed species.
are produced singly or in chains of two and measure
150–300 x 15–19 μm. Alternaria solani produces References
resilient structures called chlamydospores, which enable Brammall, R. A. 1993. Effect of foliar fungicide treatment on
the pathogen to survive in soil for a period of time. This early blight and yield of fresh market tomato in Ontario.
pathogen is seedborne in tomato and can result in
Frazer, J. T. and Zitter, T. A. 2003. Two species of Alternaria
diseased seedlings or transplants. Affected seedlings cause early blight of potato (Solanum tuberosum) and tomato
may develop collar rot in which the base of the plant is (Lycopersicon esculentum). Phytopathology 93:S27.
girdled due to a stem canker. Plants with collar rot can Gleason, M. L., MacNab, A. A., Pitblado, R. E., Ricker, M. D.,
East, D. A., and Latin, R. X. 1995. Disease early warning
become stunted, wilted, and dead. This pathogen also systems for processing tomatoes in eastern North America:
affects other solanaceous host such as potato and are we there yet? Plant Disease 79:113–121.
aubergine (eggplant). Gleason, M. L., Parker, S. K., Pitblado, R. E., Latin, R. X.,
Speranzini, D., Hazzard, R. V., Maletta, M. J., Cowgill, W. P.,
Reports indicate that the early blight Alternaria and Biederstedt, D. L. 1997. Validation of a commercial
pathogens on tomato and potato, historically both system for remote estimation of wetness duration. Plant
designated as A. solani, may be distinct species. Morph- Disease 81:825–829.
ologically and genetically the early blight isolates from Miller, D. J., Coffman, C. B., Teasdale, J. R., Everts, K. L., Abdul-
Baki, A. A., Lydon, J., and Anderson, J. D. 2002. Foliar
tomato are distinct from those from potato. Tomato disease in fresh-market tomato grown in differing bed
isolates are more virulent on tomato, and the potato strategies and fungicide spray programs. Plant Disease
isolates are more aggressive on potato. The tomato 86:955–959.
Patterson, C. L. 1991. Importance of chlamydospores as primary
isolates apparently do not produce spores very well in inoculum for Alternaria solani, incitant of collar rot and early
culture, while the potato isolates sporulate extensively. blight of tomato. Plant Disease 75:274–278.
The tomato early blight pathogen is proposed to be Pennypacker, S. P., Madden, L., and MacNab, A. A. 1983.
A. tomatophila, while the potato pathogen retains the Validation of an early blight forcasting system for tomatoes.
A. solani name. Simmons, E. G. 2000. Alternaria themes and variations
(244–286): species on Solanaceae. Mycotaxon 75:1–115.
Disease cycle Vakalounakis, D. J. 1991. Control of early blight of greenhouse
Initial inoculum of A. solani is present on infested tomato, caused by Alternaria solani, by inhibiting sporulation
with ultraviolet-absorbing vinyl film. Plant Disease
tomato crop debris and on tomato seed. In addition, the 75:795–797.
pathogen can overwinter on volunteer tomato plants Weir, T. L., Huff, D. R., Christ, B. J., and Romaine, C. P. 1998.
and on other solanaceous plants such as aubergine RAPD-PCR analysis of genetic variation among isolates of
Alternaria solani and Alternaria alternata from potato and
(eggplant), potato, and the weeds black nightshade tomato. Mycologia 90:813–821.
(Solanum nigrum) and horsenettle (S. carolinense).
F UNGAL D ISEASES
Conidia are blown onto plants via winds and splashing

water. Wet, mild conditions (with a temperature range
of 24–29° C) favor disease development. In Europe,
early blight is most important when summer tempera-
tures are high.
Athelia rolfsii (anamorph = Sclerotium rolfsii )

459
SOUTHERN BLIGHT

Southern blight, or Sclerotium stem rot, occurs on a
large number of vegetable and ornamental plants espe-
cially in warmer regions of the world. In the UK this
tomato disease is not established in the field though
southern blight has been recorded on ornamentals and
imported vegetables. This disease is found in many
tomato growing regions of the USA.

On tomato, the early symptoms consist of a water-
soaked lesion on crown and lower stem tissue that is in 459 Wilting of tomato plants caused by southern
contact with the soil. These infection sites turn light to blight disease.
dark brown and can rapidly girdle the entire crown.
Crown tissue is often cracked or split. Above-ground 460 Tomato stem 460
symptoms consist of wilting and a quick collapse of all colonized by the
foliage (459). If soil moisture conditions are suitable, southern blight
the pathogen will form a thick, white mycelial mat or pathogen.
layer on crown, lower stem, and even on the surround-
ing soil around the crown (460, 461). Small (1–2 mm in
diameter), spherical, tan to light brown sclerotia form
profusely on and in this white growth. Sclerotia are
characterized by having an outer, differentiated,
pigmented rind. Fruit in contact with infested soil can
also become infected, developing sunken, water-soaked
lesions that later support the typical white mycelial
growth and sclerotia.
Causal agent
Southern blight is caused by Sclerotium rolfsii, which is
an imperfect fungus in the mycelia sterilia category and 461 White 461
produces no asexual spores (older references list the mycelial fan of
fungus as Corticium rolfsii). Sclerotium rolfsii has a southern blight of
broad host range and forms a basidiomycete perfect tomato.
stage (Athelia rolfsii), though it is unknown whether
this stage is involved in the disease.
Disease cycle
Because of its resilient sclerotia, the pathogen can
F UNGAL D ISEASES
survive in the soil and in crop debris for many years.

The fungus is favored by high temperatures above
30° C. In the soil, sclerotia near host tissues will
germinate, form infective mycelium, and directly
penetrate root and crown tissues of tomato.
Control 462 462 Stem lesion

Rotate with non-host plants so that soil inoculum levels caused by gray
are reduced. Deep plowing of fields prior to planting, mold on tomato.
which inverts the soil profile, may help reduce inoculum
levels. Pre-plant treatment of soil with effective
fumigants will give short-term control; however, such
treatments may be too expensive to implement for pro-
cessing tomato crops.
References
Bulluck, L. R. and Ristaino, J. B. 2002. Effect of synthetic and
organic soil fertility amendments on southern blight, soil
microbial communities, and yield of processing tomatoes.
Hasan, A. and Khan, M. N. 1985. The effect of Rhizoctonia
solani, Sclerotium rolfsii, and Verticillium dahliae on the
resistance of tomato to Meloidogyne incognita. Nematologia
Mediterranea. 13:133–136.
McCarter, S. M., Jaworski, C. A., Johnson, A. W., and
Williamson, R. E. 1976. Efficacy of soil fumigants and
methods of application for controlling southern blight of
tomatoes grown for transplants. Phytopathology
66:910–913.
Punja, Z. K. 1985. The biology, ecology, and control of
Sclerotium rolfsii. Annual Revue of Phytopathology
23:97–127.
463

GRAY MOLD

Gray mold is a commonly found disease of tomato and
is manifested in several ways. Gray mold can be partic-
ularly damaging in greenhouse environments, due to
the elevated humidity in such structures.
Symptoms and diagnostic features 463 Stem lesion caused by gray mold of tomato,
Petioles and stems become infected and develop tan to showing initiation at wounds.
darker brown lesions (462). The developing lesions can
eventually girdle the entire petiole or stem and show
concentric rings due to the sporulation of the pathogen
and coloration of the lesion. Leaves may also have
F UNGAL D ISEASES
brown lesions and sporulation. The gray mold Infections on green or ripe fruit result in a soft,
pathogen often infects petioles, stems, and leaves that decayed, circular rot that can eventually envelop the
are damaged or senescing (463). Senescing petals are entire fruit. The fungus usually sporulates on the fruit
also subject to gray mold infection; if such petals are in calyx or in the center of the fruit lesion where the epi-
contact with the developing fruit, the fungus can grow dermis has split. A distinct fruit infection, called ‘ghost
from the petal and into the fruit tissue. spots’, occurs when the pathogen invades the fruit but
464 465
464 Numerous ‘ghost spots’ on a ripening tomato. 465 Gray sporulation of Botrytis cinerea on infected
tomato stem.
then dies prior to causing decay. The resulting symptom Disease cycle
is a white to yellow ring that can range from 3–10 mm Botrytis cinerea survives in and around fields as a sapro-
in diameter (464). Ghost spots do not result in fruit phyte on crop debris, as a pathogen on numerous crops
decay but cause the fruit to lose market quality. Tomato and weed plants, and as sclerotia in the soil. Conidia
transplants that are damaged during the planting develop from these sources and become windborne.
process can develop gray mold stem infections and die. When conidia land on senescent or damaged tomato
On greenhouse tomatoes, stem infections are the tissue, they will germinate if free moisture is available
most prominent problem. Cracked or wounded stems and rapidly colonize this food base. Once established,
and cut stubs remaining after fruit are harvested are the pathogen will grow into adjacent healthy stems and
primary locations for gray mold infections. Gray mold leaves, resulting in disease symptoms and the produc-
colonies that start on such wounded tissues usually tion of additional conidia. Cool temperatures, free
progress into the main stem and cause girdling. moisture, and high humidity favor the development of
the disease. Tomato tissues that are damaged from
Causal agent other diseases can become colonized by B. cinerea that
Gray mold is caused by asexual fungus Botrytis cinerea. acts as a secondary decay organism.
The sexual stage, Botryotinia fuckeliana, is rarely found
on the crop. Conidiophores of B. cinerea are long Control
(1–2 mm), become gray-brown with maturity, and Reduce plant wetness by avoiding or reducing sprinkler
branch irregularly near the apex. Conidia are clustered irrigation. Adequately ventilate greenhouses, or heat
at the branch tips and are single-celled, pale brown, them to reduce overall humidity. Fungicides may be
ellipsoid to obovoid, and measure 6–18 x 4–11 μm. The useful in protecting fruit from gray mold. It is important
pathogen can be isolated on standard microbiological to use a diversity of fungicides with different modes of
media. Some isolates sporulate poorly in culture unless action because B. cinerea commonly develops resistance
incubated under lights (12 h light/12 h dark). If formed, to such materials. For example, resistance to benzimi-
F UNGAL D ISEASES
sclerotia are black, oblong or dome-shaped, and dazole and dicarboximide materials is prevalent and
measure 4–10 mm. The fungus grows best at 18–23° C often limits their effectiveness. Dichlofluanid is useful
but is inhibited at warm temperatures above 32° C. On for control of the ghost spot symptom as it is one of the
host tissue the fungus produces characteristically few fungicides that prevents spore germination.
profuse sporulation that is dense, velvety, and grayish
brown in color (465).
References Vegetative parts of the tomato plant are also suscep-

Chastagner, G. A., Ogawa, J. M., and Manji, B. T. 1978. tible to anthracnose. Leaves develop small, circular, tan
Dispersal of conidia of Botrytis cinerea in tomato fields. to brown spots that often are ringed with yellow halos.
Roots initially show brown lesions and later rot. As
Chastagner, G. A. and Ogawa, J. M. 1979. A fungicide-wax
treatment to protect and suppress Botrytis cinerea on fresh root cortex tissue breaks down, the black microsclero-
market tomatoes. Phytopathology 69:59–63. tia of the pathogen form profusely, giving this phase of
Ferrer, J. B. and Owen, J. H. 1959. Botrytis cinerea, the cause of the disease the name black dot root rot. Black dot root
ghost-spot disease of tomato. Phytopathology 49:411–417.
rot is part of the brown root rot disease complex that
Miller, M. W. and Jeves, T. M. 1979. The persistence of benomyl
tolerance in Botrytis cinerea in glasshouse tomato crops. occurs on greenhouse-grown tomato in Europe.
Morgan, W. M. 1984. The effect of night temperatures and Causal agents
glasshouse ventilation on the incidence of Botrytis cinerea in a
late planted tomato crop. Crop Protection 3:243–251. Anthracnose is caused by several species of the fungus
O’Neill, T. M., Shtienberg, D., and Elad, Y. 1997. Effect of some Colletotrichum: C. coccodes, C. gloeosporioides, and
host and microclimate factors on infection of tomato stems by C. dematium. C. coccodes is the species most frequently
Botrytis cinerea. Plant Disease 81:36–40.
associated with the fruit disease and appears to be the
Sasaki, T., Honda, Y., Umekawa, M., and Nemoto, M. 1985.
Control of certain diseases of greenhouse vegetables with only causal agent of black dot root rot. The minute
ultraviolet-absorbing vinyl film. Plant Disease 69:530–533. (about 0.3 mm in diameter), cup-shaped acervuli
Shtienberg, D., Elad, Y., Niv, A., Nitzani, Y., and Kirshner, B. fruiting bodies are usually present in fruit lesions.
1998. Significance of leaf infection by Botrytis cinerea in stem
rotting of tomatoes grown in non-heated greenhouses.
Acervuli release single-celled, hyaline conidia that are
European Journal of Plant pathology 104:753–763. cylindrical with obtuse ends. Conidia measure 16–24 x
Vakalounakis, D. J. 1992. Control of fungal diseases of 2–5 μm. Long, brown, septate setae are usually present
greenhouse tomato under long-wave infrared-absorbing in the acervuli. The pathogen forms small (0.2–0.4
plastic film. Plant Disease 76:43–46.
mm), irregularly shaped survival structures called
microsclerotia. Colletotrichum coccodes has a broad
Colletotrichum coccodes, C. gloeosporioides, host range and can infect a number of other plants such
C. dematium as cucurbits, legumes, potato, and weeds.
ANTHRACNOSE
466
Anthracnose disease occurs in various parts of the
world where tomato is grown. The disease is usually of
minor importance unless environmental conditions
favor development of the pathogen.

The disease primarily affects the fruit. Young, green
fruit may be infected, but disease symptoms are not 466 Fruit lesions caused by anthracnose.
expressed until fruit begin to ripen. Ripe fruit initially
show small, circular, depressed lesions (466). Lesions 467
467 Dark fungal
can then become quite large (12–15 mm in diameter), structures inside
sunken, and contain concentric rings. Lesion centers are fruit lesions caused
usually tan, but become black as fungal structures by anthracnose.
F UNGAL D ISEASES
(microsclerotia and acervuli) form in the tissues (467).

If humid, wet weather occurs, the fruiting bodies in the
lesions will release pink-colored spore masses.
Harvested fruit infected with anthracnose will not ship
or store well, and are very susceptible to secondary fruit
decay organisms.
Disease cycle Lees, A.K. and Hilton, A.J. 2003. Black dot (Colletotrichum
coccodes) an increasingly important disease of potato. Plant
The fungus survives in soil in the form of microsclero- Pathology 52:3–12.
tia or as acervuli and microsclerotia on dried plant Miller, D. J., Coffman, C. B., Teasdale, J. R., Everts, K. L., Abdul-
residue. The fungus can be seedborne. The pathogen is Baki, A. A., Lydon, J., and Anderson, J. D. 2002. Foliar
disease in fresh-market tomato grown in differing bed
splashed from the soil onto tomato foliage and fruit and strategies and fungicide spray programs. Plant Disease
initiates infections. In addition, fruit that are in contact 86:955–959.
with the soil become infected by soilborne inoculum. Raid, R. N. and Pennypacker, S. P. 1987. Weeds as hosts for
Colletotrichum coccodes. Plant Disease 71:643–646.
Ripe fruit are particularly susceptible to infection. The
Schneider, R. W., Grogan, R. G., and Kimble, K. A. 1978.
root phase of anthracnose disease is often found in Colletotrichum root rot of greenhouse tomatoes in
infested greenhouse situations due to high concentra- California. Plant Disease Reporter 62:969–ß971.
tions of inoculum and favorable conditions for disease
development. Optimum temperatures for disease devel-
opment are 20–24° C. Wet, humid weather favors the
development of acervuli and conidia; conidia are spread
by splashing water.
Control Fusarium oxysporum f. sp. lycopersici

Rotate crops so that non-hosts are grown at least every FUSARIUM WILT
other year. Many weeds can support the pathogen, so
practice good weed control. Stake plants or use mulch Introduction and significance
materials to reduce the number of fruit in contact with Fusarium wilt was first characterized in 1895 and
soil. Avoid sprinkler irrigation which spreads the continues to be present worldwide. If resistant cultivars
conidia. Apply fungicides as necessary and use disease are not used, the disease can still be a serious production
forecasting programs such as TOMCAST to schedule problem.
applications. Harvest fruit in a timely manner so that
they are not overly ripe. Researchers are attempting to Symptoms and diagnostic features
develop resistant cultivars. If young seedlings are infected, plants can be stunted
and exhibit poor growth. However, the more familiar
References symptoms of Fusarium wilt occur on older plants.
Batson, W. E. and Roy, K. W. 1982. Species of Colletotrichum Initial symptoms on such plants are chlorosis of lower
and Glomerella pathogenic to tomato fruit. Plant Disease leaves followed by wilting of that foliage. Character-
66:1153–1155.
istically, the yellow to yellow-gold discoloration and
Blakeman, J. P. and Hornby, D. 1966. The persistence of
Colletotrichum coccodes and Mycosphaerella ligulicola in wilting symptoms often first occur on only one side of
soil with special reference to sclerotia and conidia. the plant. As disease progresses, the entire plant will
turn chlorotic, wilt, and then collapse and dry up (468).
Byrne, J. M., Hausbeck, M. K., and Latin, R. X. 1997. Efficacy
and economics of management strategies to control The vascular tissue is discolored and turns brown (469)
anthracnose fruit rot in processing tomatoes in the midwest. with the discoloration extending into the upper stems.
Plant Disease 81:1167–1172. This extensive browing is a helpful feature in distin-
Dillard, H. R. 1989. Effect of temperature, wetness duration, and
inoculum density on infection and lesion development of
guishing this disease from Fusarium crown and root
Colletotrichum coccodes on tomato fruit. Phytopathology rot, in which the vascular browning is found only in the
79:1063–1066. lower stem. Fusarium wilt vascular browning tends to
Farley, J. D. 1976. Survival of Colletotrichum coccodes in soil. be darker than the vascular discoloration caused by
F UNGAL D ISEASES
Gleason, M. L., MacNab, A. A., Pitblado, R. E., Ricker, M. D.,

Verticillium wilt, though this distinction is not always
East, D. A., and Latin, R. X. 1995. Disease early warning clear. Disease symptoms can be accentuated if the
systems for processing tomatoes in eastern North America: infected plant is bearing a heavy load of fruit or is
are we there yet? Plant Disease 79:113–121.
stressed by some other factor. The overall symptoms are
Last, F. T. and Ebben, M. H. 1966. The epidemiology of tomato
brown root rot. Annals of Applied Biology 57:95–112. similar to those caused by Verticillium wilt; hence
disease confirmation will require laboratory analysis.
468 469
468 Fusarium wilt causing severe yellowing of tomato. 469 Vascular discoloration caused
by Fusarium wilt of tomato.
Causal agent
Fusarium wilt is caused by the fungus Fusarium wilt may be more severe if plants are grown under
oxysporum f. sp. lycopersici. The pathogen morphology certain nutrient conditions. For example, low nitrogen,
and colony characteristics are similar to other low phosphorus, high potassium, and ammoniacal
F. oxysporum fungi. The fungus forms one- or two- forms of nitrogen may enhance disease.
celled, oval- to kidney-shaped microconidia on mono-
phialides, and four- to six-celled, fusiform, curved Control
macroconidia. Microconidia measure 5–12 x 2–4 μm, Use resistant cultivars. Use nitrate-based fertilizers
while macroconidia range from 25–45 x 3–5 μm (four- instead of ammoniacal ones. Do not plant tomato in
celled) to 35–60 x 3–5 μm (six-celled). Macroconidia fields having high populations of root knot nematode
are usually produced in cushion-shaped structures (Meloidogyne species) as this nematode can cause the
called sporodochia. Chlamydospores are also formed. plant’s Fusarium wilt resistance to be overcome.
The pathogen is usually readily isolated from symp- Practice good field sanitation so that infested soil and
tomatic vascular tissue. Semi-selective media like mud are not spread to uninfested fields.
Komada’s medium can help isolate the pathogen if
secondary rot organisms are present. This pathogen is References
apparently host specific to tomato and can be Bao, J. R. and Lazarovitis, G. 2001. Differential colonization of
seedborne. Three races (races 1, 2, and 3) have been tomato roots by nonpathogenic and pathogenic Fusarium
oxysporum strains may influence Fusarium wilt control.
documented. A Petri-plate technique can be used to Phytopathology 91:449–456.
differentiate this vascular wilt Fusarium from the crown Borrero, C., Trillas, M. I., Ordovas, J. Tello, J. C., and Aviles, M.
and root rot Fusarium (see Sanchez, et al.). 2004. Predictive factors for the suppression of Fusarium wilt
of tomato in plant growth media. Phytopathology
94:1094–1101.
Disease cycle Boyer, A. and Charest, P. M. 1989. Use of lectins for
F UNGAL D ISEASES
Like other Fusarium wilt pathogens, F. oxysporum f. sp. differentiating between Fusarium oxysporum f. sp. radicis-
lycopersici is a soil inhabitant that can survive in the soil lycopersici and Fusarium oxysporum f. sp. lycopersici in pure
culture. Canadian Journal of Plant Pathology 11:14–21.
for indefinite periods of time due to the production of Cai, G., Gale, L. R., Schneider, R. W., Kistler, H. C., Davis, R. M.,
overwintering chlamydospores. The fungus is favored Elias, K. S., and Miyao, E. M. 2003. Origin of race 3 of
by warm temperatures, and optimum wilt development Fusarium oxysporum f. sp. lycopersici at a single site in
California. Phytopathology 93:1014–1022.
takes place at 28° C. Researchers find that Fusarium
Davis, R. M., Kimble, K. A., and Farrar, J. J. 1988. A third race of

Fusarium oxysporum f. sp. lycopersici identified in 470
California. Plant Disease 72:453.
Elias, K. S. and Schneider, R. W. 1991. Vegetative compatibility
groups in Fusarium oxysporum f. sp. lycopersici.
Erb, W. A. and Rowe, R. C. 1992. Screening tomato seedlings for
multiple disease resistance. Journal of the American Society
for Horticultural Science 117:622–627.
Katan, T., Shlevin, E., and Katan, J. 1997. Sporulation of
Fusarium oxysporum f. sp. lycopersici on stem surfaces of
tomato plants and aerial dissemination of inoculum.
Mai, W. F. and Abawi, G. S. 1987. Interactions among root knot
nematodes and Fusarium wilt fungi on host plants. Annual
Review of Phytopathology 25:317–338.
Marlatt, M. L., Correll, J. C., Kaufmann, P., and Cooper, P. E.
1996. Two genetically distinct populations of Fusarium 470 Internal discoloration caused by Fusarium
oxysporum f. sp. lycopersici race 3 in the United States. Plant oxysporum f. sp. radicis-lycopersici.
Disease 80:1336–1342.
Mes, J. J., Weststeijn, E. A., Herlaar, F., Lambalk, J. J. M.,
Wijbrandi, J., Haring, M. A., and Cornelissen, B. J. C. 1999.
Biological and molecular characterization of Fusarium more rapidly and collapse completely. A tan to brown
oxysporum f. sp. lycopersici divides race 1 isolates into
separate virulence groups. Phytopathology 89:156–160.
discoloration develops in the vascular tissue of the root
Sanchez, L. E., Endo, R. M., and Leary, J. V. 1975. Rapid and extends into the adjacent tissues of the lower stem,
technique for identifying clones of Fusarium oxysporum f. sp. as well (470). However, such internal stem discol-
lycopersici causing crown and root rot of tomato. oration remains in the lower stem and does not extend
Scott, J. W., Agrama, H. A., and Jones, J. P. 2004. RFLP-based
beyond 10–30 cm above the soil line. This limited,
analysis of recombination among resistance genes to lower discoloration is a helpful feature in distinguishing
Fusarium wilt races 1, 2, and 3 in tomato. Journal of the this disease from Fusarium wilt, in which the vascular
browning can extend far into the upper stems.
Weststeijn, G. 1973. Soil sterilization and glasshouse disinfection
to control Fusarium oxysporum f. sp. lycopersici in tomatoes Examination of the outside surface of plant crowns and
in the Netherlands. Netherlands Journal of Plant Pathology lower stems may reveal the presence of large, irregular,
79:36–40 brown, necrotic cankers (471). On occasion orange
spore deposits may form on these cankers.
Fusarium oxysporum f. sp. radicis-lycopersici Causal agent

FUSARIUM CROWN & ROOT ROT Fusarium crown and root rot is caused by the fungus
Fusarium oxysporum f. sp. radicis-lycopersici. The
Introduction and significance pathogen morphology and colony characteristics are
Fusarium crown and root rot is found in many parts similar to other F. oxysporum fungi. The fungus forms
of the world on both field and greenhouse grown one- or two-celled, oval to kidney shaped microconidia
tomatoes. The disease can be particularly severe in on monophialides, and four- to six-celled, fusiform,
greenhouse production environments. curved macroconidia. Microconidia measure 5–12 x
2–4 μm, while macroconidia range from 25–45 x 3–5
Symptoms and diagnostic features μm (four-celled) to 35–60 x 3–5 μm (six-celled). Macro-
The initial symptom is chlorosis of the lower leaves that conidia are usually produced in cushion-shaped struc-
F UNGAL D ISEASES
often is initiated along the margins of the leaves. Such tures called sporodochia and appear orange-colored in
leaves later become necrotic and then wither. In many culture or on infected stem cankers. Chlamydospores
cases, successively younger leaves develop chlorosis and are also formed. The pathogen is usually readily
necrosis until only the upper part of the plant has isolated from symptomatic vascular tissue. Semi-
healthy, functional foliage. Infected plants can be selective media like Komada’s medium can help isolate
stunted and not productive. In other cases plants decline the pathogen if secondary rot organisms are present.
A Petri-plate technique can be used to differentiate References

this crown and root rot Fusarium from the vascular wilt Boyer, A. and Charest, P. M. 1989. Use of lectins for
Fusarium (see Sanchez, et al.). Under experimental con- differentiating between Fusarium oxysporum f. sp. radicis-
lycopersici and Fusarium oxysporum f. sp. lycopersici in pure
ditions, researchers found that this pathogen can also culture. Canadian Journal of Plant Pathology 11:14–21.
infect plants such as bean, beet, clover, cucumber, Chellemi, D. O., Olson, S. M., and Mitchell, D. J. 1994. Effects
aubergine (eggplant), pepper, and others. of soil solarization and fumigation on survival of soilborne
pathogens of tomato in northern Florida. Plant Disease
78:1167–1172.
Disease cycle Gillespie, D. R. and Menzies, J. G. 1993. Fungus gnats vector
Like Fusarium wilt pathogens, F. oxysporum f. sp. Fusarium oxysporum f. sp. radicis-lycopersici. Annals of
radicis-lycopersici is a soil inhabitant that can survive in Applied Biology 123:539–544.
Hartman, J. R. and Fletcher, J. T. 1991. Fusarium crown and root
the soil for indefinite periods of time due to the produc- rot of tomatoes in the U. K. Plant Pathology 40:85–92.
tion of overwintering chlamydospores. In addition to Jarvis, W. R. and Thorpe, H. J. 1980. Effects of nitrate and
soil inoculum, the pathogen can also grow saprophyti- ammonium nitrogen on severity of Fusarium foot and root
cally and produce conidia on decaying organic matter. rot and on yield of greenhouse tomatoes. Plant Disease
64:309–310.
In greenhouses, microconidia can reach tomato plants Krikun, J., Nachmias, A., Cohn, R., and Lahkim-Tsror, L. 1982.
by becoming airborne or by being transported by The occurrence of Fusarium crown and root rot of tomato in
fungus gnats. Optimum disease development takes Israel. Phytoparasitica 10:113–115.
place at temperatures between 20–22° C. Following Menzies, J. G., Koch, C., and Seywerd, F. 1990. Additions to the
host range of Fusarium oxysporum f. sp. radicis-lycopersici.
initial infection at the base of the stem, there appears to Plant Disease 74:569–572.
be an incubation period of several days before there is Mihuta-Grimm, L., Erb, W. A., and Rowe, R. C. 1990. Fusarium
secondary spread through the vascular system of sus- crown and root rot of tomato in greenhouse rock wool
systems: sources of inoculum and disease management with
ceptible cultivars. benomyl. Plant Disease 74:996–1002.
Rekah, Y., Shtienberg, D., and Katan, J. 1999. Spatial
Control distribution and temporal development of Fusarium crown
In greenhouses, steam the soil and then apply fungicides and root rot of tomato and pathogen distribution in field soil.
prior to transplanting tomato. For infested outdoor Rekah, Y., Shtienberg, D., and Katan, J. 2001. Population
fields, no control measures have been developed. In Dynamics of Fusarium oxysporum f. sp. radicis-lycopersici in
such cases, use crop rotations that do not include host relation to the onset of Fusarium crown and root rot of
tomato. European Journal of Plant pathology 107:367–375.
plants. Some resistant cultivars are being developed for
Rodriquez-Molina, M. C., Medina, I., Torres-Vila, L. M. and
this disease. Cuartero, J. 2003. Vascular colonisation patterns in
susceptible and resistant tomato cultivars inoculated with
Fusarium oxysporum f. sp. radicis-lycopersici races 0 and 1.
471 Tomato stem Rosewich, U. L., Pettway, R. E., Katan, T., and Kistler, H. C.
471
lesions caused by 1999. Population genetic analysis corroborates dispersal of
Fusarium crown Fusarium oxysporum f. sp. radicis-lycopersici from Florida to
Europe. Phytopathology 89:623–630.
and root rot
Rowe, R. C. 1980. Comparative pathogenicity and host ranges
of Fusarium oxysporum isolates causing crown and root rot
of greenhouse and field-grown tomatoes in North America
and Japan. Phytopathology 70:1143–1148.
Rowe, R. C., Farley, J. D., and Coplin, D. L. 1977. Airborne
spore dispersal and recolonization of steamed soil by
Fusarium oxysporum in tomato greenhouses.
Rowe, R. C. and Farley, J. D. 1981. Strategies for controlling
F UNGAL D ISEASES
Fusarium crown and root rot in greenhouse tomatoes. Plant

Disease 65:107–112.
Sanchez, L. E., Endo, R. M., and Leary, J. V. 1975. Rapid
technique for identifying clones of Fusarium oxysporum f. sp.
lycopersici causing crown and root rot of tomato.
Leveillula taurica (anamorph = Oidiopsis taurica), Causal agents

Oidium neolycopersici, O. lycopersici For L. taurica, the asexual (anamorph) stage is named
POWDERY MILDEW Oidiopsis taurica. Conidiophores develop only from
endophytic mycelium and emerge through stomata in
Introduction and significance the lower leaf epidermis. Conidiophores can be
Powdery mildew disease can significantly limit tomato branched and carry one, or sometimes two, conidia.
production in various parts of the world. Severe disease Conidia are hyaline, single-celled, and dimorphic.
can cause early plant senescence and reduced yields. Primary (terminal) conidia are lanceolate with distinct
apical points. Secondary conidia are ellipsoid–cylindric
Symptoms and diagnostic features and lack the apical point. Conidial dimensions for both
There are two different types of powdery mildew fungi types vary according to the host plant but generally are
that infect tomato. Leveillula taurica (anamorph = 50–70 x 16–24 μm. For both conidial types, length-to-
Oidiopsis taurica) initially causes light green, irregularly width ratios are greater than 3.
shaped leaf spots. Spots can have diffuse margins, but Globose cleistothecia of the Leveillula teleomorph
often tend to appear angular and vein-delimited. As have numerous hypha-like appendages, contain up to
the spots age, the tissue becomes chlorotic and then 20 asci, but are rarely observed. Asci contain two
necrotic (472, 473). Careful examination of the under- ascospores that are cylindrical to pyriform and measure
sides of these leaves reveals the white powdery growth 24–40 x 12–22 μm. Leveillula taurica appears to have
of this pathogen (474). Leveillula taurica usually infects a broad host range of numerous crops and weeds, and
the older leaves; the younger leaves escape infection has been reported to infect plants in over 50 plant
until they mature. In some regions, severe disease can families. However, there may be distinct subpopula-
result in extensive shriveling of foliage, reduced growth, tions that have more restricted host ranges. This
and significant yield loss when fruit are exposed to the pathogen is found on tomato throughout the world and
sun and become sunburned. is often associated with drier climates.
The other powdery mildew on tomato is caused by In contrast to L. taurica, Oidium species produce
one or more species of Oidium. This powdery mildew epiphytic, conidiophore-bearing mycelium that grows
disease results in white colonies on upper and lower superficially on host surfaces. Oidium neolycopersici
surfaces of leaves and on stems and petioles (475). On produces conidia singly; conidia measure 22–46 x
occasion the colonies may take on a grayish white color. 10–20 μm and are ellipsoid–ovoid in shape. This species
The infected, underlying tissue may initially turn purple is widespread and can be found on tomato in many
but later becomes chlorotic and necrotic. Severe infec- regions of the world. Oidium lycopersici produces
tions cause leaves to be twisted and deformed. conidia in chains of three to five spores; conidia
472 473
F UNGAL D ISEASES
472 Yellow lesions caused by Leveillula taurica. 473 Yellow lesions caused by Leveillula taurica.
474
474 Sporulation 475
475 Sporulation
of powdery of powdery
mildew of tomato mildew of tomato
caused by caused by Oidium
Leveillula taurica. spp.
measure 25–40 x 12–18 μm and are elliptical to Correll, J. C., Gordon, T. R., and Elliott, V. J. 1987. Host range,
specificity, and biometrical measurements of Leveillula
doliform in shape. This species has only been confirmed taurica in California. Plant Disease 71:248–251.
in Australia. The sexual cleistothecia stage has yet to be Correll, J. C., Gordon, T. R., and Elliott, V. J. 1988. Powdery
observed for either of these Oidium species. mildew of tomato: the effect of planting date and triadimefon
on disease onset, progress, incidence and severity.
Disease cycle Fletcher, J. T., Smewin, B. J., and Cook, R. T. A. 1988. Tomato
Powdery mildew species are obligate pathogens and powdery mildew. Plant Pathology. 37:594–598.
survive on overwintering tomato, alternate hosts, or Khodaparast, S. A., Takamatsu, S., and Hedjaroude, G.-A. 2001.
Phylogenetic structure of the genus Leveillula
possibly as cleistothecia from their respective perfect (Erysiphales:Erysiphaceae) inferred from the nucleotide
stages. The asexual conidia of these fungi are dispersed sequences of the rDNA ITS region with special reference to
by winds. Powdery mildew development is favored by the L. taurica species complex. Mycological Research
105:909–918.
mild temperatures below 30° C. Interestingly, in green-
Kiss, L., Cook, R. T. A., Saenz, G. S., Cunnington, J. H.,
houses where humidity is extremely high (95% RH), Takamatsu, S., Pascoe, I., Bardin, M., Nicot, P. C., Sato, Y.,
powdery mildew caused by O. lycopersici may be sup- and Rossman, A. Y. 2001. Identification of two powdery
mildews, Oidium neolycopersici sp. nov. and Oidium
pressed. Many new reports document recent occur-
lycopersici, infecting tomato in different parts of the world.
rences of O. neolycopersici in various regions. However, Mycological Research 105:684–697.
researchers found that this pathogen is present on Palti, J. 1971. Biological characteristics, distribution, and control
preserved herbarium plants that are over 50 years old. of Leveillula taurica. Phytopathologia Mediterranea
10:139–153.
Price, T. V. 1981. Powdery mildew of tomato in Australia.
Control Australasian Plant Pathology 10:38–40.
Fungicides, such as sulfur, may be needed if the disease Reuveni, R. and Rotem, J. 1973. Epidemics of Leveillula taurica
becomes severe. Irrigation systems may influence on tomatoes and peppers as affected by conditions of
humidity. Phytopathologische Zeitschrift 76:153–157.
disease severity; studies indicate that furrow irrigated
Vakalounakis, D. J. and Papadakis, A. 1992. Occurrence of a
tomato may have more severe powdery mildew than new powdery mildew of greenhouse tomato in Greece, caused
sprinkler irrigated plantings. No other control options by Erysiphe sp. Plant Pathology 41:372–373.
F UNGAL D ISEASES
are available. Whipps, J. M. and Budge, S. P. 2000. Effect of humidity on

development of tomato powdery mildew (Oidium
lycopersici) in the glasshouse. European Journal of Plant
References Pathology 106:395–397.
Arredondo, C. R., Davis, R. M., and Rizzo, D. M. 1996. First Whipps, J. M., Budge, S. P., and Fenlon, J. S. 1998.
report of powdery mildew of tomato in California caused by Characteristics and host range of tomato powdery mildew.
an Oidium sp. Plant Disease 80:1303. Plant Pathology 47:36–48.
Phytophthora capsici, P. cryptogea, P. drechsleri,

477
P. parasitica (= P. nicotianae var. parasitica)
PHYTOPHTHORA ROOT ROT

There are several soilborne Phytophthora species that
cause diseases on tomato. Different tomato-producing
regions throughout the world may have different
species involved in this disease. In recent years these
pathogens have increased in importance on various
vegetable crops in the USA.

Diseases caused by Phytophthora spp. are manifested as
seed decays, seedling damping-off, root rots, and fruit
rots. Symptoms of Phytophthora root rot initially
consist of water-soaked root lesions that later turn dark
gray to brown. The discoloration can occur on both the
fine feeder and larger taproots. As lesions expand, indi-
vidual roots become girdled or entirely rotted. The dis-
coloration will affect both vascular and stele tissues of
the root and can move up the main taproot and into the 477 Foliar dieback caused by Phytophthora.
plant crown and lower main stem (476). In advanced
stages, the roots will be soft and decayed. The plant
crown can show surface and internal discoloration.
Above-ground symptoms consist of foliage that first Phytophthora fruit disease is called buckeye rot.
turns dull gray-green, then later wilts. The entire plant Buckeye rot almost always occurs on fruit that are
canopy can rapidly collapse and die (477, 478). touching infested soil. Green and ripe fruit can show
similar symptoms. The disease begins as small, brown
spots on fruit surfaces in contact with soil. Spots grow
476 Darkened into large, circular or irregularly oblong lesions that can
476
tomato stems cover more than half of the fruit. The lesions are char-
caused by acterized by concentric rings of alternating light and
Phytophthora dark brown discoloration (479). Diseased fruit are
capsici. initially firm, but will later become soft and rotted. The
white mycelium of the pathogen can sometimes be
observed when the lesion breaks open and rots. The
early, firm lesion symptoms on the fruit may resemble
the fruit infections caused by the late blight pathogen.
Causal agents
Phytophthora root rot is caused by several species
F UNGAL D ISEASES
including P. capsici, P. cryptogea, and P. parasitica

(= P. nicotianae var. parasitica). Buckeye rot is caused by
P. capsici, P. drechsleri, and P. parasitica. All three
species are oomycetes, soil inhabitants, and can persist
in soils for extended periods of time. Phytophthora
capsici forms irregularly shaped sporangia that can be
478
Disease cycle
Phytophthora species are spread by surface water and
movement of infested soil. Both fruit and root diseases
require wet soil conditions. Compacted, finely textured,
and poorly draining soils create conditions favorable
for root rot. Excess soil moisture or splashing water is
required for significant fruit rot development. These
Phytophthora species can infect pepper, cucurbits, and
other hosts.
Control
Plant tomato in fields having soils that drain well.
Prepare soil so that drainage is enhanced and low areas
are avoided. Carefully manage irrigation so that excess
soil water is reduced. Stake plants to keep fruit off
the ground, or use plastic mulches on bed tops. Keep
bed tops dry by using subsurface drip irrigation. Some
fungicides may help manage both root and fruit
infections.
References
478 Collapsing plants caused by Phytophthora root rot Blaker, N. S. and Hewitt, J. D. 1987. Comparison of resistance to
of tomato. Phytophthora parasitica in tomato. Phytopathology
77:1113–1116.
Cafe-Filho, A. C. and Duniway, J. M. 1995. Dispersal of
Phytophthora capsici and Phytophthora parasitica in furrow-
479 Pathology 44:1025–1032.
Neher, D. and Duniway, J. M. 1992. Dispersal of Phytophthora
parasitica in tomato fields by furrow irrigation. Plant Disease
76:582–586.
Neher, D. A., McKeen, C. D., and Duniway, J. M. 1993.
Relationships among Phytophthora root rot development,
Phytophthora parasitica populations in soil, and yield of
tomatoes under commercial field conditions. Plant Disease
77:1106–1111.
Ristaino, J. B. and Duniway, J. M. 1989. Effect of preinoculation
and postinoculation water stress on severity of Phytophthora
root rot in processing tomatoes. Plant Disease 73:349–352.
Ristaino, J. B., Duniway, J. M., and Marois, J. J. 1988. Influence
of frequency and duration of furrow irrigation on
development of Phytophthora root rot. Phytopathology
479 Buckeye rot symptoms on tomato fruit caused by
78:1701–1706.
Phytophthora. Ristaino, J. B., Duniway, J. M., and Marois, J. J. 1989.
Phytophthora root rot and irrigation schedule influence
growth and phenology of processing tomatoes. Journal of the
American Society for Horticultural Science 114:556-561.
spherical, ovoid, elongated, or have more than one Swiecki, T. J. and MacDonald, J. D. 1991. Soil salinity enhances
F UNGAL D ISEASES
apex. Sporangia are papillate, deciduous, have pedicels Phytophthora root rot of tomato but hinders asexual
that are 10 or more μm in length, and measure 30–60 x reproduction by Phytophthora parasitica. Journal of the
25–35 μm. Phytophthora parasitica sporangia vary
Workneh, F., van Bruggen, A. H. C., Drinkwater, L. E., and
greatly and can be ellipsoidal, ovoid, pyriform, or Shennan C. 1993. Variables associated with corky root and
spherical with distinct papilla. Sporangia are not Phytophthora root rot of tomatoes in organic and
conventional farms. Phytopathology 83:581–589.
deciduous and measure 11–60 x 20–45 μm.
Phytophthora infestans Symptoms and diagnostic features

LATE BLIGHT Initial late blight symptoms on tomato foliage are irreg-
ularly shaped, pale green, water-soaked spots and areas
Introduction and significance on leaves. These areas rapidly expand into large brown
Late blight disease of potato is one of the world’s most to gray leaf lesions that in severe cases can kill the entire
well known plant diseases because of its historic signif- leaf. If environmental conditions are suitable, the leaf
icance and role in the Irish potato famine of the 1840s. undersides can be covered with the velvet white growth
Late blight is also an important tomato disease. of the pathogen (480). Stems and petioles can also
Worldwide, late blight reemerged in the 1990s through develop the water-soaked and later brown to gray
early 2000s as a very serious disease concern for both lesions (481). The pathogen can rapidly colonize
potato and tomato crops, and devastating epidemics tomato foliage and cause entire plants to turn brown,
have been chronicled on various continents. shrivel, and die (482). Infected green fruit develop
circular to oval to irregularly shaped lesions that are
480 Late blight 480
green-brown to dark brown in color (483). Such lesions
sporulation on can become quite large, sometimes covering the entire
tomato leaf. fruit. Characteristically these green fruit lesions are very
firm and do not break down and rot unless the infec-
tions are old and secondary decay organisms are
present in the fruit.
Causal agent
Late blight is caused by the oomycete Phytophthora
infestans. Phytophthora infestans is heterothallic and
requires two distinct mating types (A1 and A2) to
undergo sexual reproduction and produce the sexual
spore, the oospore. The presence and importance of
oospores appears to differ depending on where the crop
is grown. In parts of the USA including California, even
if both mating types are present in one area, it appears
that sexual recombination is not common; the oospore
is rarely found in host plant tissue in these areas. In
481 Stem lesions 481
Canada (British Columbia), Central Mexico, and parts
caused by late of Europe (Netherlands, Poland, Russia), the oospore is
blight of tomato. more readily found and genetic evidence indicates a
greater diversity is present in populations, which pre-
supposes sexual recombination.
The fungus is sometimes difficult to maintain in
culture, though cultures can be grown on V-8 juice, pea,
rye B, and other media. Incubating the symptomatic
tissue at low temperatures (below 20° C) and with high
humidity will also encourage the fungus to grow and
sporulate after only one to a few days. Mycelium is
F UNGAL D ISEASES
coenocytic (lacking cell cross walls) and produces ellip-

soidal to ovoid, hyaline, semi-papillate sporagia that
measure 21–38 x 12–23 μm. Sporangia are deciduous
(=caducous), have pedicels measuring up to 3 μm long,
and are distributed by winds and splashing water.
Sporangia can germinate directly and infect tomato
482
482 Tomato plants infected with late blight.
tissues, or can produce swimming zoospores that are and overwhelmingly belonged to the US-1 clonal
released and infect the host. Optimum temperature for lineage group that is sensitive to the widely used
growth of the fungus is 20° C. Tomato and potato are fungicide metalaxyl.
the main hosts, though other plants in the Solanaceae However, the recent serious outbreaks were often
can also support the pathogen. Examples of other hosts caused by novel lineages. In North America, four such
are hairy nightshade (S. sarrachoides), S. physalifolium, lines caused significant damage to crops: US-6 MR (A1
and petunia (Petunia species). mating type; resistant to metalaxyl; highly virulent to
The recent increase in late blight severity coincides tomato), US-7 (A2 mating type; resistant to metalaxyl;
with worldwide changes in the population genetics of highly virulent to tomato); US-8 (A2 mating type;
P. infestans. Recent advances in molecular methods and
DNA technology have enabled researchers to precisely 483
characterize isolates and obtain some insight into
reasons for this increased severity. Research reveals that
P. infestans is a very complex organism. While all
F UNGAL D ISEASES
P. infestans isolates belong to one of two mating types,

all individuals also simultaneously belong to one of a
series of distinct clonal lineages that are asexual descen-
dants from single genotypes. Prior to the 1980s, the
various regions of the world were primarily populated
by P. infestans isolates that were of the A1 mating type 483 Fruit infections caused by late blight of tomato.
resistant to metalaxyl; highly virulent to potato), and Control

US-11 (A1 mating type; resistant to metalaxyl; highly Fungicides are key tools for managing late blight. Apply
virulent on potato and tomato). The occurrence and protectant fungicides prior to late blight infection. The
spread of these new pathogen lines is most likely due to pathogen has developed resistance to some fungicide
the shipment of potato seed tubers, tomato fruit, and products such as metalaxyl. Late blight forecasting
tomato transplants between areas and continents. systems may be helpful in deciding when fungicides
These population genetics are in flux, because novel should best be applied. Several forecasting systems are
clonal lineages replace older ones after only a few used for identifying late blight infection periods in
seasons. Significant changes in P. infestans population potato crops. In the UK, Smith periods define when
structures have also been documented in Europe, South weather conditions are favorable for blight infection. A
America, and Asia. These new aggressive isolates can full Smith period requires relative humidity greater than
reproduce more rapidly than older genotypes, thereby 90% for a minimum of 11 hours on two consecutive
shortening the disease cycle to 5–7 days under favorable days and temperatures above 10º C.
conditions. Additional changes in virulence and Avoid or reduce the use of sprinklers for irrigation.
fungicide insensitivity could occur more frequently in Destroy old tomato fields after harvest is completed.
the future because sexual reproduction will likely be Eliminate pathogen reservoir sources such as potato
more common now that both mating types are widely tuber or tomato fruit cull piles and volunteer potato or
distributed. tomato plants. Because disease can develop on trans-
One additional parameter of P. infestans diversity is plants inside greenhouses, carefully inspect tomato
aggressiveness of isolates. Studies indicate that only transplants and remove suspect plants and trays. Some
some isolates are highly virulent to tomato, while all resistant cultivars are available.
tested isolates were highly virulent on potato.
Therefore, P. infestans can be further divided up into References
tomato-aggressive and tomato-nonaggressive isolates. Adler, N. E., Erselius, L. J., Chacon, M. G., Flier, W. G., Ordonez,
This factor is an important management consideration; M. E., Kroon, L. P. N. M., and Forbes, G. A. 2004. Genetic
diversity of Phytophthora infestans sensu lato in Ecuador
if a tomato-nonaggressive isolate is present in a tomato provides new insight into the origin of this important plant
field, then crop loss due to late blight is likely to be pathogen. Phytopathology 94:154–162.
limited and fungicides may be needed less frequently. Anderson, B., Johansson, M., Jonsson, B. 2003. First report of
Solanum physalifolium as a host plant for Phytophthora
There is some evidence that the A2 mating type occurs infestans in Sweden. Plant Disease 87:1538.
more frequently on tomato than on potato. Bakonyi, J., Láday, M., Dula, T., and Érsek, T. 2002.
Characterisation of isolates of Phytophthora infestans from
Disease cycle Hungary. European Journal of Plant pathology
108:139–146.
In contrast to most other Phytophthora species, Cohen, Y., Farkash, S., Reshit, Z., and Baider, A. 1997. Oospore
P. infestans usually is not considered a soilborne fungus, production of Phytophthora infestans in potato and tomato
though this aspect might change if both mating types leaves. Phytopathology 87:191–196.
are present and oospores are formed that can persist in Cook, D. E. L., Young, V., Birch, P. R. J., Toth, R., Gourlay, F.,
Day, J. P., Carnegie, S. F., and Duncan, J. M. 2003. Phenotypic
the soil. The fungus overwinters in volunteer host and genotypic diversity of Phytophthora infestans
plants, potato cull piles, and residential gardens. Potato populations in Scotland (1995–1997). Plant Pathology
plants and cull tubers may be an important source of 52:181–192.
Deahl, K. L., Pagani, M. C., Vilaro, F. L., Perez, F. M., Moravec,
inoculum for tomato fields. When high humidity and B., Cooke, L. R. 2003. Characteristics of Phytophthora
moderate temperatures are present, sporangia are infestans isolates from Uruguay. European Journal of Plant
produced, released into the air, and blown onto suscep- Pathology 109:277–281.
F UNGAL D ISEASES
tible crops. Optimum growth of the fungus is at Deahl, K. L., Shaw, D. S., and Cooke, L. R. 2004. Natural
occurrence of Phytophthora infestans on black nightshade
18–22° C. A striking feature of late blight is the speed of (Solanum nigrum) in Wales. Plant Disease 88:771.
disease development and spread. If conditions are Fry, W. E. and Goodwin, S. B. 1997. Re-emergence of potato and
suitable for the pathogen, entire fields can become tomato late blight in the United States. Plant Disease
81:1349–1357.
infected after only a few days.
Fry, W. E., Goodwin, S. B., et al. 1993. Historical and recent Phytophthora spp., Pythium spp., Rhizoctonia solani
migrations of Phytophthora infestans: chronology, pathways,
and implications. Plant Disease 77:653–661. DAMPING-OFF, FRUIT ROTS
Fry, W. E., Goodwin, S. B., Matuszak, J. M., Spielman, L. J., and
Milgroom, M. G. 1992. Population genetics and Introduction and significance
intercontinental migrations of Phytophthora infestans.
Annual Review of Phytopathology 30:107–129. Several soilborne pathogens cause seed, seedling, and
Goodwin, S. B. 1997. The population genetics of Phytophthora. transplant diseases of tomato. Pathogens include species
Phytopathology 87:462–473. of Phytophthora, Pythium, and Rhizoctonia. These
Goodwin, S. B., Cohen, B. A., Deahl, K. L., and Fry, W. E. 1994. pathogens can also infect tomato fruit and cause field
Migration from northern Mexico as the probable cause of
recent genetic changes in populations of Phytophthora and postharvest fruit rots.
infestans in the United States and Canada. Phytopathology
84:553–558. Symptoms and diagnostic features
Goodwin, S. B. and Drenth, A. 1997. Origin of the A2 mating
These diseases have various phases. Tomato seeds can
type of Phytophthora infestans outside Mexico.
Phytopathology 87:992–999. be infected prior to germination and result in seed
Goodwin, S. B., Smart, C. D., Sandrock, R. W., Deahl, K., Punja, death. Newly germinated seedlings can be infected to
Z. K., and Fry, W. E. 1998. Genetic change within such a degree that plants do not emerge above the soil
populations of Phytophthora infestans in the United States
and Canada during 1994 to 1996: Role of migration and (pre-emergence damping-off). Seedlings might emerge
recombination. Phytopathology 88:939–949. from the ground but become diseased after soil
Goodwin, S. B., Sujkowski, L. S., and Fry, W. E. 1996. emergence (post-emergence damping-off). Finally,
Widespread distribution and probable origin of resistance to
metalaxyl in clonal genotypes of Phytophthora infestans in
transplants placed in the ground can develop root rots
the United States and western Canada. Phytopathology or stem lesions from these same pathogens. Initial
86:793–800. symptoms of post-emergence damping-off occur on
Knapova, G. and Gisi, U. 2002. Phenotypic and genotypic seedling stems in contact with the soil. These symptoms
structure of Phytophthora infestans populations on potato
and tomato in France and Switzerland. Plant Pathology consist of shriveled stems that have discolored, tan to
51:641–653. dark brown lesions. With time the lower stem collapses,
Koh, Y. J., Goodwin, S. B., Dyer, A. T., Cohen, B. A., Ogoshi, A., roots decay, and the cotyledons and leaves wilt. Such
Sato, N., and Fry, W. E. 1994. Migrations and displacements
of Phytophthora infestans populations in East Asian
plants usually bend over. Damping-off diseases often
countries. Phytopathology 84:922–927. result in death of the seedling and subsequent reduction
Legard, D. E., Lee, T. Y., and Fry, W. E. 1995. Pathogenic of plant stands. However, even if plants do not succumb
specialization in Phytophthora infestans: aggressiveness on to these pathogens, the surviving plant may be stunted
tomato. Phytopathology 85:1356–1361.
Matuszak, J. M., Fernandez-Elquezabal, J., and Villarreal-
and delayed in development.
Gonzalez, M.. 1994. Sensitivity of Phytophthora infestans These three pathogens can also infect roots and
populations to metalaxyl in Mexico: distribution and crowns of older plants as well as fruit. Phytophthora
dynamics. Plant Disease 78:911–916.
fruit infections are called buckeye rot (see Phytophthora
Porter, L. D. and Johnson, D. A. 2004. Survival of Phytophthora
infestans in surface water. Phytopathology 94:380–387. root rot section, page 359) and can be caused by several
Tumwine, J., Frinking, H. D., and Jeger, M. J. 2002. Integrating species of Phytophthora. Pythium fruit infections are
cultural control methods for tomato late blight called watery rot and usually infect ripe tomato fruit.
(Phytophthora infestans) in Uganda. Annals of Applied
Biology 141:225–236. Symptoms consist of irregular, water-soaked lesions on
fruit that are in contact with the soil. Once infected, the
fruit is rapidly colonized by the Pythium pathogen, the
epidermis breaks, and the fruit becomes soft and
watery. White mycelial growth can be observed on the
rotted tissues. Rhizoctonia fruit rot can affect immature
F UNGAL D ISEASES
green fruit but is mostly a problem on ripe fruit. Dark

brown, circular to oblong lesions develop on ripe fruit
that are touching the soil. These lesions enlarge and
break down into a mushy, soft rot. Rhizoctonia solani
will form characteristic brown, persistent hyphae on the
fruit surface.
Causal agents provide control for some of these pathogens. Avoid

Phytophthora and Pythium species are in the oomycete planting too soon into fields that still have extensive
group. Phytophthora capsici and P. parasitica usually crop residue in the soil. Rotate crops, as consecutive
infect roots of older plants, but can cause damping-off. tomato plantings will increase the populations of the
A number of Pythium species cause damping-off: soilborne pathogens. For transplants, prepare good-
P. aphanidermatum, P. arrhenomanes, P. debaryanum, quality beds and do not plant too deep.
P. myriotylum, P. ultimum. All these organisms survive To avoid fruit rots, keep bed tops dry by carefully
in the soil as saprophytes and are favored by wet soil managing the irrigation or by using buried drip irri-
conditions. With the exception of P. ultimum, these gation. Prepare soil to enhance drainage and avoid low
pathogens usually produce zoospores that swim to and areas. Stake plants or use plastic mulches on the bed
infect susceptible tissues. Sexual structures—antheridia, tops to keep fruit off the ground. Some fungicides may
oogonia, and oospores—are produced by all species. In help manage both root and fruit infections.
addition to tomato, these pathogens can infect
numerous other plants. References
Rhizoctonia solani is a soilborne fungus with a very Cafe-Filho, A. C. and Duniway, J. M. 1995. Dispersal of
broad host range. Rhizoctonia solani has no asexual Phytophthora capsici and Phytophthora parasitica in furrow-
spores, but produces characteristically coarse, brown, Pathology 44:1025–1032.
approximately right-angle branching hyphae. The Golden, J. K. and Van Gundy, S. D. 1975. A disease complex of
hyphae are distinctly constricted at branch points, and okra and tomato involving the nematode Meloidogyne
incognita, and the soil-inhabiting fungus, Rhizoctonia solani.
cross walls with dolipore septa are deposited just after Phytopathology 65:265–273.
the branching. Hyphal cells are multi-nucleate. Small, Pearson, R. C. and Hall, D. H. 1973. Ripe fruit rot of tomato
tan to brown loosely aggregated clumps of mycelia caused by Pythium ultimum and Pythium aphanidermatum.
function as sclerotia. This fungus can survive by Plant Disease Reporter 57:1066–1069.
infecting and thriving on a great number of plant hosts,

besides tomato, and can also persist in the soil as a
saprophyte. The teleomorph stage, Thanatephorus Pyrenochaeta lycopersici
cucumis, is not commonly observed. CORKY ROOT ROT
Disease cycle Introduction and significance

Most of these soilborne pathogens survive in fields for Corky root rot, or brown rot, was first described from
indefinite amounts of time. Wet soil conditions and cool Europe but now also occurs in North America. Corky
temperatures (15–20° C) generally favor these organ- root rot is important where tomato crops are grown
isms and their ability to grow and infect hosts. repeatedly in the same soil.
However, for pathogens such as P. aphanidermatum
and P. myriotylum, warmer soil conditions (32–37° C) Symptoms and diagnostic features
are favorable. The seedling stage is most susceptible to Initial symptoms consist of plants that show poor vigor,
infection, though these pathogens can infect the feeder are stunted, and begin to wilt. Leaves may show inter-
roots of mature plants. veinal chlorosis and later fall off the plant. The most
characteristic symptoms occur on larger roots and
Control consist of brown lesions that have a rough corky or
Damping-off is primarily controlled by creating condi- wrinkled texture (484, 485). Such lesions often appear
tions unfavorable for the pathogens. Plant on raised as horizontal bands across the length of the root; lesions
F UNGAL D ISEASES
beds and in soils that drain well so that overly wet soil are dry and have cracks that run lengthwise along the
conditions are reduced. Carefully manage irrigation root. Smaller feeder roots may either show the brown,
and do not apply excess water. Plant seed that has been rough lesions or may be completely rotted. Internal
treated with fungicides, and avoid planting seed too tissues of the larger roots do not exhibit discoloration
deeply, which delays seedling emergence and increases or symptoms. Affected plants rarely collapse and die,
the chance of infection. Post-plant fungicides may but can experience a reduction in yield.
Causal agent 484

Corky root is caused by the fungus Pyrenochaeta lycop-
ersici. This pathogen is a slow-growing fungus that
forms gray colonies on standard microbiological media
but is difficult to isolate without using semi-selective
media. In culture, the pathogen forms brown to black
pycnidia that measure 150–300 μm in diameter.
Pycnida release spores through a circular pore (ostiole)
that is ringed with three to twelve light brown, septate
setae. Single-celled, cylindrical to allantoid, hyaline
conidia measure 4–8 x 1.5–2 μm and are borne on coni-
diophores within the pycnidial body. The fungus forms
microsclerotia that measure 63.5 x 448 μm.
Disease cycle 484 Root banding caused by corky root rot of tomato.
Pyrenochaeta lycopersici is a soilborne organism and
can survive for long periods of time as microsclerotia in 485 Root banding 485
soil or on old tomato roots. The fungus prefers cool caused by corky
conditions and optimum disease development takes root rot of tomato.
place at 15–20° C, though the range is from 8–32° C.
The pathogen can also infect aubergine (eggplant),
melon, pepper, safflower, spinach, and squash. Pyreno-
chaeta lycopersici often co-infects tomato roots with the
black dot pathogen (Colletotrichum coccodes).
Control
Apply fumigants to field soil, and steam or fumigants to
greenhouse planting areas. Rotate away from tomato
to avoid buildup of inoculum. Delay planting until later
in the spring when soils are warmer. Some European
tomato cultivars are resistant to this pathogen.
Additional control measures include grafting to
resistant rootstocks and mounding soil around the stem
base to allow new adventitious roots to grow.
References
Campbell, R. N., Schweers, V. H., and Hall, D.H. 1982. Corky Workneh, F., van Bruggen, A. H. C., Drinkwater, L. E., and
root of tomato in California caused by Pyrenochaeta Shennan C. 1993. Variables associated with corky root and
lycopersici and control by soil fumigation. Plant Disease Phytophthora root rot of tomatoes in organic and
66:657–661. conventional farms. Phytopathology 83:581–589.
Grove, G. G. and Campbell, R. N. 1987. Host range and survival Workneh, F. and van Bruggen, A. H. C. 1994. Suppression of
in soil of Pyrenochaeta lycopersici. Plant Disease corky root of tomatoes in soils from organic farms associated
71:806–809. with soil microbial activity and nitrogen status of soil and
Hockey, A. G. and Jeves, T. M. 1984. Isolation and identification tomato tissue. Phytopathology 84:688–694.
F UNGAL D ISEASES
of Pyrenochaeta lycopersici, causal agent of tomato brown

root rot. Transactions of the British Mycological Society
82:151–152.
Shishkoff, N. and Campbell, R. N. 1990. Survival of
Pyrenochaeta lycopersici and the influence of temperature
and cultivar resistance on the development of corky root of
tomato. Plant Disease 74:889–894.
Sclerotinia minor, S. sclerotiorum Disease cycle

WHITE MOLD, For detailed descriptions of the disease cycles, see the
SCLEROTINIA ROT bean white mold section in the chapter on legume
diseases.
White mold, or Sclerotinia rot, is an occasional tomato Control
problem. Both pathogens occur on tomato throughout For an integrated approach to Sclerotinia control, see
the world. Disease caused by the S. sclerotiorum species the bean white mold section in the chapter on legume
is the more important Sclerotinia disease. diseases. For high value greenhouse tomato crops, soil
sterilization with heat or chemical treatments may be
Symptoms and diagnostic features cost-effective.
The types of symptoms seen on tomato depend on
which species of Sclerotinia is involved. Sclerotinia
minor only infects tomato tissues that are in contact References
with the soil. Sclerotinia minor causes a water-soaked Abawi, G. S. and Grogan, R. G. 1979. Epidemiology of diseases
lesion to develop at the crown and lower stem (486). caused by Sclerotinia species. Phytopathology 69:899–904.
Kohn, L. M. 1979. Delimitation of the economically important
The lesion enlarges and can girdle the plant, resulting in
plant pathogenic Sclerotinia species. Phytopathology
the collapse of the canopy and foliage (487). With time, 69:881–886.
the crown and stem lesions turn light tan to off-white in Lobo, M., Lopes, C. A., and Silva, W. L. C. 2000. Sclerotinia rot
color. White mycelium and small (3–5 mm), black, losses in processing tomatoes grown under centre pivot
irrigation in central Brazil. Plant Pathology 49:51–56.
irregularly shaped sclerotia form around and within the
Purdy, L. H. 1979. Sclerotinia sclerotiorum: history, diseases and
decayed crown. symptomatology, host range, geographic distribution, and
Sclerotinia sclerotiorum is the other species that can impact. Phytopathology 69:875–880.
attack tomato. Because S. sclerotiorum has an airborne
spore stage, infections can occur throughout the tomato
canopy. These above-ground infections usually occur
on damaged stems or petioles, or where a nutrient
source, such as a senescent flower petal, falls onto stems
or petioles. These infections are water-soaked lesions
that gradually enlarge and encircle the stems. Older
infections turn off-white to white-gray in color (488).
White mycelium can be observed on infected lesions if
conditions are favorable. The large, black sclerotia can
grow on the outer surface or in the central cavity of
stems (489). S. sclerotiorum can also infect tomato
crowns and lower stems. Fruit can become infected and
develop a soft, watery rot (490). This pathogen
produces white mycelium and black, oblong or dome-
shaped sclerotia. Sclerotia are significantly larger
(5–10 mm long) than those of S. minor.
Causal agent
F UNGAL D ISEASES
For detailed descriptions of S. sclerotiorum and

S. minor, see the bean white mold section in the chapter
on legume diseases (page 262).
486 488
486 Tomato stems infected by Sclerotinia minor. 488 Bleached stems and black sclerotia from Sclerotinia
sclerotiorum on tomato.
489 Black sclerotia

487 489
from Sclerotinia
sclerotiorum
forming inside
tomato stems.
490
F UNGAL D ISEASES
487 Collapsed tomato plants caused by Sclerotinia 490 Tomato fruit showing white mycelium of
minor. Sclerotinia sclerotiorum.
491
VERTICILLIUM WILT

Verticillium wilt is a well-known disease that affects
hundreds of different crops and is an important tomato
production factor throughout the world. The closely
related pepper and aubergine (eggplant) are also subject
to this disease.

On tomato, early symptoms consist of the chlorosis of 491 Angular tomato leaf lesion caused by
leaf margins and tips of older, lower leaves; these Verticillium wilt.
yellowed areas are sometimes angular in shape and
interveinal (491). The chlorotic sections later turn 492
necrotic and die (492). Shoot tips and foliage wilt, espe-
cially during the warmer times of the day, and recover
at night. Internal vascular tissue discolors to a tan to
light brown color (493). This coloring is most evident
in the main stems closer to the crown; such discol-
oration may not be evident in the upper, smaller stems.
Verticillium wilt vascular discoloration tends to be
lighter and subtler than the vascular discoloration
caused by Fusarium wilt, though this distinction is not
always clear. Disease symptoms can be accentuated if
the infected plant is bearing a heavy load of fruit or is
stressed by some other factor. Even if diseased plants do 492 Dieback of tomato foliage due to Verticillium wilt.
not collapse completely, plant growth and yields can be
significantly reduced, sometimes by over 20%. The 493
overall symptoms are similar to those caused by
Fusarium wilt; hence disease confirmation will require
laboratory analysis. On tomato, Verticillium wilt tends
to develop more slowly than Fusarium wilt.
Causal agent
The causal agent is Verticillium dahliae. The pathogen
can be isolated on standard microbiological media,
though semi-selective media such as NP-10 can be
useful for isolation. On general purpose media, the
pathogen forms the characteristic hyaline, verticillate
conidiophores bearing three to four phialides at each
node, and hyaline, single-celled, ellipsoidal conidia that 493 Vascular discoloration of tomato stems affected by
F UNGAL D ISEASES
measure 2-8 x 1-3 μm. Older cultures form dark brown Verticillium wilt.
to black torulose microsclerotia that consist of groups
of swollen cells formed by repeated budding. Micro-
sclerotia size varies greatly and is in the range of time (up to 8 to 10 years). Verticillium dahliae has an
15–100 μm in diameter. Microsclerotia enable the extensive host range of crops and weeds. Two distinct
pathogen to survive in the soil for extended periods of tomato races have been documented.
Disease cycle Alfalfa mosaic virus

The pathogen survives in the soil as dormant microscle- ALFALFA MOSAIC
rotia, but can also persist as epiphytes on non-host
roots. Cool to moderate weather conditions favor the Introduction and significance
pathogen, and disease is enhanced at temperatures Alfalfa mosaic virus (AMV) is present throughout the
between 20–24° C. The fungus enters host roots world but is a serious production concern in only
through wounds, and later systemically infects tomato certain regions.
vascular tissue.
Control Tomato plants that are infected early in their develop-
Plant resistant or tolerant cultivars. Plants with the Ve ment may die. Leaves will develop irregularly shaped,
gene are resistant to tomato race 1; however, resistance bright yellow patches and a bronze discoloration.
has not yet been identified for tomato race 2. It seems Foliage of severely diseased plants will curl downward.
likely that new races of V. dahliae will continue to A red to red-brown discoloration occurs in the vascular
emerge and overcome the currently available genetic tissue of the lower main stem. Symptomatic fruit can be
resistance. Pre-plant treatment of soil with effective distorted and exhibit irregularly shaped, sunken, dark
fumigants will give short-term control but will not brown, necrotic spots, rings, and patches (494).
eradicate the pathogen from fields. For greenhouse pro-
duction, steaming of soil can also provide short-term Causal agent
control. Rotate crops so that tomato is not planted in AMV is the only member of the alfamovirus group and
fields having a history of the problem. Rotation with has particles that are bacilliform and measure 30–56 x
non-host crops, such as small grains and corn, can 18 nm. The particles contain three single-stranded
lower inoculum levels but will not eradicate the genomic RNAs and a fourth subgenomic RNA. AMV
pathogen. Minimize spread of infested soil to other, is transmitted by a number of aphid vectors and can be
uninfested areas. seedborne in tomato.
References Disease cycle

Ashworth, L. J., Huisman, O. C., Harper, D. M., and Stromberg, Disease is usually most severe when tomato fields are
L. K. 1979. Verticillium wilt disease of tomato: influence of planted close to infected alfalfa plantings. AMV is also
inoculum density and root extension upon disease severity.
Phytopathology 69:490–492. seedborne in tomato.
Baergen, K. D., Hewitt, J. D., and St. Clair, D. A. 1993.
Resistance of tomato genotypes to four isolates of Verticillium Control
dahliae race 2. HortScience 28:833–836.
Follow general suggestions in Part 1. Use seed that does
Bletsos, F. A., Thanassoulopoulos, C. C., and Roupakias, D. G.
1999. Water stress and Verticillium wilt severity on eggplant not have significant levels of the pathogen
(Solanum melongena L.). Journal of Phytopathology
147:243–248.
Erb, W. A. and Rowe, R. C. 1992. Screening tomato seedlings for
multiple disease resistance. Journal of the American Society
for Horticultural Science 117:622–627. 494
Grogan, R. G., Ioannou, N., Schneider, R. W., Sall, M. A., and
Kimble, K. A. 1979. Verticillium wilt on resistant tomato
cultivars in California: virulence of isolates from plants and
soil and relationship of inoculum density to disease incidence.
Harrington, M. A. and Dobinson, K. F. 2000. Influences of
V IRAL D ISEASES
cropping practices on Verticillium dahliae populations in

commercial processing tomato fields in Ontario.
Nagao, H., Shiraishi, T., Oshima, S., Koike, M., Iijima, T. 1997.
Assessment of vegetative compatibility of race-2 tomato wilt 494 Fruit symptoms caused by Alfalfa mosaic virus on
isolates of Verticillium dahliae in Japan. Mycoscience
38:379–385. tomato.

495
BEET CURLY TOP

Beet curly top virus (BCTV) occurs in North and South
America, Asia, the Middle East, and the Mediterranean
region. This virus is an important pathogen of many
crops such as tomato, pepper, and Chenopodium
plants.

If infected early in development, tomato plants will die.
Plants that are infected later will remain extremely 495 Stunted and chlorotic symptoms of Beet curly top
stunted and become very chlorotic with a bronze or virus on tomato.
purple tinge (495). Leaves become thick and brittle in
texture, chlorotic with purple veins, and roll upwards 496
(496). Fruit ripen prematurely and are small, wrinkled,
and red.
Causal agent
or in pairs. The BCTV genome is a single-stranded
circular DNA. BCTV is vectored in a persistent manner
by the beet leafhopper (Circulifer tenellus). Circulifer
opacipennis is a vector in the Mediterranean region. In
the plant, BCTV is restricted to the phloem tissue. On a
BCTV from North America and the Middle East and 496 Leaf curling and purple vein symptoms of Beet
found them to be similar, providing evidence that these curly top virus on tomato.
various BCTV strains share a common origin.

This virus infects many weed and crop hosts. Recent Briddon, R. W., Stenger, D. C., Bedford, I. D., Stanley, J.,
research on curly top disease as it occurs in Izadpanah, K., Markham, P. G. 1998. Comparison of a beet
Amaranthaceae, Fabaceae, Solanaceae, and other crops those from the new world. European Journal of Plant
indicates that the viral agent may differ depending upon Pathology 104:77–84.
the host being considered. Beet curly top as a disease Martin, M. W. and Thomas, P. E. 1986. Increased value of
resistance to infection if used in integrated pest management
may actually be caused by one of four different curly control of tomato curly top. Phytopathology 76:540–542.
top virus species: Beet curly top virus (BCTV), Beet mild Soto, M. J. and Gilbertson, R. L. 2003. Distribution and rate of
curly top virus (BMCTV), Beet severe curly top virus movement of the curtovirus Beet mild curly top virus (family
(BSCTV), and Spinach curly top virus (SCTV). Geminiviridae) in the beet leafhopper. Phytopathology
93:478–484.
Research is ongoing to further determine the relation-
V IRAL D ISEASES
Thomas, P. E. and Martin, M. W. 1972. Characterization of a

ships of these various viruses. factor of resistance in curly top virus-resistant tomatoes.
Control Wang, H., Gurusinghe, P. de A., and Falk, B. W. 1999. Systemic
insecticides and plant age affect beet curly top virus
Follow general suggestions for managing virus diseases transmission to selected host plants. Plant Disease
(see Part 1). 83:351–355.
Cucumber mosaic virus 497 Strap-leaf 497

CUCUMBER MOSAIC symptoms of
Cucumber mosaic
Introduction and significance virus on tomato.
Cucumber mosaic virus (CMV) is commonly found
throughout the world and can cause disease on over
800 crop and weed hosts, including tomato and many
other vegetable crops. CMV is most prevalent in
temperate regions.

CMV severely stunts tomato plant growth and early
infections result in small, yellow, bushy plants. Leaves
may show a mottled pattern. A most striking symptom
occurs when leaf blades do not develop and the leaf
takes on an elongated, filiform shape known as ‘shoe-
string’ or ‘strap-leaf’ (497). Infected plants may not
produce many fruit, or fruit that do develop are small
and slow to mature.

CMV is a cucumovirus with particles that are isometric Potato virus Y
in shape (29 nm in diameter) and contain three single- POTATO VIRUS Y
stranded RNAs. Many CMV strains have been docu-
mented, and on tomato alone many different strains Introduction and significance
have been found. CMV is transmitted in a nonpersistent Potato virus Y (PVY) is a pathogen of solanaceous
manner by several aphid vectors. plants around the world and is of major economic
importance.
Control
CMV is difficult to control because of its extremely Symptoms and diagnostic features
wide host range. Follow general suggestions for Symptoms can vary greatly but generally consist of
managing virus diseases (see Part 1). Use seed that does veinbanding, in which dark green bands form along leaf
not have significant levels of the pathogen. veins, and a downward rolling of the leaves. Mottle and
mosaic patterns and some leaf distortions can also
References occur. As disease develops, leaves can show brown,
Fuchs, M., Provvidenti, R., Slightom, J. L., and Gonsalves, D. necrotic interveinal lesions. Fruit usually do not exhibit
1996. Evaluation of transgenic tomato plants expressing the symptoms.
coat protein gene of cucumber mosaic virus strain WL under
field conditions. Plant Disease 80:270–275.
Gallitelli, D. 2000. The ecology of cucumber mosaic virus and Causal agent and disease cycle
sustainable agriculture. Virus Research 71:9–21. PVY is a potyvirus with long (730 x 11 nm) flexuous
Hellwald, K.-H., Zimmermann, C., and Buchenauer, H. 2000. rods that contain single-stranded RNA. It is vectored in
RNA 2 of cucumber mosaic virus subgroup I strain NT-CMV
is involved in the induction of severe symptoms in tomato. a nonpersistent manner by several aphids, with Myzus
European Journal of Plant Pathology 106:95–99. persicae being particularly important. This virus is also
V IRAL D ISEASES
Palukaitis, P., Roossinck, M. J., Dietzgen, R. G., and Francki, R. readily transmitted mechanically.
I. B. 1992. Cucumber mosaic virus. Advances in Virus
Control
(see Part 1).
Tobacco mosaic virus,Tomato mosaic virus References

TOBACCO MOSAIC, Broadbent, L. 1976. Epidemiology and control of tomato mosaic
TOMATO MOSAIC virus. Annual Review of Phytopathology 14:75–96.
Mayhew, D. E., Hedin, P., and Thomas, D. L. 1984. Corky
ringspot: a new strain of tomato mosaic virus in California.
Introduction and significance Plant Disease 68:623–625.
Tobacco mosaic (TMV) and Tomato mosaic (ToMV) Pelham, J. 1972. Strain-genotype interaction of tobacco mosaic
viruses are two closely related virus pathogens. Both virus in tomato. Annals of Applied Biology 71:219–228.
viruses can infect tomato and other solanaceous plants.

TMV and ToMV both can infect tomato and cause
light and dark green mottling or mosaics on foliage.
Leaflets may be deformed and narrow, giving the leaf a Tomato spotted wilt virus
fern-like appearance (498). Fruit set may be reduced, TOMATO SPOTTED WILT
and fruit may ripen unevenly.
Causal agents and disease cycle In some regions this virus is very common on tomato,
TMV and ToMV are viruses in the tobamovirus group. pepper, and many other crops.
These viruses have straight rod particles that measure
300 x 18 nm and contain single-stranded, linear RNA Symptoms and diagnostic features
genomes. TMV has no known vector and is readily Tomato spotted wilt virus (TSWV) causes leaves to
transmitted mechanically. ToMV also lacks a known develop irregularly shaped to circular, black, small
vector, is transmitted mechanically, and can be (3-8 mm in diameter) spots (499). Stems and shoots
seedborne in tomato. may have black streaks or lesions on the epidermis
(500). Severely affected plants may wilt or be stunted.
Control Symptomatic fruit will develop chlorotic rings, patches,
Follow general suggestions for managing virus diseases and lesions (501, 502).
(see Part 1). Because ToMV is seedborne in tomato, use
seed that does not have significant levels of the Causal agent
pathogen. Seed infested with ToMV can also be treated TSWV is a tospovirus and has isometric particles,
with dry heat (70° C for 2 to 4 days) or with trisodium measuring approximately 80–110 nm, which are
phosphate (10% for 15 minutes). surrounded with membranes. TSWV has a genome
consisting of three linear single-stranded RNAs and is
vectored by several species of thrips; at least eight
498
species are found to be vectors. The western flower
(Frankliniella occidentalis) and tobacco (F. fusca) thrips
are probably the most important vectors.
Disease cycle
TSWV has one of the most extensive host ranges of any
known plant virus and can infect over 900 different cul-
tivated and weedy plant species. Therefore initial
inoculum can come from any number of landscape
V IRAL D ISEASES
plants, weeds, and other plants. Thrips insects vector

the virus to the tomato crops. It is well documented that
thrips insects can only acquire the virus as larvae that
498 Distorted tomato leaves caused by Tobacco mosaic feed on diseased plants; after acquiring the virus, the
virus. Healthy leaf is in the center. insects carry the virus for the rest of their lives.
499 501
499 Leaf lesions due to Tomato spotted wilt virus on 501 Green fruit symptoms caused by Tomato spotted
tomato. wilt virus on tomato.
500 502
500 Stem lesions due to Tomato spotted wilt virus on 502 Ripe fruit symptoms caused by Tomato spotted wilt
tomato. virus on tomato.
Control
Follow general suggestions for managing virus diseases Groves, R. L., Walgenbach, J. F., Moyer, J. W., and Kennedy, G.
(see Part 1). The broad host range of TSWV and the dif- G. 2002. The role of weed hosts and tobacco thrips,
Frankliniella fusca, in the epidemiology of tomato spotted
ficulty in controlling thrips makes this disease particu- wilt virus. Plant Disease 86:573–582.
larly difficult to manage. Krishna Kumar, N. K., Ullman, D. E., and Cho, J. J. 1993.
Evaluation of Lycopersicon germ plasm for tomato spotted
wilt tospovirus resistance by mechanical and thrips
References
transmission. Plant Disease 77:938–941.
Best, R. J. 1968. Tomato spotted wilt virus. Advances in Virus Momol, M. T., Olson, S. M., Funderburk, J. E., Stavisky, J., and
Research 13:66–146. Marois, J. J. 2004. Integrated management of tomato spotted
V IRAL D ISEASES
Cho, J. J., Mau, R. F. L., Gonsalves, D., and Mitchell, W. C. wilt on field grown tomatoes. Plant Disease 88:882–890.
1986. Reservoir weed hosts of tomato spotted wilt virus.
Greenough, D. R., Black, L. L., and Bond, W. P. 1990.
Aluminum-surfaced mulch: an approach to the control of
tomato spotted wilt virus in solanaceous crops. Plant Disease
74:805–808.
Tomato yellow leaf curl virus

504
TOMATO YELLOW LEAF CURL

Tomato yellow leaf curl virus (TYLCV) is one of the
most damaging tomato virus diseases in tropical and
sub-tropical areas, where entire tomato plantings can
become infected if vector populations are high. The
disease has become widely distributed and has been
reported in the Mediterranean region (particularly in
southern Europe), the Middle East (Israel), Africa, and
recently in North America (Caribbean area, southeast-
ern USA, and Mexico).
Symptoms and diagnostic features 504 Yellow, distorted tomato foliage caused by Tomato
If infected at a young stage, tomato plants can be yellow leaf curl virus.
severely stunted and will not produce fruit (503).
Foliage shows an upright or erect growth habit, leaves
curl upwards and may be crumpled. Interveinal Control
chlorosis is also observed in the leaves (504). Follow general suggestions for managing virus diseases
(see Part 1).
TYLCV is a geminivirus that consists of twinned icosa- References
hedral particles and single-stranded DNA genomes. Accotto, G. P., Navas-Castillo, J., Noris, E., Moriones, E., and
Bean, pepper, and several weeds are also hosts. TYLCV Louro, D. 2000. Typing of tomato yellow leaf curl viruses in
Europe. European Journal of Plant Pathology 106:179–186.
is vectored in a persistent manner by the sweet potato
Delatte, H., Dalmon, A., Rist, D., Soustrade, I., Wuster, G., Lett,
whitefly (Bemisia tabaci). This virus is apparently not J. M., Goldbach, R. W., Peterschmitt, M., and Reynaud, B.
seedborne in tomato. Researchers in Europe believe 2003. Tomato yellow leaf curl virus can be acquired and
transmitted by Bemisia tabaci (Gennadius) from tomato fruit.
two distinct species of this virus exist: Tomato yellow Plant Disease 87:1297–1300.
leaf curl-Sardinia (TYLCV-Sar), Tomato yellow leaf Lapidot, M., Friedmann, M., Lachman, O., Yehezkel, A.,
curl-Israel (TYLCV-Is). Nahon, S., Cohen, S., and Pilowsky, M. 1997. Comparison of
resistance level to tomato yellow leaf curl virus among
commercial cultivars and breeding lines. Plant Disease
81:1425–1428.
McGlashan, D., Polston, J. E., and Bois, D. 1994. Tomato yellow
leaf curl virus in Jamaica. Plant Disease 78:1219.
503 Nakhla, M. K., Maxwell, D. P., Martinez, R. P., Carvalho, M. G.,
and Gilbertson, R. L. 1994. Widespread occurrence of the
Eastern Mediterranean strain of tomato yellow leaf curl
geminivirus in tomatoes in the Dominican Republic. Plant
Disease 78:926.
Polston, J. E. and Anderson, P. K. 1997. The emergence of
whitefly-transmitted geminiviruses in tomato in the western
hemisphere. Plant Disease 81:1358–1369.
Salati, R., Nahkla, M. K., Rojas, M. R., Guzman, P., Jaquez, J.,
Maxwell, D. P., and Gilbertson, R. L. 2002. Tomato yellow
V IRAL D ISEASES
leaf curl virus in the Dominican Republic: characterization of

an infectious clone, virus monitoring in whiteflies, and
identification of reservoir hosts. Phytopathology 92:487–496.
Zubiaur, Y. M., Zabalgogeazcoa, I., de Blas, C., Sanchez, F.,
Peralata, E. L., Romero, J., and Ponz, F. 1996. Geminivirus
associated with diseased tomatoes in Cuba. Journal of
503 Stunted tomato plant affected by Tomato yellow Phytopathology 144:277–279.
leaf curl virus.
BLOSSOM END ROT Causal agent

Blossom end rot is caused by a calcium deficiency in the
Symptoms and diagnostic features tissues at that end of the fruit. Calcium is not particu-
Blossom end rot is a physiological disorder of tomato larly mobile in plant tissues, so the distal end of the fruit
fruit. Initial symptoms can occur on green fruit and can experience shortages of this nutrient. Plants that are
consist of small, light brown flecks and lesions that are growing rapidly, subject to water stress, and fertilized
usually clustered on the blossom end of the developing with high nitrogen rates may be more susceptible.
fruit. As the disorder worsens, the blossom end has a Uneven watering practices contribute to the develop-
circular to oblong lesion that is dark brown to black in ment of the disorder. Pepper and squash fruit can also
color, firm in texture, and sunken (505, 506, 507). The develop similar symptoms due to calcium deficiencies.
lesion can take up most of the blossom end. Secondary
decay organisms may colonize the lesion and result in a Control
fruit rot. To minimize damage from this disorder, do not over
fertilize with high-nitrogen fertilizers. Irrigate crops
regularly and with appropriate amounts of water.
Calcium fertilizer supplements may help in some cases,
but these treatments are generally ineffective. Choose
cultivars that tend to develop this problem less fre-
quently than others.
References
Bangerth, F. 1979. Calcium related physiological disorders of
505
plants. Annual Review of Phytopathology 17:97–122.
Banuelos, G. S., Offermann, G. P., and Seim, E. C. 1985. High
relative humidity promotes blossom end rot on growing
tomato fruit. HortScience 20:894–895.
Evans, H., and Troxler, R. 1953. Relation of Ca nutrition to the
incidence of blossom end rot in tomatoes. Proceedings of the
Taylor, M. D. Locascio, S. J., and Alligood, M. R. 2004.
Blossom-end rot incidence of tomato as affected by irrigation
quantity, calcium source, and reduced potassium.
HortScience 39:1110–1115.
Van Goor, B. 1968. The role of Ca and cell permeability in the
disease blossom end rot of tomatoes. Physiologia Plantarum
21:1110–1121.
505 Fruit symptom of blossom end rot.
506 507 A BIOTIC D ISORDERS
506 Fruit symptom of blossom end rot. 507 Internal fruit symptom of blossom end rot.
Spinacia oleracea Spinach
SPINACH (Spinacia oleracea) is in the Amaranthaceae (amaranth family) and has become an
important leafy vegetable crop in many parts of the world. The plant probably originated in Iran
(formerly Persia). Leaves of this plant are high in antioxidants and nutrients, and hence spinach
is gaining popularity as a fresh salad and cooked vegetable commodity. In the USA spinach is
now commonly grown on broad beds (2 meters wide) with extremely high seed density; such
plantings can be harvested early for ‘baby leaf’ spinach or held longer and cut for standard fresh
market spinach. Spinach in the USA is often harvested mechanically.
Pseudomonas syringae pv. spinaciae 508 Initial water-

508
BACTERIAL LEAF SPOT soaked lesions due
to bacterial leaf
Introduction and significance spot of spinach.
Bacterial leaf spot was first reported on spinach in
Europe (Italy) in 1988. Since that time the disease has
also been detected in Japan and in the USA (California).
The disease thus far is a minor problem.

Initial symptoms consist of water-soaked, irregularly
shaped spots that measure 2–5 mm in diameter (508).
As the disease develops, these small spots enlarge to as
much as 10–15 mm in diameter, are angular in shape
due to delimiting from leaf veins, and turn dark brown
with streaks of black (509). On occasion, faint yellow
halos surround the spots. On leaves having numerous 509 Advanced
509
spots, the spots sometimes merge together, resulting in water soaked
the death of large areas of the leaf (510). Spots are symptom of
visible from both top and bottom sides of leaves. The bacterial leaf spot
disease occurs on both newly expanded and mature of spinach.
foliage.
Causal agent
Bacterial leaf spot is caused by the bacterium Pseudo-
monas syringae pv. spinaciae. This pathogen is an

aerobic, Gram-negative bacterium. The pathogen can
be isolated on standard microbiological media and
produces cream-colored colonies typical of most
pseudomonads. Strains are non-fluorescent when
cultured on Kings medium B. The pathogen appears to
be host specific to spinach.
S PINACIA O LERACEA 369
510 Advanced leaf

Albugo occidentalis
510
spots due to WHITE RUST
bacterial leaf spot
of spinach. Introduction and significance
White rust is a very damaging disease of spinach that
occurs only in the USA. Thus far the disease is found in
states that are east of the Rocky Mountains.

Initial symptoms consist of small chlorotic spots and
lesions. As the disease develops, raised white pustules or
blisters appear in and around these chlorotic areas and
can be seen on both leaf surfaces (511). These pustules
often develop in concentric circles or in rings that
surround the yellow lesion. In advanced stages of the
disease, the white pustules coalesce, lesions appear
grainy due to the presence of oospores, and the leaf
tissues can become necrotic.
Disease cycle Causal agent

Disease epidemiology is still being determined. White rust is caused by the obligate pathogen Albugo
Pseudomonas syringae pv. spinaciae may possibly be occidentalis, an oomycete organism. Albugo occident-
seedborne; if this is the case, then seedborne inoculum alis can infect spinach and some Chenopodium species.
may be the primary means of pathogen introduction to Distinct physiological races have not been identified.
spinach fields. Weed or other reservoir hosts have not The pathogen produces hyaline, globose to oval
been identified. sporangia that measure 10–14 μm in diameter when
they are dry and 10–19 x 20–22 μm when hydrated.
Control Sporangia are borne in chains. Yellowish oospores have
Until the source of the pathogen is identified, control a finely reticulate surface and are 44–62 μm in diameter.
strategies will be incomplete. Avoid using overhead
sprinkler irrigation because splashing water will spread Disease cycle
the pathogen and encourage infection and disease Sporangia are produced within the white rust pustules
development. (sori) and are released when the leaf epidermis that
References 511
Bazzi, C., Gozzi, R., Stead, D., and Sellwood, J. 1988. A bacterial
leaf spot of spinach caused by a non-fluorescent
Pseudomonas syringae. Phytopathologia Mediterranea
27:103–107.
Koike, S. T., Azad, H. R., and Cooksey, D. C. 2002. First report
of bacterial leaf spot of spinach, caused by a Pseudomonas
syringae pathovar, in California. Plant Disease 86:921.
Ozaki, K., Kimura, T., and Matsumoto, K. 1998. Pseudomonas
syringae pv. spinaciae, the causal agent of bacterial leaf spot of
F UNGAL D ISEASES
spinach in Japan. Annals Phytopathological Society of Japan

64:264–269.
511 Spinach leaf showing white rust signs and

symptoms.
encloses the sori ruptures. They are then blown onto Aphanomyces cochlioides, Fusarium oxysporum,
leaf surfaces via winds and splashing water and usually Pythium aphanidermatum, P. irregulare,
Rhizoctonia solani
germinate indirectly by releasing six to nine motile
zoospores. The zoospores encyst and produce germ DAMPING-OFF, ROOT ROTS
tubes that penetrate the surface and infect the leaf.
Optimum temperatures for sporangia production and Introduction and significance
germination are 22° C and 12–16° C, respectively. At Spinach is very susceptible to damping-off and root rot
least 12 hours of leaf wetness is required for infection, diseases and overwatering situations. Significant plant
and disease severity increases with wetness duration up stand loss can be the result of damping-off that occurs
to 84 hours. Oospores are produced extensively in early in the crop cycle.
infected tissues. Due to their resilient nature, oospores
are an important survival structure for A. occidentalis Symptoms and diagnostic features
and probably are a major source of primary inoculum. With pre-emergence damping-off, spinach seed and
However, their precise role in white rust epidemiology newly germinated seedlings are attacked and rotted
is uncertain. prior to the above-ground emergence of the seedling.
Control Symptoms of post-emergence damping-off consist of
Plant resistant cultivars. Practice crop rotation to help stunted plants, yellowed lower leaves, general poor
reduce soil inoculum levels. Apply preplant and foliar growth (512), wilting, and eventual collapse and death
fungicides such as metalaxyl. Weather data are being of plants. Roots of infected plants appear water-soaked
used to attempt to schedule fungicide applications. or brown to black in color (513). Areas of the taproot
may be girdled or damaged by a necrotic lesion. In
References severe cases, nearly all roots may be girdled or rotted
Brandenberger, L. P., Correll, J. C., Morelock, T. E., and McNew, off. Care must be taken when diagnosing these soil-
R. W. 1994. Characterization of resistance of spinach to white borne diseases because symptoms resulting from abiotic
rust (Albugo occidentalis) and downy mildew (Peronospora
farinosa f. sp. spinaciae). Phytopathology 84:431–437. problems, caused by factors such as overwatering and
Dainello, F. J., Black, M. C., and Kunkel, T. E. 1990. Control of poor planting technique, can look identical to
white rust of spinach with partial resistance and multiple soil symptoms caused by damping-off pathogens. As a
applications of metalaxyl granules. Plant Disease
74:913–916.
plant, spinach is very sensitive to excess soil moisture.
Sullivan, M. J. and Damicone, J. P. 2003. Development of a
weather-based advisory program for scheduling fungicide
applications for control of white rust of spinach. Plant
Disease 87: 923–928.
512 513
F UNGAL D ISEASES
512 Pythium damping-off of spinach. 513 Root lesions of Pythium damping-off of spinach.
Causal agents Cladosporium variabile

Damping-off diseases are caused by several pathogens, CLADOSPORIUM LEAF SPOT
including the following: Fusarium oxysporum,
Pythium aphanidermatum, P. irregulare, Aphanomyces Introduction and significance
cochlioides, and Rhizoctonia solani. In some areas, the Cladosporium leaf spot is regularly found in regions
Fusarium wilt pathogen (F. oxysporum f. sp. spinaciae) such as California, but the disease is rarely severe on
can cause damping-off. In Europe, Phytophthora production spinach unless there are significant rains
cryptogea causes spinach root rot disease. In California, during the growing season. However, the disease can
there are fields where Fusarium, Pythium, and significantly damage spinach seed crops.
Rhizoctonia all are present and contribute to root rot
problems. Symptoms and diagnostic features
This disease is characterized by mostly round, tan leaf
Disease cycle spots that rarely exceed 1 cm in diameter (514, 515).
These organisms are soil inhabitants and are therefore Dark green spores and mycelium later develop in the
permanent residents in infested soils. Damping-off can
result from the activity of an individual pathogen or
from a complex of several of these agents working
simultaneously. Severity of damping-off is influenced by 514
cultivar, soil texture and profile, irrigation management,
production technique, and pathogen populations.
Severe damping-off is often associated with warmer
temperatures, heavy textured or poorly draining soils,
low areas in the field, and fields that have a history of
frequent spinach production.
Control
Plant spinach in soils that drain well. Do not plant
spinach seeds too deeply into the soil. Prepare seed beds
so that even, rapid germination is enhanced. Carefully
manage the irrigation schedule to prevent flooding and
saturated soil conditions. Plant seed that is treated with
fungicides. Applying metalaxyl to spinach seed lines 514 Leaf spots due to Cladosporium leaf spot of
immediately after planting can help control Pythium spinach.
species.
515
References
Larsson, M. 1994. Prevalence and pathogenicity of spinach root
pathogens of the genus Pythium in Sweden. Plant Pathology
43: 261–268.
Larsson, M. and Gerhardson, B. 1992. Disease progression and
yield losses from root diseases caused by soilborne pathogens
of spinach. Phytopathology 82:403–406.
Larsson, M. and Olofsson, J. 1994. Prevalence and pathogenicity
of spinach root pathogens of the genera Aphanomyces,
F UNGAL D ISEASES
Phytophthora, Fusarium, Cylindrocarpon, and Rhizoctonia

in Sweden. Plant Pathology 43: 251–260.
Sumner, D. R., Kays, S. J., and Johnson, A. W. 1976. Etiology
and control of root diseases of spinach. Phytopathology
66:1267–1273.
515 Close-up of Cladosporium leaf spots.

centers of these spots and are characteristic signs of this References

pathogen. The presence of dark green sporulation dis- Correll, J. C., Morelock, T. E., Black, M. C., Koike, S. T.,
tinguishes Cladosporium leaf spot from anthracnose Brandenberger, L. P., and Dainello, F. J. 1994. Economically
important diseases of spinach. Plant Disease 78:653–660.
and Stemphylium leaf spot diseases, both of which also
David, J. C. 1995. Cladosporium variabile. Descriptions of
form circular lesions. The disease is commonly seen on Pathogenic Fungi and Bacteria No. 1229. International
spinach seed crops grown in the northwest USA, Mycological Institute, Surrey, England.
especially if weather is cool and moist. For seed crops, du Toit, L. J., Derie, M. L., and Hernandez-Perez, P. 2005.
Evaluation of fungicides for control of leaf spot in spinach
disease severity is greater if pollen from spinach flowers seed crops, 2004. Fungicide & Nematicide Tests 60:V044.
falls on leaves prior to infection. du Toit, L. J., Derie, M. L., and Hernandez-Perez, P. 2005.
Evaluation of yield loss caused by leaf spot fungi in spinach
seed crops, 2004. Fungicide & Nematicide Tests 60:V047.
Causal agent
du Toit, L. J. and Hernandez-Perez, P. 2005. Efficacy of hot water
Cladosporium leaf spot is caused by the fungus Clado- and chlorine for eradication of Cladosporium variabile,
sporium variabile (formerly named Heterosporium Stemphylium botryosum, and Verticillium dahliae from
variabile). Conidiophores of C. variabile emerge from spinach seed. Plant Disease 89:1305–1312.
Hernandez-Perez, P. and du Toit, L. J. 2006. Seedborne
leaf tissue and appear in clusters. Conidiophores are Cladosporium variabile and Stemphylium botryosum in
straight, unbranched, geniculate, and are light brown in spinach. Plant Disease 90:137–145.
color. Conidia are borne in short chains (three to five Inglis, D. A., Derie, M. L., and Gabrielson, R. L. 1997.
spores) and are ellipsoidal to subglobose with rounded Cladosporium leaf spot on spinach seed crops and control
measures. Washington State University Extension Bulletin
ends, brown to green-brown, and roughly textured No. 865.
(verrucose). Conidia have zero to three septa and
measure 5–30 x 3–13 μm. In culture C. variabile forms
aerial hyphae that are characteristically twisted and
coiled (torulose).
Disease cycle
The complete epidemiology of this disease has not been
documented. The pathogen is seedborne and has been
detected on spinach seed produced in both Europe and
the USA. Conidia are dispersed by winds and splashing
water from rain and sprinkler irrigation. In California
the disease is always most severe in early spring
(February through April) if there is rainy weather.
Control
No control recommendations are available for produc-
tion spinach in the field. Disease severity may increase
if overhead sprinkler irrigation is used. Use seed that
does not have significant levels of the pathogen. Hot
water or 1.2% bleach seed treatments can significantly
reduce seedborne inoculum.
F UNGAL D ISEASES
Colletotrichum dematium f. sp. spinaciae the spinach isolates. Such research indicates that host
ANTHRACNOSE specificity for this pathogen, indicated by the forma
specialis (f. sp.) designation, is demonstrated.
Anthracnose outbreaks occur sporadically in spinach Disease cycle
growing areas. In Europe, Asia, and North America it The fungus survives as dormant mycelium in infected
is usually only a minor problem. plant debris. Seedborne inoculum is also possible,
though this source of the pathogen is not well docu-
Symptoms and diagnostic features mented. Conidia are moved from plant to plant by
Initial symptoms are small, circular, water-soaked splashing water from rain or sprinklers. Wet conditions,
lesions on both young and old leaves (516). Lesions along with dense leaf canopies, limited air movement,
later enlarge, first turning chlorotic and then later and low plant fertility favor infection and disease devel-
brown to tan in color (517). The brown lesions can opment. This fungus also acts as a secondary decay
become dry, thin, and papery in texture. In severe cases, organism on spinach and readily colonizes tissue
lesions coalesce and result in severe blighting of foliage. damaged by pathogens such as the white rust pathogen
Tiny, black fruiting bodies (acervuli) form profusely in (Albugo occidentalis).
diseased tissue and are a characteristic sign of the
pathogen. The presence of acervuli distinguishes Control
anthracnose from Cladosporium and Stemphylium leaf Reduce leaf wetness by eliminating overhead sprinkler
spot diseases, both of which also form circular lesions. irrigations, or by irrigating by sprinklers early in the
day. Provide adequate fertilizer for the spinach crop.
Causal agent Effective fungicides are not registered, and resistant
Anthracnose is caused by the fungus Colletotrichum cultivars are still under development.
dematium f. sp. spinaciae. The fungus produces a cup-
shaped acervulus fruiting body that usually contains References
long, dark brown setae along with the hyaline, fusi- Correll, J. C., Morelock, T. E., and Guerber, J. C. 1993.
form, slightly curved conidia having acute apices and Vegetative compatibility and virulence of the spinach
anthracnose pathogen, Colletotrichum dematium. Plant
measuring 20–24 x 2–3 μm. Conidia are extruded in a Disease 77:688–691.
light pink gelatinous matrix that is primarily spread by Koike, S. T. and Correll, J. C. 1993. First report of spinach
splashing water. When C. dematium isolates from anthracnose caused by Colletotrichum dematium in
spinach, tomato, and onion were inoculated onto
spinach, the non-spinach isolates were less virulent than
516 517
F UNGAL D ISEASES
516 Water soaked lesions caused by anthracnose of 517 Advanced lesions and acervuli caused by
spinach. anthracnose of spinach.
Fusarium oxysporum f. sp. spinaciae

518
FUSARIUM WILT

Fusarium wilt is an important disease of spinach
worldwide. However, disease incidence varies from
region to region. In the extensive spinach industry in
California, this disease occurs only sporadically.

Typical symptoms include plant stunting, chlorosis and
necrosis of older leaves, wilting of the older leaves, and
plant collapse (518). The vascular tissue of the diseased
plant is often discolored and can be brown, dark 518 Chlorosis and decline due to Fusarium wilt of
brown, or black. In particular, the vascular tissue of the spinach.
taproot tip may show the greatest degree of discol-
oration and the surrounding root cortex may be 519
necrotic and black (519).
Causal agent
Fusarium wilt is caused by the soilborne fungus
Fusarium oxysporum f. sp. spinaciae. The pathogen
morphology and colony characteristics are similar to
other F. oxysporum fungi. The fungus forms one- or
two-celled, oval to kidney-shaped microconidia on
monophialides, and three- to five-celled, fusiform,
curved macroconidia. Macroconidia are usually pro-
duced in cushion-shaped structures called sporodochia.
Chlamydospores are also formed. The pathogen is
usually readily isolated from symptomatic vascular 519 Darkened roots due to Fusarium wilt of spinach.
tissue. The pathogen is host specific to spinach and may
be seedborne. In some spinach producing regions this
pathogen can also contribute to damping-off disease. References
Bassi, A., Jr. and Bode, M. J. 1978. Fusarium oxysporum f. sp.
Disease cycle spinaciae seedborne in spinach. Plant Disease Reporter
62:203–205.
The pathogen produces chlamydospores that enable it
Fiely, M. B., Correll, J. C., and Morelock, T. E. 1995. Vegetative
to survive long periods of time in the soil. If spinach is compatibility, pathogenicity, and virulence diversity of
planted in the field, pathogen propagules germinate and Fusarium oxysporum recovered from spinach. Plant Disease
79:990–993.
invade the spinach plants via the roots. From the roots,
O’Brien, M. J. and Winters, H. F. 1977. Evaluation of spinach
the pathogen can become systemic and grow into accessions and cultivars for resistance to Fusarium wilt: I.
spinach vascular tissue. Greenhouse method. Journal of the American Society for
F UNGAL D ISEASES
Reyes, A. A. 1979. Populations of the spinach wilt pathogen,

Control Fusarium oxysporum f. sp. spinaciae, in the root tissues,
Plant resistant cultivars as they become available. rhizosphere, and soil in the field. Canadian Journal of
Practice crop rotation so that soilborne inoculum does Microbiology 25:227–229.
not build up to high levels. Avoid planting in fields with Takehara, T., Kuniyasu, K., Mori, M., and Hagiwara, H. 2003.
Use of a nitrate-nonutilizing mutant and selective media to
history of severe Fusarium wilt. examine population dynamics of Fusarium oxysporum f. sp.
spinaciae in soil. Phytopathology 93:1173–1181.
Peronospora farinosa f. sp. spinaciae

520
DOWNY MILDEW, BLUE MOLD

Downy mildew, or blue mold, is one of the most wide-
spread and destructive diseases of spinach. In most
areas, downy mildew is generally considered the most
important disease of spinach.

Early symptoms consist of initially light green to dull
yellow, irregularly shaped lesions on cotyledons and
true leaves (520). These lesions later turn bright yellow.
With time, the lesions can enlarge and become tan and 520 Leaf chlorosis caused by downy mildew of spinach.
dry, or if wet conditions persist the tissue can become
soft and necrotic. Examination of the underside of the
leaf, opposite the yellow area, usually reveals the purple 521
growth of the pathogen (521). Such sporulation can at
times occur on the top leaf surfaces. If disease develop-
ment is extensive, leaves can appear curled and
distorted and may take on a blighted effect due to the
numerous infection sites.
Causal agent
Downy mildew is caused by Peronospora farinosa f. sp.
spinaciae, which belongs in the oomycete group of
organisms. Older literature names the pathogen as
P. effusa. The conidiophores of this pathogen emerge
from leaf stomates, branch extensively, and have
tapered tips on which blue-gray conidia are borne. 521 Sporulation of downy mildew on underside of
Conidia are ovoid to ellipsoid and measure 21–27 x spinach leaf.
16–19 μm. Peronospora farinosa f. sp. spinaciae is het-
erothallic and requires two mating types for the pro-
duction of the sexual oospore. Oospores are spherical, Disease cycle
thick walled, and measure 20–38 μm. Peronospora Like most downy mildews, this pathogen requires cool,
farinosa f. sp. spinaciae is a complex pathogen and wet conditions for infection and disease development.
consists of multiple races. Races are identified by testing The heavy canopy of densely planted spinach retains
their virulence on differential sets of spinach cultivars much moisture and creates ideal conditions for
having various resistance genes. In the early 2000s, infection and disease development. Spores are dispersed
races 5 and 6 were prevalent in the USA, while races 5 in the air from plant to plant and field to field by winds
and 7 occurred in Europe. However, additional new and to a lesser extent splashing water. Lesion develop-
races are being detected in both the USA (race 10) and ment is enhanced at temperatures between 15–25° C.
F UNGAL D ISEASES
Europe (race 8). This pathogen infects only spinach and If favorable temperatures and leaf wetness are present,
a few Chenopodium weed species, such as C. album downy mildew can progress rapidly and result in sig-
(lamb’s quarters or fat hen). nificant disease. Resilient oospores have been detected
on spinach seed and presumably can occur in leaf tissue.
However, the role of oospores in disease epidemiology
is uncertain.
Control Stemphylium botryosum

Use resistant cultivars, as this is the most satisfactory STEMPHYLIUM LEAF SPOT
means of controlling spinach downy mildew.
Historically, single gene resistance has been relied on to Introduction and significance
breed resistant cultivars. When new races of the This new disease of spinach was first documented in
pathogen develop, however, cultivars with this type of 2001 in the Salinas Valley of California, though the
resistance are readily infected and new sources of resist- problem may have been present for many years before.
ance must be found. To prevent downy mildew on Since that time Stemphylium leaf spot has been found
young seedlings, treat seed with metalaxyl, or apply elsewhere in the USA (Arizona, Delaware, Florida,
metalaxyl post-plant to the seed lines. Apply foliar Maryland, and Washington) and in Europe. This
fungicides to protect emerged crops. disease occurs both on production spinach and spinach
seed crops.
References
Brandenberger, L. P., Correll, J. C., and Morelock, T. E. 1991.
522
Identification of and cultivar reactions to a new race (race 4)
of Peronospora farinosa f. sp. spinaciae on spinach in the
United States. Plant Disease 75:630–634.
Brandenberger, L. P., Correll, J. C., Morelock, T. E., and McNew,
R. W. 1994. Characterization of resistance of spinach to white
rust (Albugo occidentalis) and downy mildew (Peronospora
farinosa f. sp. spinaciae). Phytopathology 84:431–437.
Brandenberger, L. P., Morelock, T. E., and Correll, J. C. 1992.
Evaluation of spinach germplasm for resistance to a new race
(Race 4) of Peronospora farinosa f. sp. spinaciae. HortScience
27:1118–1119.
Brandenberger, L. P., Correll, J. C., and Morelock, T. E. 1991.
Nomenclature of the downy mildew fungus on spinach.
Mycotaxon 41:157–160.
Byford, W. J. 1967. Host specialization of Peronospora farinosa
on Beta, Spinacia and Chenopodium. Transactions of the
British Mycological Society 50: 603–607.
Correll, J. C., Morelock, T. E., Black, M. C., Koike, S. T.,
Brandenberger, L. P., and Dainello, F. J. 1994. Economically
important diseases of spinach. Plant Disease 78:653–660.
Frinking, H. D., Harrewijn, J. L., and Geerds, C. F. 1985. Factors
governing oospore production by Peronospora farinosa f. sp. 522 Initial gray spots of Stemphylium leaf spot of
spinaciae in cotyledons of spinach. Netherlands Journal of spinach.
Inaba, T. and Morinaka, T. 1984. Heterothallism in Peronospora
effusa. Phytopathology 74:214–216. 523
Inaba, T. and Morinaka, T. 1985. The relationship between
conidium and oospore production in spinach leaves infected
with Peronospora effusa. Annals Phytopathological Society
of Japan 51:443–449.
Inaba, T., Takahashi, K., and Morinaka, T. 1983. Seed
transmission of spinach downy mildew. Plant Disease
67:1139–1141.
Irish, B. M., Correll, J. C., Koike, S. T., Schafer, J., and Morelock,
T. E. 2003. Identification and cultivar reaction to three new
races of the spinach downy mildew pathogen from the United
F UNGAL D ISEASES
States and Europe. Plant Disease 87:567–572.

Koike, S. T., Smith, R. F., and Schulbach, K. F. 1992. Resistant
cultivars, fungicides combat downy mildew of spinach.
California Agriculture 46:29–31.
523 Advanced tan spots of Stemphylium leaf spot of

spinach.
Symptoms and diagnostic features There are also indications that Cladosporium and
Initial symptoms consist of small, 2–6 mm diameter, Stemphylium spinach pathogens can form a complex
circular to oval, gray-green leaf spots on leaves (522). and result in severe disease in seed fields.
As the disease progresses, leaf spots enlarge, remain
circular to oval in shape, and turn tan in color. Older Control
spots coalesce, dry up, and become papery in texture For production spinach, this disease appears to be of
(523). Visual signs of fungal growth are generally minor importance and no controls are currently rec-
absent from the spots; hence this problem is readily dif- ommended. Overhead sprinkler irrigation may cause
ferentiated from foliar diseases in which purple growth the disease to be worse. Use seed that does not have
(downy mildew), green spores (Cladosporium leaf significant levels of the pathogen. Hot water or 1.2%
spot), or acervuli (anthracnose) develop within lesions. bleach seed treatments can significantly reduce seed-
Overall, symptoms can closely resemble the tan, borne inoculum.
circular spots caused by pesticide or fertilizer damage.
This disease can cause significant leaf spots to develop References
on seed spinach crops, especially if pollen from spinach du Toit, L. J. and Derie, M. L. 2001. Stemphylium botryosum
flowers falls on leaves prior to infection. pathogenic on spinach seed crops in Washington. Plant
Disease 85:920.
du Toit, L. J., Derie, M. L., and Hernandez-Perez, P. 2005.
Causal agent Evaluation of fungicides for control of leaf spot in spinach
The pathogen is presently named Stemphylium botry- seed crops, 2004. Fungicide & Nematicide Tests 60:V044.
osum, though this fungus may be a new, different du Toit, L. J., Derie, M. L., and Hernandez-Perez, P. 2005.
Evaluation of yield loss caused by leaf spot fungi in spinach
species of Stemphylium. Stemphylium botryosum seed crops, 2004. Fungicide & Nematicide Tests 60:V047.
isolates from spinach are host specific to spinach. On du Toit, L. J. and Hernandez-Perez, P. 2005. Efficacy of hot water
V-8 juice agar incubated under lights, the pathogen and chlorine for eradication of Cladosporium variabile,
Stemphylium botryosum, and Verticillium dahliae from
produces dark green-brown mycelium and abundant spinach seed. Plant Disease 89:1305–1312.
conidia after approximately 10 days. Conidiophores Everts, K. L. and Armentrout, D. K. 2001. Report of leaf spot of
are mostly unbranched, 5 μm wide with distinctly spinach caused by Stemphylium botryosum in Maryland and
swollen apical cells (7 μm wide) having darkly Delaware. Plant Disease 85:1209.
Hernandez-Perez, P. and du Toit, L. J. 2006. Seedborne
pigmented bands. The multicelled conidia are brown- Cladosporium variabile and Stemphylium botryosum in
colored, broadly ellipsoidal to ovoid, and borne singly. spinach. Plant Disease 90:137–145.
A conspicuous constriction is present at the median Koike, S. T., Henderson, D. M., and Butler, E. E. 2001. Leaf spot
transverse septum. Outer conidial walls are roughly disease of spinach in California caused by Stemphylium
botryosum. Plant Disease 85:126–130.
textured (verrucose). Conidia dimensions are mostly Koike, S. T., Matheron, M. E., and du Toit, L. J. 2005. First
19–28 x 14–19 μm, and the mean length/width ratio is report of leaf spot of spinach caused by Stemphylium
1.46. Pseudothecia from an ascomycete perfect stage, botryosum in Arizona. Plant Disease 89:1359.
Pleospora herbarum, have been found on spinach seed
and senescent leaf infections. The role of P. herbarum in
the disease cycle has not been clearly established.
Disease cycle
Details on disease development are lacking. The
pathogen is seedborne, and has been detected on
spinach seed from the USA, Europe, and New Zealand.
F UNGAL D ISEASES
In production fields the disease spreads slowly and

economic damage is usually limited. In spinach seed
production fields, however, the epidemiology of the
disease is much more complex. Spinach pollen that falls
onto leaves can provide a food base for the pathogen
and therefore favor spore germination and infection.
Verticillium dahliae Symptoms and diagnostic features

VERTICILLIUM WILT Symptoms typically begin to show when seed crop
plants begin to bolt and enter their reproductive phase.
Introduction and significance Interveinal tissue of lower leaves turns yellow while
Verticillium wilt has not yet been detected as a problem veins remain green (524). Such leaves later wilt. The
of production spinach in the field, but significant outside lower stems can be red in color. Vascular tissue
disease can be observed in spinach seed fields in the of roots and crowns is light tan to brown. In severe
Pacific northwest USA. The ability of the pathogen to cases plants can be significantly stunted and die (525).
be seedborne in spinach may create opportunities for Vascular discoloration caused by Verticillium wilt is
this pathogen to cause spinach problems in the future. noticeably lighter in color than the vascular discol-
In addition, infested spinach seed could introduce the oration seen with Fusarium wilt (526).
pathogen to fields that later are planted to susceptible
rotation crops. Causal agent
Verticillium wilt is caused by the fungus Verticillium
dahliae. The pathogen can be isolated on standard
524 526
524 Chlorosis of lower spinach leaves caused by 526 Light discoloration of spinach vascular tissue
Verticillium wilt. caused by Verticillium wilt (center) versus dark
discoloration from Fusarium wilt (right). Healthy plant
is on the left.
525 527
F UNGAL D ISEASES
525 Foliage dieback and stem necrosis caused by 527 Dissected spinach stem showing small, black
Verticillium wilt. microsclerotia of Verticillium dahliae.
microbiological media, though semi-selective media Beet curly top virus

such as NP-10 can be useful for isolation. On general BEET CURLY TOP
purpose media, the pathogen forms the characteristic
hyaline, verticillate conidiophores bearing three to four Introduction and significance
phialides at each node, and hyaline, single-celled, ellip- Beet curly top virus (BCTV) occurs in North and South
soidal conidia. Older cultures form dark brown to America, Asia, the Middle East, and the Mediterranean
black torulose microsclerotia that consist of groups of region. This virus is an important pathogen of many
swollen cells formed by repeated budding. Micro- crops such as pepper, tomato, and Chenopodium
sclerotia size varies greatly and is in the range of 15–100 plants. Occurrence on spinach varies between regions.
μm in diameter. This pathogen is seedborne in spinach,
and has been detected in spinach seed from both the Symptoms and diagnostic features
USA and Europe. Therefore, infested spinach seed BCTV infections on spinach initially appear as leaf
could be a means of spreading the pathogen to previ- stunting and chlorosis (528). Affected plants appear
ously uninfested fields. compact and yellow. Younger leaves in the center of the
plant are often very pale yellow, curled, and brittle in
Disease cycle texture. Plants can die a few weeks after symptoms
The pathogen survives in the soil as dormant microscle- appear.
rotia for extended periods of time (up to 8 to 10 years)
but can also persist as an epiphyte on non-host roots. Causal agent
Diseased tissue can also harbor microsclerotia (527). BCTV is a geminivirus with isometric particles that
Cool to moderate weather conditions favor the measure 18–22 nm in diameter and which occur singly
pathogen, and disease is enhanced at temperatures or in pairs. The BCTV genome is a single-stranded
between 20–24º C. The microsclerotia germinate, and circular DNA. BCTV is vectored in a persistent manner
infective hyphae enter host roots through wounds. On by the beet leafhopper (Circulifer tenellus). Circulifer
spinach seed plants, disease severity becomes greater as opacipennis is a vector in the Mediterranean region. In
plants mature and develop seed stalks (bolting). the plant, BCTV is restricted to the phloem tissue. On a
Control BCTV from North America and the Middle East and
For production spinach, no control measures are yet found them to be similar, providing evidence that these
recommended, though growers should be aware that various BCTV strains share a common origin.
infested spinach seed is a source of the pathogen.
For spinach seed crops, use seed that has been treated
or found to be uninfested. Hot water or 1.2% bleach
seed treatments can significantly reduce seedborne 528
inoculum. Avoid planting spinach seed crops in fields
having a history of Verticillium wilt.
References
du Toit, L. J., Derie, M. L., and Hernandez-Perez, P. 2005.
Verticillium wilt in spinach seed production. Plant Disease
89:4–11.
du Toit, L. J. and Hernandez-Perez, P. 2005. Efficacy of hot water
and chlorine for eradication of Cladosporium variabile,
Stemphylium botryosum, and Verticillium dahliae from
V IRAL D ISEASES
spinach seed. Plant Disease 89:1305–1312.

Snyder, W. C. and Wilhelm, S. 1962. Seed transmission of
Verticillium wilt of spinach. Phytopathology 52:365.
van der Spek, J. 1973. Seed transmission of Verticillium dahliae.
Mededelingen van de Faculteit Landbouwwetenschappen, 528 Stunting and leaf chlorosis due to Beet curly top
Rijksuniversiteit Gent 38(3):1427–1434.
virus.

This virus infects many weed and crop hosts. Recent BWYV infections on spinach appear as interveinal and
research on curly top disease as it occurs in leaf margin chlorosis on older leaves (529, 530). Leaf
Chenopodiaceae, Fabaceae, Solanaceae, and other veins and areas adjacent to the veins usually remain
crops indicates that the viral agent may differ depending green. This yellows symptom may be confused with
upon the host being considered. Beet curly top as a various nutrient deficiency symptoms, notably those
disease may actually be caused by one of four different caused by nitrogen, iron, or magnesium deficiency. As
curly top virus species: Beet curly top virus (BCTV), the disease progresses, the yellowing increases and the
Beet mild curly top virus (BMCTV), Beet severe curly older, lower leaves become completely chlorotic. Older
top virus (BSCTV), and Spinach curly top virus symptomatic leaves are sometimes colonized by
(SCTV). Research is on-going to further determine the secondary fungi which contribute further to the decline
relationships of these various viruses. in quality.
Control Causal agent and disease cycle

Follow general suggestions in Part 1. BWYV is a polerovirus and has isometric particles with
diameters of 25 nm and single-stranded, linear RNA
References genomes. BWYV may be found in numerous crop and
Baliji, S., Black, M. C., French, R., Stenger, D. C., and Sunter, G. weed plants, and the host list is extensive, including over
2004. Spinach curly top virus: a newly described curtovirus 150 plant species. Some isolates or strains of this virus
species from southwest Texas with incongruent gene
phylogenies. Phytopathology 94:772–779. have different abilities to infect certain plants; thus, not
Briddon, R. W., Stenger, D. C., Bedford, I. D., Stanley, J., all strains of BWYV may be able to infect all known
Izadpanah, K., Markham, P. G. 1998. Comparison of a beet hosts, greatly complicating the etiology of this disease.
those from the new world. European Journal of Plant
The role of different strains for spinach has not been
Pathology 104:77–84. clarified. BWYV is vectored by several aphid vectors,
Sams, D. W. and Bienz, D. R. 1974. Relative susceptibility of especially the green peach aphid (Myzus persicae), in a
spinach plant introduction accessions to curly top. persistent manner.
HortScience 9:600–601.
Soto, M. J. and Gilbertson, R. L. 2003. Distribution and rate of
movement of the curtovirus Beet mild curly top virus (family Control
Geminiviridae) in the beet leafhopper. Phytopathology Follow general suggestions for managing virus diseases
93:478–484.
(see Part 1).

529

species that affect chenopodium crops. Beet western
yellows virus (BWYV) is prevalent in the USA and
elsewhere and infects many other plants in addition to
beet, Swiss chard, and spinach. Beet mild yellowing
virus (BMYV) is the most important yellows virus on
Chenopodiaceae hosts in the UK and Western Europe.
V IRAL D ISEASES
A third Polerovirus pathogen is Beet chlorosis virus

(BCHV).
529 Chlorosis and green vein symptoms of BWYV on

spinach.
530 Symptoms and diagnostic features

Symptoms of CMV infection on spinach include a slight
to moderate chlorosis (531) and a narrowing of young
leaves. Leaves also can have an inward rolling of
margins and be extremely wrinkled and distorted. In
advanced stages of disease, the plants usually appear
stunted and the immature leaves in the center of the
plant may become completely blighted, killing the
growing point (532). In some reports this disease is
called spinach blight.

(29 nm in diameter) and contain three single-stranded
530 Close-up of chlorosis and green vein symptoms of RNAs. Many CMV strains have been documented.
BWYV on spinach. CMV is transmitted by several aphid vectors in a non-
persistent manner. CMV occurs in many weed hosts
and can also be seedborne in spinach
Control
CMV is difficult to control because of its extremely
Cucumber mosaic virus wide host range. Follow general suggestions for
CUCUMBER MOSAIC managing virus diseases (see Part 1). Some resistant
spinach cultivars are available, though such resistance
Introduction and significance may not be complete. Use spinach seed that does not
Cucumber mosaic virus (CMV) is commonly found have the virus.
throughout the world and can cause disease on over
800 plant (crop and weed) hosts, including plants in the References
Chenopodiaceae. CMV is most prevalent in temperate Yang, Y., Kim, K. S., and Anderson E. J. 1997. Seed transmission
regions. of cucumber mosaic virus in spinach. Phytopathology
87:924931.
531 532
V IRAL D ISEASES
531 Yellowing of spinach leaf caused by Cucumber 532 Severe symptoms of Cucumber mosaic virus on
mosaic virus. spinach.
Specialty and herb crops

SPECIALTY CROPS is a category that usually refers to agricultural or horticultural
commodities that are grown in a very limited volume, comprise small production areas,
are new crops, tend to be produced or consumed by certain ethnic groups, or are used for
specialized cooking purposes. Both organic and conventionally grown specialty items find their
way to farmers’ markets, specialty grocery stores, and other specialized outlets. This chapter
outlines some disease problems found on various specialty vegetables, gourmet commodities,
and herbs and spices. In many cases these specialty vegetables are susceptible to the same range
of pathogens that affect more familiar, widely grown vegetables that are in the same plant
families as the specialty items. However, in contrast to the more well-known vegetables, the
specialty crops face particular challenges with regard to disease management. Research projects
and funding are often not available for dealing with specialty crop problems. Therefore, precise
information on specialty crop diseases is usually very limited. Commercial plant breeding efforts
can rarely be justified for specialty crops that are planted on such a small scale. Specialty crops
are often omitted from fungicide registrations, or such registrations are not approved in all
regions or countries. For example, a fungicide product such as azoxystrobin may be registered
in the Eastern USA on some minor crops, but the California label may not include those same
crops; therefore, chemical control options may not be available for use
on specialty commodities.
Controlling diseases of specialty crops follows the general integrated disease
management strategies used for other vegetable crops. Choose and plant resistant cultivars,
if such are available. Rotate specialty crops so that the same commodity is not planted in the
same location for back-to-back plantings or in the same season; this strategy is particularly
important for soilborne pathogens. Select the area to be planted so as to favor plant development
and discourage pathogens; for example, selection of well-draining, lighter textured soils will help
reduce disease pressure caused by Pythium and other damping-off pathogens. Avoid fields and
locations that have a history of the diseases of concern. As mentioned, fungicides are often not
registered for these crops, though some mineral products (sulfur, copper) are generally
approved. When possible, use appropriate cultural practices to create conditions unfavorable for
disease development: avoid using overhead sprinkler irrigation, do not plant until the previous
crop residues have dissipated, use seed that does not have significant levels of the pathogen, use
transplants that do not show disease symptoms, practice good weed and insect management.
Refer to the appropriate sections in this book that discuss the same pathogens and diseases
as found on the crops in this chapter.
S PECIALTY AND H ERB C ROPS 383
Amoracia rusticana Albugo candida

HORSERADISH White rust
White rust or white blister is a common and sometimes
Horseradish is a crucifer plant (family Brassicaceae) cul- severe foliar disease on horseradish. The undersides of
tivated for its leaves and fleshy, white, pungent roots affected leaves bear small, white or pale brown raised
that are processed into the horseradish condiment. blisters. These blisters break open to release powdery
Horseradish is propagated from root cuttings. This white spores. The pathogen is Albugo candida, the
plant is probably native to southeast Europe and same pathogen that affects other crucifers. Perennial
western Asia. Horseradish has escaped from cultivation plantings of horseradish facilitate A. candida survival
and become widely naturalized in Europe, North and re-infection, and the pathogen can infect the fleshy
America, and New Zealand. Fungicide recommenda- roots of horseradish. Hot water treatment of root
tions exist for some of these diseases in some countries. cuttings (44º C for 10–15 minutes) may control root
infection. For more information see the white rust
section in the crucifer chapter
533 Cercospora Cercospora amoraciae

533
leaf spot of horse- Cercospora leaf spot
radish. This disease produces round to angular, pale brown leaf
spots (533, 534). Some spots have a darker margin and
chlorotic halo. Lesions are often numerous on older
leaves and coalesce to produce large pale blotches or
severe blighting of foliage. Cercospora leaf spot is very
prevalent on wild horseradish in the UK. The pathogen,
Cercospora amoraciae, forms hyaline spores that
measure 50–140 x 3-5 μm, have 7 to 18 septa, and are
broader at the attachment point and tapered at the
distal end. Young lesions caused by C. amoraciae may
be difficult to distinguish from Alternaria brassicae
lesions.
Peronospora parasitica
(= Hyaloperonospora parasitica)
Downy mildew
534
This disease is occasionally reported on horseradish and
causes irregular, angular-shaped leaf lesions. The
pathogen is Peronospora parasitica. The precise rela-
tionship between the horseradish downy mildew
pathogen and P. parasitica isolates from other brassica
hosts requires additional research. For more informa-
tion see the downy mildew section in the crucifer
chapter.
Ramularia amoraciae
H ORSERADISH
Ramularia leaf spot

This disease is common in Europe and North America
and sometimes causes significant losses. Ramularia leaf
spot produces circular to irregular-shaped, pale green or
534 Close-up of Cercospora leaf spot of horseradish.
yellowish spots that measure up to 10 mm in diameter 535

(535). Spots later turn white and develop dark margins.
These lesions coalesce to form larger blotches. Severe
infection results in death of the leaves; affected leaves
can have a tattered appearance as the dead areas tear
away. The pathogen is Ramularia amoraciae. Spores
are visible on the undersurfaces of lesions and have one
septum or none and measure 8–30 x 3–4 μm. The
pathogen overwinters as black stromata on fallen
leaves; stromata produce new conidia in the spring.
This pathogen apparently infects only horseradish; the
reported occurrence of R. amoraciae on oilseed rape
(Brassica napus) in France is now considered to involve
the white leaf spot pathogen.
535 Ramularia leaf spot of horseradish.
Turnip mosaic virus (TuMV)
Turnip mosaic
This virus disease causes a chlorotic, blotchy mottle,
sometimes with vein clearing. As the leaves age, a more Xanthomonas campestris pv. amoraciae
general chlorosis develops followed by necrotic rings at Black rot
the edge of the chlorotic patches. Affected plants have Black rot causes localized leaf spots that tend to be
stunted growth. Flecking and streaking occur on the angular in shape and resemble those of bacterial leaf
petioles and leaf veins and this may extend into the spot disease caused by Pseudomonas syringae pv.
roots. TuMV is a potyvirus. maculicola. Black rot of horseradish is caused by
Xanthomonas campestris pv. amoraciae. This pathogen
Verticillium dahliae is closely related to X. campestris pv. campestris, causal
Verticillium wilt agent of the systemic black rot disease that affects many
Horseradish plants affected by Verticillium wilt may brassica plants. Xanthomonas campestris pv. amor-
not show foliar symptoms. If symptoms of the foliage aciae from horseradish is only weakly pathogenic to
occur, these consist of wilting, chlorosis, necrosis, and cabbage and cauliflower. For more information see the
overall stunting of growth; lower leaves are affected black rot section in the brassica chapter (page 159).
first. The vascular tissue of the roots (and also plant
petioles) shows dark brown to black discoloration and References
streaking. This discoloration later spreads to the root Atibalentja, N. and Chang, R. J. 1998. Verticillium dahliae
cortex and core, making the harvested root unusable resistance in horseradish germ plasm from the University of
Illinois collection. Plant Disease 82:176–180.
for processing. The main causal agent is Verticillium
Babadoost, M., Chen, W., Bratsch, A. D., and Eastman, C. E.
dahliae. Microsclerotia enable the pathogen to survive 2004. Verticillium longisporum and Fusarium solani: two
in the soil for extended periods of time (up to 8 to 10 new species in the complex of internal discoloration of
horseradish roots. Plant Pathology 53:669–676.
years). Because horseradish is propagated vegetatively,
Brun H., Renard M., Jouan B., Tanguy, X., and Lamarque, C.
cuttings and plant divisions probably spread this 1979. Observations préliminaires sur quelques maladies du
pathogen to new plantings. For more information see colza en France: Sclerotinia sclerotiorum, Cylindrosporium
the Verticillium wilt section in the brassica chapter concentricum, Ramularia amoraciae. Sciences Agronomiques
Rennes (1979), 7–77.
(page 194). Resistant or tolerant cultivars are being Eastburn, D. M. and Chang, R. J. 1994. Verticillium dahliae: a
H ORSERADISH
developed. This disease of horseradish may be caused causal agent of root discoloration of horseradish in Illinois.
by a complex of soilborne pathogens; researchers Plant Disease 78:496–498.
recently have also implicated V. longisporum and Percich, J. A. and Johnson, D. R. 1990. A root rot complex of
horseradish. Plant Disease 74:391–393.
Fusarium solani with vascular discoloration.
Anethum graveolens Anthriscus cerefolium

DILL CHERVIL
Dill is produced for its foliage and is used as a culinary Chervil, or salad chervil, another member of the
herb and for seasonings. The plant is in the Apiaceae Apiaceae, is produced for its foliage and is used as a
family. culinary herb, garnish, salad ingredient, and tea.
Erysiphe heraclei Erysiphe heraclei

Powdery mildew Powdery mildew
On dill, powdery mildew forms white mycelium and On chervil, powdery mildew forms white mycelium
conidia on leaves, stems, and flower stalks. The disease and conidia on both sides of leaves (536), causes slight
causes slight twisting of foliage and early senescence. twisting of foliage, and results in quality loss of the
Conidia form singly, are cylindric, and measure 30–40 harvested product. Severely affected plants are not
x 12–15 um. Conidia lack fibrosin bodies and ger- harvested. Conidia form singly, are cylindric, and
minate at the ends with either a very short or a long measure 40–50 x 15–17 um. Conidia lack fibrosin
germ tube forming a lobed appressorium (polygoni- bodies and germinate at the ends with either a very
type). Spherical cleistothecia have been observed. The short or a long germ tube forming a lobed appressorium
pathogen is Erysiphe heraclei. (polygoni-type). No cleistothecia have been observed.
The pathogen is Erysiphe heraclei.
Itersonilia perplexans
Itersonilia blight
This is a minor disease of dill that has been reported
only occasionally. Initial symptoms consist of a gray-
green discoloration and wilting of the tips of dill leaves.
As disease develops, many of the leaves discolor and
collapse, which gives the foliage a blighted appearance
536
and makes the leaves unsuitable for harvest. The
pathogen is the fungus Itersonilia perplexans. In culture
the fungus produces slow-growing colonies that are
cream-colored, velutinous, and flat with minimal aerial
mycelium. Mycelium is hyaline and has clamp connec-
tions. Ovoid to subglobose sporogenous cells are
produced and measure 11–14 x 12–16 μm. Spores are
ballistospores that are bilaterally symmetrical, lunate,
16–18 x 12–13 μm, and germinate with hyphae or
secondary ballistospores. Studies indicate I. perplexans
consists of pathogenic forms that are host-specific to
either chrysanthemum and closely related Compositae,
or to Apiaceae plants such as dill, carrot, parsley, and
parsnip.
References
Koike, S. T. and Tjosvold, S. A. 2001. A blight disease of dill in
D ILL , C HERVIL
California caused by Itersonilia perplexans. Plant Disease

85:802.
Soylu, E. M. and Soylu, S. 2003. First report of powdery mildew
caused by Erysiphe heraclei on dill (Anethum graveolens) in 536 White fungal growth of powdery mildew on
Turkey. Plant Pathology 52:423. chervil.
Sclerotinia sclerotiorum Beta vulgaris subsp. cicla

White mold SWISS CHARD
White mold infections cause tan to gray lesions to
develop on crowns and lower sections of stems (537). Swiss chard is in the Amaranthaceae family and is
These lesions are surrounded by pink to orange-colored closely related to beet. However, Swiss chard is grown
tissue, which is similar in color to celery petioles infected exclusively for its leaves and is most often used as a
by this same fungus. Affected stems wilt and plants cooked vegetable. In California, Swiss chard is also
eventually collapse and rot. White mycelium and large, grown for only a few weeks and then harvested for a
irregular, black sclerotia (5–10 mm in diameter) are small, ‘baby leaf’ fresh vegetable used in salads. Two
observed on infected stems and crowns. The pathogen common chard types are the green leaf varieties that
is Sclerotinia sclerotiorum. For more information see have white petioles and the red-green to purple-green
the white mold on bean section in the legume chapter leaf types that have red petioles. Table beet (Beta
(page 262). vulgaris subsp. vulgaris), or beetroot, is in the same
plant family as Swiss chard and is grown for its swollen,
References fleshy taproot that is eaten as a cooked or pickled
Koike, S. T. and Saenz, G. S. 2004. First report of powdery commodity.
mildew caused by Erysiphe heraclei on chervil in California.
Beet curly top virus (BCTV)
Koike, S. T. 1999. Stem and crown rot of chervil, caused by
Sclerotinia sclerotiorum. Plant Disease 83:1177. Beet curly top
Beet curly top virus can result in severely stunted,
chlorotic Swiss chard plants (538). Such plants have
older leaves that turn dull to bright yellow and are
brittle, thickened, and rolled. BCTV is vectored by the
beet leafhopper (Circulifer tenellus) and other leafhop-
per species. For more information see the beet curly top
section in the beet chapter (page 148).
537 538
C HERVIL
537 Chervil crown infected with Sclerotinia 538 Chlorosis and leaf deformity of Swiss chard
sclerotiorum. infected with Beet curly top virus.
539 540
539 Cercospora leaf spot of Swiss chard. 540 Powdery mildew on Swiss chard.
Cercospora beticola 541 Infected 541

Cercospora leaf spot crown and
Initial symptoms are small, angular leaf spots that are emerging leaves of
brown or tan with purple to red borders (539). As spots Swiss chard caused
enlarge, the tissue becomes tan to gray in color and may by downy mildew.
or may not retain the purple border. In severe cases the
spots can coalesce and cause large sections of the leaf to
die. The pathogen is Cercospora beticola, and it can
infect both Swiss chard and table beet. The fungus is
seedborne. For more information see the Cercospora
leaf spot section in the beet chapter.
Erysiphe polygoni
Powdery mildew
Swiss chard and table beet are susceptible to powdery
mildew caused by Erysiphe polygoni. The pathogen
appears as typical white to gray mycelium and conidia
growing on both top and bottom sides of leaves (540).
If disease is severe, the leaves may be twisted and 542 Infected
542
distorted. See also the powdery mildew section in the leaves of Swiss
beet chapter. chard caused by
downy mildew.
Peronospora farinosa f. sp. betae
Downy mildew
On both Swiss chard and table beet, downy mildew
causes leaves to twist, curl, and grow in abnormal ways.
The newest leaves and growing point can be extremely
deformed (541). If conditions are favorable, affected
tissue can be covered with the purple-gray growth of the
fungus (542). This pathogen (Peronospora farinosa f.
S WISS C HARD
sp. betae) does not infect spinach; spinach downy

mildew is caused by the closely related P. farinosa f. sp.
spinaciae. See also the downy mildew section in the beet
chapter (page 142).
Pseudomonas syringae pv. aptata

543
Bacterial leaf spot
Initial symptoms of bacterial leaf spot on Swiss chard
and table beet consist of water-soaked leaf spots that
measure 2–3 mm in diameter (543). As bacterial leaf
spot develops, spots become circular to ellipsoid in
shape, measure 3–8 mm in diameter, and are tan with
distinct brown to black borders (544). Spots are visible
from both top and bottom sides of leaves. The pathogen
is Pseudomonas syringae pv. aptata. This pathogen also
infects sugar beet.
Rhizoctonia solani, Pythium spp.

Damping-off 543 Early symptoms of bacterial leaf spot of Swiss
Symptoms of damping-off of Swiss chard occur on chard.
newly emerging plants and consist of wilting, brown
necrosis of crown tissue, and eventual death of seedlings 544
(545). If Swiss chard is planted in high plant densities,
disease incidence can increase rapidly and affect large
numbers of seedlings. Damping-off pathogens are
Rhizoctonia solani and species of Pythium.
Uromyces betae
Rust
On both Swiss chard and table beet, the most obvious
indication of rust is the presence of discrete, brown to
orange-brown pustules on both sides of the infected leaf
(546, 547). The brown spores emerge in large numbers
from these pustules. If infected severely, the leaf can turn
yellow and begin to decline. The pathogen is Uromyces
betae. For more information see the rust section in the 544 Advanced leaf spots of bacterial leaf spot of
beet chapter. Swiss chard.
References 545
Koike, S. T., Henderson, D. M., Bull, C. T., Goldman, P. H., and
Lewellen, R. T. 2003. First report of bacterial leaf spot of
Swiss chard caused by Pseudomonas syringae pv. aptata in
Koike, S. T. and Subbarao, K. V. 1999. Damping-off of Swiss
chard, caused by Rhizoctonia solani, in California. Plant
Disease 83:695.
S WISS C HARD
545 Damping-off of Swiss chard caused by Rhizoctonia

solani. Healthy plants are on the right.
Brassica rapa subsp. rapa

546
BROCCOLI RAAB
Broccoli raab, also known as rapini, broccoletto di

rapa, or cima de rapa, is a crucifer vegetable (family
Brassicaceae) grown for its succulent young shoots,
leaves, and immature flower buds. In addition to
bacterial blight, broccoli raab is susceptible to
Alternaria leaf spot and powdery mildew (see the
brassica chapter).
Pseudomonas syringae pv. alisalensis

Bacterial blight
546 Rust pustules on Swiss chard. Initial symptoms consist of small (2–4 mm), angular,
water-soaked flecks on lower foliage that are visible on
both sides of the leaves (548). These flecks expand and
547
become surrounded by bright yellow borders. As the
disease progresses, multiple leaf spots coalesce and
result in large, irregular necrotic areas and extensive leaf
yellowing. Affected leaf tissue later dries, turns tan, and
becomes papery in texture (549). Disease progresses
upwards from these lower leaves to leaves higher in the
plant canopy. If symptoms develop on the uppermost
leaves attached to the flower stalks, the shoot loses
market quality and will not be harvested. Under condi-
tions favorable for disease development, leaf infections
can be extensive and cause significant reduction in plant
growth. Bacterial blight is caused by Pseudomonas
syringae pv. alisalensis. This pathogen also causes
bacterial blight on broccoli. See also the bacterial blight
547 Advanced rust on Swiss chard. section in the brassica chapter (page 157).
548 549
B ROCCOLI R AAB
548 Water-soaked spots of early bacterial blight 549 Leaf lesions of advanced bacterial blight infection
infection of broccoli raab. of broccoli raab.
References 550
Cintas, N. A., Koike, S. T., and Bull, C. T. 2002. A new pathovar,
Pseudomonas syringae pv. alisalensis pv. nov., proposed for
the causal agent of bacterial blight of broccoli and broccoli
raab. Plant Disease 86:992–998.
Koike, S. T., Cintas, N. A., and Bull, C. T. 2000. Bacterial blight,
a new disease of broccoli caused by Pseudomonas syringae in
Koike, S. T., Henderson, D. M., Azad, H. R., Cooksey, D. A., and
Little, E. L. 1998. Bacterial blight of broccoli raab: a new
disease caused by a pathovar of Pseudomonas syringae. Plant
Disease 82:727–731.
Brassica spp.
MUSTARDS
550 White rust pustules of Japanese mustard.
Specialty leafy mustard crops are grown for use as fresh
vegetables for salads. Japanese or mizuna mustard 551
(Brassica campestris ssp. nipposinica) is a dark green
leafy mustard that usually has finely dissected, feathery
leaves. Red Asian mustard (B. juncea ssp. rugosa),
known also as purple or giant-leafed mustard, is a dark
red to red green leafy mustard that has spatulate leaves.
Tatsoi or tah tsai (B. campestris ssp. narinosa) is a leafy
mustard that has oval, dark green leaves and almost
white petioles.
Albugo candida
White rust
On Japanese mustard and tah tsai, white rust causes
typical white raised pustules to develop profusely on the 551 Alternaria leaf spot of Japanese mustard.
lower sides of leaves (550). Leaf hypertrophy is
observed only on infected Japanese mustard. The
pathogen is Albugo candida. Spherical sporangia Pseudocercosporella capsellae
diameters range from 18–19 μm. Red mustard is appar- White leaf spot
ently not a host. For more information see the white On leafy mustards, white leaf spot causes round to oval,
rust section in the brassica chapter (page 162). light tan to off-white leaf spots measuring 2–8 mm in
diameter (552). White sporulation is common on leaf
Alternaria brassicae spot surfaces, and the hyaline, cylindrical conidia
Alternaria leaf spot measure 60–79 μm x 2–3 μm. Isolations onto acidified
Alternaria leaf spot symptoms consist of small (2–6 mm potato-dextrose agar (2 ml 25% lactic acid/liter) yield
in diameter), circular to oblong brown spots that slow-growing, raised, black, stromatic colonies that
contain concentric rings (551 and also 553). On tah produce few conidia. On 2% water agar, colony mor-
tsai, yellow borders may develop around the spots. phology is similar to that on PDA, but colonies also
M USTARDS
Elongated, brown spots also develop on leaf petioles. release a purple-pink pigment into the media. The
The pathogen is Alternaria brassicae. For more infor- pathogen is Pseudocercosporella capsellae. For more
mation see the Alternaria leaf spot section in the information see the white leaf spot section in the
brassica chapter (page 164). brassica chapter (page 176).
Cichorium endivia, C. intybus

552 552 White leaf
spot of red ENDIVE/ESCAROLE, RADICCHIO
mustard.
There are several head-forming leafy vegetables that are
in the chicory plant group (family Asteraceae). These
crops are grown for leaves that are used fresh in salads
or cooked in other foods. Endive (Cichorium endivia)
and escarole (the broad-leaf type of C. endivia) are
green, open headed types that form dense rosettes that
have a growth habit similar to low, prostrate leaf
lettuces. Radicchio or red chicory (C. intybus) typically
is a dark red to red-green chicory that is field grown (in
contrast to witloof chicory that is forced in dark, indoor
incubation conditions) and forms rosettes that later
develop into enclosed heads. Some C. intybus types
grow more like romaine lettuce and have an open archi-
tecture.
553
Alternaria cichorii
Alternaria leaf spot
Symptoms of Alternaria leaf spot on endive and
escarole consist of small (1–2 mm diameter), necrotic,
circular leaf spots (554). The pathogen is Alternaria
cichorii. The fungus sporulates on the leaf spots.
Conidia from leaves are obclavate in shape (larger at the
base) with slender, unbranched beaks extending from
the narrow end of the spore body. Spore body dimen-
sions measure 56–78 x 14–20 μm, and beaks measure
36–81 x 1–2 μm. Spore bodies have seven to nine trans-
verse septa. Longitudinal septa are usually not present.
553 White leaf spot (left) and Alternaria leaf spot (right)
of tatsoi mustard.
References 554
Koike, S. T. 1996. Outbreak of white rust, caused by Albugo
candida, on Japanese mustard and tah tsai in California. Plant
Disease 80:1302.
Koike, S. T. 1996. Japanese mustard, tah tsai, and red mustard as
E NDIVE /E SCAROLE , R ADICCHIO
hosts of Alternaria brassicae. Plant Disease 80:822.

Koike, S. T. 1996. Red mustard, tah tsai, and Japanese mustard
as hosts of Pseudocercosporella capsellae in California. Plant
Disease 80:960.
554 Alternaria leaf spot of endive.

555
On radicchio the pathogen causes circular to oblong,
necrotic spots ranging in diameter from 3–20 mm and
having concentric zones of darker tissue (555, 556).
Beet western yellows virus (BWYV)

Beet western yellows
Symptoms of this virus disease in endive and escarole
resemble those of lettuce infected with the same virus.
The leaves develop yellow blotches in interveinal tissue.
This yellowing continues until the oldest, lower leaves
are bright yellow to sometimes almost white in color
(557), with the main leaf veins remaining green. It
appears that this virus does not cause significant
555 Early leaf spots of Alternaria leaf spot of radicchio. stunting or reduction in plant size. Overall symptoms of
this yellows disease may resemble nutrient deficiencies,
such as iron chlorosis. BWYV is spread by aphid
556
vectors. For more information see the beet western
yellows section in the lettuce chapter (page 317).
Erwinia spp., Pseusdomonas spp.

Bacterial soft rot
Bacterial soft rot is a problem on many vegetables,
including endive and escarole. On endive and escarole,
symptoms consist of a brown to black, soft mushy rot
of lower leaves as well as leaves within the tightly
whorled heads (558). Such leaves are usually slimy and
wet. Bacterial soft rot occurs when plant tissue is
damaged from tipburn, disease infections, and other
factors. This problem is usually considered to be a
556 Advanced leaf spots of Alternaria leaf spot of secondary decay and is caused by a complex of Erwinia,
radicchio. Pseudomonas, and other bacteria.
557
Powdery mildew
On endive and radicchio, powdery mildew forms white
mycelium and conidia on both sides of leaves (559),
causes slight twisting of foliage, and results in quality
loss of the harvested product. Infected leaves must be
trimmed off the plant at harvest. Conidia are produced

in chains. The pathogen is Golovinomyces cicho-
racearum (previously named Erysiphe cichoracearum).
557 Endive infected with Beet western yellows virus.

558 560
558 Leaf and petiole decay of bacterial soft rot of 560 Bacterial leaf spot of Italian dandelion
endive. (=C. intybus).
559 561
559 Sporulation of powdery mildew of radicchio. 561 Rust pustules on endive.
Pseudomonas syringae Puccinia hieracii

Bacterial leaf spot Rust
Italian dandelion (Cichorium intybus) is a chicory plant Endive and escarole are susceptible to a rust disease.
related to radicchio. Italian dandelion does not form a The most obvious indication of this problem is the
head, but rather grows long, upright, loose foliage that presence of the rust pathogen itself. The fungus forms
superficially looks similar to true dandelion (Taraxa- discrete, dark brown to red-brown pustules on both
cum officinale). Early symptoms of bacterial leaf spot sides of the diseased leaf (561). The red brown spores
are angular, vein delimited, dark, water-soaked leaf emerge in large numbers from these pustules. If infected
spots that measure 2–7 mm in diameter. As disease severely, the leaf can turn yellow and begin to decline.
develops, spots retain the angular edges but exhibit The pathogen is Puccinia hieracii.
various irregular shapes (560). Spots commonly form
along the edges of the leaves; in some cases these spots
develop into long lesions that measure between 10 and
30 mm in length. Spots are visible on both the top and
bottom sides of the leaf and at maturity are a dull black
color. The pathogen is Pseudomonas syringae.
562
Rhizoctonia solani
(teleomorph = Thanatephorus cucumis)
Rhizoctonia blight
On endive and escarole, Rhizoctonia blight causes a
soft, watery, brown decay of the leaves (562). In the
tightly appressed heads of these plants, the decay
generally spreads in a concentric circle, resulting in
circular whorls of brown, rotted leaves within diseased
heads. Such infections make the heads unmarketable.
The pathogen is Rhizoctonia solani. The perfect stage
of this fungus, Thanatephorus cucumeris, is not
commonly observed on these hosts.
Sclerotinia minor
562 Leaf and petiole decay of Rhizoctonia blight of White mold
endive. In coastal California, Sclerotinia minor is the main
Sclerotinia species on these crops. White mold affects
563
endive, escarole, and radicchio. Plants nearing maturity
wilt and collapse (563). Crown tissues become necrotic
and develop a soft rot. White mycelium and small
(0.5–3.0 mm) black sclerotia form on infected tissues
(564). Isolates of S. minor are able to infect both lettuce
and these chicory species. Sclerotinia sclerotiorum can
also infect these plants. For more information see the
white mold on bean section in the legume chapter (page
262).
Tomato spotted wilt virus (TSWV)

Tomato spotted wilt
On radicchio, TSWV causes chlorotic spots, streaks,
563 Collapsed radicchio infected with Sclerotinia mottles, and other symptoms on leaves (565). If radic-
minor. chio is infected when young, the plants can be stunted
and leaves deformed and twisted. TSWV is vectored by
564
thrips. For more information see the tomato spotted
wilt section in the tomato chapter (page 364).
564 Mycelium and sclerotia of Sclerotinia minor on

radicchio.
565 566
565 Radicchio leaves infected with Tomato spotted wilt 566 Tipburn disorder on radicchio.
virus.
Tipburn 567
Tipburn is a physiological disorder of leafy vegetables
caused by an imbalance of calcium in leaf tissue.
Symptoms occur on the margins of developing leaves
and consist of light to dark brown speckling, lesions,
and necrosis (566, 567). In severe cases tipburn can
result in extensive damage to these leaf margins.
Symptomatic leaves are usually found within the inner
whorls of chicory heads. Calcium deficiency occurs
when conditions cause plants to grow so rapidly that
the plant cannot supply sufficient calcium to leaf
margins. This disorder is similar to tipburn in lettuce
and spinach, blackheart of celery, and blossom end rot
of tomato. For more information see the tipburn section
in the lettuce chapter (page 326). 567 Tipburn disorder on endive.
References
di Mario, E. 1968. Alternaria porri f. sp. cichorii on endive and Koike, S. T. and Subbarao, K. V. 1995. First report of endive and
chicory in Apulia (Italy). Phytopathologia Mediterranea escarole as hosts of Sclerotinia minor. Plant Disease 79:642.
7:7–14. Koike, S. T. and Subbarao, K. V. 1995. First report of radicchio as
Koike, S. T. and Butler, E. E. 1998. Leaf spot of radicchio caused a host of Sclerotinia minor. Plant Disease 79:966.
by Alternaria cichorii in California. Plant Disease 82:448. Schober, B. M. and Vermeulen, T. 1999. Enzymatic maceration
Koike, S. T. and Bull, C. T. 2006. First report of bacterial leaf spot of witloof chicory by the soft rot bacteria Erwinia carotovora
of Italian dandelion (Cichorium intybus) caused by a subsp. carotovora: the effect of nitrogen and calcium
Pseudomonas syringae pathovar in California. Plant Disease treatments of the plant on pectic enzyme production and
90:245. disease development. European Journal of Plant Pathology
Koike, S. T and Saenz, G. S. 1996. Occurrence of powdery 105:341–349.
mildew, caused by Erysiphe cichoracearum, on endive and Vakalounakis, D. J. and Christias, C. 1985. Light intensity,
radicchio in California. Plant Disease 80:1080. temperature and conidial morphology in Alternaria cichorii.
Koike, S. T. and Subbarao, K. V. 1999. Leaf blight of endive and Transactions of the British Mycological Society 85:425–430.
escarole, caused by Rhizoctonia solani, in California. Plant
Disease 83:1070.
Coriandrum sativum 568 Foliar

568
CILANTRO symptoms of
Cilantro yellow
Also known as Chinese parsley or Mexican parsley, blotch virus of
Cilantro is a leafy vegetable in the Apiaceae family and cilantro.
is grown for use as a fresh herb, salad ingredient, and
seasonings in cooking. The same plant is also grown for
its seed, which is used in seasoning and cooking. The
seed crop is usually called coriander.
Cilantro yellow blotch virus (CYBV)

Cilantro yellow blotch
Symptoms on leaves consist of chlorotic blotches with
diffuse margins, yellowed veins, and slight leaf defor-
mities (568). Some cultivars can be mildly stunted. This
disease reduces the quality of the harvested product.
When symptomatic leaves are examined with an elec-
tron microscope, unusual virus-like particles measuring 569
approximately 2 μm in length can be observed. Particle
morphology resembles that of closteroviruses, but with
a broadly twisted symmetry. In thin-sectioned leaf
material, aggregates of virus-like particles are seen in
phloem tissue. The pathogen is not yet fully character-
ized and is tentatively named Cilantro yellow blotch
virus.
Fusarium oxysporum f. sp. corianderii

Fusarium wilt
This disease has been documented in Argentina, India,
and the USA (California). Affected plants show stunting
and poor growth, yellowing and reddening of foliage,
and eventual collapse (569). Vascular tissues in crowns 569 Yellowing and reddening of cilantro infected by
and large roots have a light tan to orange discoloration. Fusarium oxysporum. Healthy plant on right.
Infected cilantro roots become translucent and later rot.
The pathogen is the soilborne fungus Fusarium oxy-
570
sporum f. sp. corianderii. In preliminary experiments
this pathogen appears to be host specific to cilantro.
C ILANTRO
570 Bacterial leaf spot of cilantro.

Pseudomonas syringae pv. coriandricola Cymbopogon citratus

Bacterial leaf spot LEMONGRASS
Bacterial leaf spot initially causes water-soaked, vein
delimited lesions on leaves. These spots rapidly turn Lemongrass is a perennial, aromatic grass species
dark brown in color, remain angular in shape, and can (family Poaceae) that has a lemon-like scent to its
be seen from both top and bottom sides of leaves (570). foliage. The crop is grown for its edible stem and oil.
If disease is severe, the foliage can take on a blighted
appearance when leaf spots coalesce. The pathogen is Puccinia nakanishikii/P. cymbopogonis
Pseudomonas syringae pv. coriandricola. This pseudo- Rust
monad has both fluroescent and nonfluorescent strains Symptoms of rust consist of elongated, stripe-like, dark
and is seedborne on cilantro. brown lesions that develop on both sides of leaf surfaces
A new foliar disease of cilantro was found in 1999 in (571). Only lesions on bottom leaf surfaces erupt and
Australia. A Microdochium species caused light gray, produce dark, cinnamon brown pustules (uredinia).
irregular, sunken stem lesions on seed crops. Initial Lesion development can be substantial, and coalescing
studies indicate this fungus infects cilantro but not other lesions can result in significant foliage drying and death.
Apiaceae plants. Several rust pathogens, such as Puccinia nakanishikii
and P. cymbopogonis, are known to infect lemongrass.
References It appears possible that more than one rust pathogen
Cooksey, D. A., Azad, H. R., Paulus, A. O., and Koike, S. T. may occur on the crop in any particular area.
1991. Leaf spot of cilantro in California caused by a
nonfluorescent Pseudomonas syringae. Plant Disease 75:101.
Dennis, J. I. 2003. New disease of coriander in Australia
associated with a Microdochium species. Plant Pathology 571 Lemongrass 571
52:408. leaves infected
Koike, S. T. and Gordon, T. R. 2005. First report of Fusarium with rust.
wilt of cilantro caused by Fusarium oxysporum in California.
Madia, M., Gaetan, S., and Reyna, S. 1999. Wilt and crown rot
of coriander by a complex of Fusarium species in Argentina.
Fitopatologia 34:155–159.
Mayhew, D. E. 2002. Cilantro yellow blotch. Compendium of
Umbelliferous Crop Diseases, p.55. R. M. Davis and R. N.
Raid, editors. American Phytopathological Society Press. St.
Paul, Minnesota.
Taylor, J. D. and Dudley, C. L. 1980. Bacterial disease of
coriander. Plant Pathology 29:117–121.
Toben, H. M. and Rudolph, K. 1996. Pseudomonas syringae pv.
coriandricola, incitant of bacterial umbel blight and seed
decay of coriander in Germany. Journal of Phytopathology
144:169–178.
Srivastava, U. S. 1972. Effect of interaction of factors on wilt of
coriander caused by Fusarium oxysporum f. sp. corianderii.
Indian Journal of Agricultural Sciences 42:618–621.
References
Bandara, J. M. R. S. 1981. Puccinia rust of citronella and
L EMONGRASS
lemongrass in Sri Lanka. Plant Disease 65:164.

Gardner, D. E. 1985. Lemongrass rust caused by Puccinia
nakanishikii in Hawaii. Plant Disease 69:1100.
Koike, S. T. and Molinar, R. H. 1999. Rust disease on lemongrass
in California. Plant Disease 83:304.
Cynara scolymus agents infecting artichoke. AILV has also been reported
ARTICHOKE from Greece.
Artichoke is in the Asteraceae family and is an herba- Ascochyta hortorum

ceous thistle. These plants are grown for the edible Ascochyta rot or black rot
bracts and receptacles of immature flower buds. Ascochyta rot, or black rot, is an important disease in
Artichokes traditionally have been grown as large, Mediterranean Europe. Symptoms usually develop first
perennial shrubs that were propagated by crown on the tips of the outermost bracts of the flower bud.
divisions. In recent years artichokes have also been Under dry conditions there is little further development
grown as annuals that are started as transplants in of the disease, and infections remain as superficial
greenhouses. blemishes. However, in wet weather the pathogen
spreads externally and internally within the artichoke
Artichoke curly dwarf virus (ACDV) flower bud. The entire bud may be affected by a dark
Artichoke curly dwarf wet rot; secondary soft rot often follows. Cultivars with
Artichoke curly dwarf disease causes significant compact buds are more prone to Ascochyta rot than
reduction in growth and vigor. Diseased plants later types with more open bud structure. The pathogen is
become severely stunted. Leaves are distorted and have Ascochyta hortorum. Older lesions have numerous
dark, necrotic spots and sections. Infected plants are less black pycnidia that produce one-septate conidia.
productive, with up to 40% less yield than healthy Brown lesions also occur on stems and foliage.
plants. Buds that are produced are often deformed and Ascochyta rot may sometimes develop on old downy
hence unmarketable. Severely affected plants may die. mildew (Bremia lactucae) lesions. The presence of
The virus particle is filamentous, measures 582 nm in pycnidia distinguishes Ascochyta rot from Itersonilia
length, and is possibly a member of the potexvirus rot caused by Itersonilia perplexans.
group. The virus has no known vector. Artichokes
infected with ACDV are apparently always co-infected
with Artichoke latent virus. However, Artichoke latent
virus by itself apparently causes no disease symptoms in
artichoke. Therefore, the exact etiology of artichoke
curly dwarf disease has not been determined. ACDV is
spread to new plantings when diseased plants are
divided for propagation material. In the field, only
artichoke has been found to be a natural host of ACDV.
Under experimental conditions, ACDV can also infect 572
other plants in the Asteraceae family such as cardoon,
sunflower, and zinnia.
Artichoke Italian latent virus (AILV)/

Artichoke yellow ringspot virus (AYRSV)
Artichoke Italian latent/Artichoke yellow ringspot
Both of these nepoviruses occur in Europe and are
thought to be transmitted by the needle nematode
(Longidorus fasciatus). AYRSV is also carried in seed,
pollen, and plant material and produces bright yellow
blotches, ringspots, and line patterns. AILV may be
A RTICHOKE
symptomless in some cultivars but can cause yellowing

and stunting in others. Artichoke mosaic, Bean yellow
mosaic, Broad bean wilt, Tobacco streak, and Arti- 572 Collapsed artichoke plants due to bacterial
choke mottle crinkle viruses are some of the other crown rot.
Erwinia chrysanthemi
574
Bacterial crown rot
Plants with bacterial crown rot may be stunted and
show poor growth. The leaves wilt during the day when
temperatures are warm. In advanced stages of the
disease, plants may collapse entirely (572). New leaves
in the center of plants may not expand and instead turn
brown and dry. Crown and tap root tissues are soft,
rotted, and turn brown or black (573). Blackened
crown tissues can be readily observed when perennial
plantings are pruned back at ground level, exposing the
black, discolored cross sections of the crowns and
stems.
After cutting, infected plants may fail to sprout, or
will re-grow more slowly than healthy plants. The cause 574 Bract infection of gray mold of artichoke.
of bacterial crown rot is Erwinia chrysanthemi. This
bacterium is a Gram-negative, non-spore producing rod 575
and is in the Erwinia soft rot group. On CVP medium,
E. chrysanthemi forms iridescent, translucent colonies
in pits or depressions in the agar surface. Little infor-
mation is available on disease development. It is likely
that the pathogen is spread to other plants by the
machines used to cut the plants. The digging and
dividing of infected crowns for propagation results in
diseased new plantings. The bacterium probably
survives on both plant tissue and on dead organic
matter. Other bacterial pathogens of artichokes include
a Xanthomonas species that is usually associated with
frost injury, and Ralstonia solanacearum that causes
bacterial wilt. 575 Infected flower bud and mycelium of gray mold of
artichoke.
573
Botrytis cinerea
(teleomorph = Botryotinia fuckeliana)
Gray mold
In the field, individual flower bracts turn brown and
later dry up (574). The top of the artichoke flower bud
can also turn brown if infected. Characteristic gray to
gray-brown, fuzzy growth of the fungus develops on
the inner surfaces of the bracts and in the center of the
bud apex (575). In the field, artichoke foliage generally
is not affected by this pathogen. Gray mold can be a
postharvest problem, with boxed and stored artichoke
buds showing the same brown infections and fungal
A RTICHOKE
growth. The cause of gray mold is Botrytis cinerea.

Botrytis cinerea survives in and around fields as a sapro-
573 Discolored crown symptom of bacterial crown rot phyte on senescent leaves and crop debris, as a
of artichoke. pathogen on numerous crops and weed plants, and as
sclerotia in the soil. Conidia develop from these sources Golovinomyces cichoracearum
and become windborne. When conidia land on Leveillula taurica (anamorph = Oidiopsis taurica)
senescent or damaged flower bracts, they will germinate Powdery mildew
if free moisture is available and rapidly colonize this There are two powdery mildew fungi that infect arti-
food source. The fungus usually invades bracts that chokes. Leveillula taurica (anamorph = Oidiopsis
have been damaged by insects, snails and slugs, frost, or taurica) is found primarily colonizing the undersides of
other factors. Cool temperatures, free moisture, and older leaves. Careful examination of the undersides of
high humidity favor the development of the disease. these leaves reveals the white powdery growth of this
Gray mold is typically more severe following periods of pathogen (577); however, the profuse white hairs of the
wet weather. leaf can obscure this sign. Severely infected leaves will
first turn yellow, then brown (578). The brown leaves
Calcium deficiency dry up and become papery and tattered. Leveillula
Calcium deficiency manifests itself in artichokes by taurica infects only the older leaves; the younger leaves
causing the young, developing flower buds to develop escape infection until they mature (579). For L. taurica,
black lesions on the tips of the bracts (576). Such bracts all conidiophores develop from endophytic mycelium
later shrivel and curl inwards. Sunken, brown sections and emerge through stomata. Conidiophores can be
develop on inner bracts within the flower bud. The branched and carry one or sometimes two conidia.
young leaves that encircle the artichoke flower buds can Research suggests that L. taurica isolates from arti-
also develop black lesions and spots. Calcium deficien- choke are distinct from the ones occurring on tomato
cy occurs when conditions cause plants to grow rapidly and other vegetable hosts.
or are stressed. This disorder is similar to tipburn in Another powdery mildew on artichoke, Golovino-
lettuce and spinach, blackheart of celery, and blossom myces cichoracearum (previously named Erysiphe
end rot of tomato. cichoracearum), usually results in less severe symptoms.
The white to gray growth of this fungus develops on the
outside of flower bracts and on upper surfaces of both
young and old leaves. Underlying tissue can turn purple
to brown. Erysiphe cichoracearum produces epiphytic
mycelium that grows superficially on host surfaces.
577 Sporulation 577

576
of Leveillula
taurica on an
artichoke leaf.
A RTICHOKE
576 Blackened tips of bracts and leaves caused by

calcium deficiency.
578 580
578 Severe (first two leaves on the left) and light 580 Collapse of articoke plants caused by Pythium root
infection (third leaf from the left) of Leveillula taurica of rot.
artichoke. Leaf on the right is healthy.
Pythium spp.
579
Pythium root rot
Newly planted seedling artichokes, either direct seeded
or transplanted, wilt and collapse. Foliage becomes dull
green and later brown and dry. Root tissues are discol-
ored, decayed, and soft. Severely infected seedlings
rarely recover and will die (580). Seedlings that do live
can be stunted and delayed in their development. In
California, artichokes were traditionally propagated
vegetatively by digging up crowns of older plantings,
dividing them into large pieces, then planting them into
new fields. Recent production practices now use seed or
transplants to initiate new plantings. Therefore this root
rot problem, which occurs mainly on seedling arti-
chokes, has only recently occurred in California. Root
rot is caused by various species of the soilborne
organism Pythium, including P. aphanidermatum.
Pythium aphanidermatum is an oomycete that
579 Leveillula taurica on older foliage of artichoke. produces coenocytic mycelium, swollen, toruloid
sporangia, and spherical, thick-walled oospores.
Sporangia develop and release zoospores in soil water.
Conidiophores are borne on this surface mycelium. The pathogen has a broad host range and can infect the
Conidia are produced in long chains, are hyaline, seed and seedlings of many plant species. Pythium is
ellipsoid to barrel-shaped, and measure 25–45 x favored by wet soil conditions that enable it to grow,
14–25 μm. Like L. taurica, E. cichoracearum likely produce swimming zoospores, and infect host roots.
exists as different physiological strains that have slightly The disease has most often been observed on crops
different host ranges. grown in sandy soil.
A RTICHOKE
Ramularia cynarae
Ramularia leaf spot patchy lesions will form (584), causing the bracts to curl
Initial symptoms of Ramularia leaf spot consist of small and dry out. Symptoms on flower bracts usually make
(2–5 mm in diameter) pale to yellow-green circular the artichoke bud unmarketable.
spots. With time the spots expand up to 20 mm in The pathogen is Ramularia cynarae. Conidiophores
diameter and turn brown (581). Spots are visible from develop in the center of the leaf spots and grow in
both upper and lower surfaces of leaves. If disease is clustered groups (fascicles) that arise from stromata.
severe, lesions will coalesce and the entire leaf can turn Conidiophores are simple, rarely branch, geniculate,
brown and dry up. White growth of the fungus (582) and measure 5–60 μm long. Conidia are catenulate,
will usually develop in the center of leaf lesions. This ellipsoid–ovoid to fusiform in shape, have from zero to
pathogen can also cause elongated lesions on stems three septa, are hyaline with thickened and darkened
(583). Ramularia leaf spot is economically important hila, and measure 10–5 x 2–5 μm. Ramularia leaf spot
when the pathogen moves from the leaves to the flower is managed by applying fungicides when leaf disease is
bud bracts. On bracts, brown, irregularly shaped, significant and prior to flower bract infection.
581
581 Leaf spots due 583
583 Stem lesions
to Ramularia leaf due to Ramularia
spot of artichoke. leaf spot of
artichoke.
582 584
A RTICHOKE
582 Sporulation of Ramularia cynarae on an artichoke 584 Bract lesions of Ramularia leaf spot on artichoke
leaf. flower buds.
Verticillium wilt for extended periods of time (up to 8–10 years).
Verticillium wilt symptoms initially consist of wilting of Infected artichoke plants may not always exhibit
foliage, often on only one side of the plant. Such foliage symptoms of disease; it is possible that only stressed
turns chlorotic and later brown and dry. Infected plants plants show indications of infection. Annual artichoke
grow poorly and are stunted. In severe cases an varieties appear to be more susceptible to V. dahliae
artichoke can lose all leaves and result in the plant con- than perennial cultivars such as Green Globe.
sisting of only the bare, tall, thick green branches (585,
586). The vascular tissue of the lower stems, crowns, References
and roots shows dark brown to black discoloration and Aly, M. M. and Abd El Ghafar, N. Y. 2000 Bacterial wilt of
streaking (587, 588). Diseased plants produce smaller artichoke caused by Ralstonia solanacearum in Egypt. Plant
Pathology 49: 807.
flower buds, and in severe cases the buds are discolored
Bhat, R. G., Subbarao, K. V., and Bari, M. A. 1999. First report
and dried. The causal agent is Verticillium dahliae. of Verticillium dahliae causing artichoke wilt in California.
Microsclerotia enable the pathogen to survive in the soil Plant Disease 83:782.
587 Crown 587

585
discoloration due
to Verticillium wilt
of artichoke.
585 Collapsed artichoke plant infected with

Verticillium wilt.
586
588 Close-up 588
of vascular
discoloration in an
artichoke stem
infected with
Verticillium wilt.
A RTICHOKE
586 Collapsed plants due to Verticillium wilt of

artichoke. Healthy plant is on the right.
Braun, U. 1998. A Monograph of Cercosporella, Ramularia, and Eruca sativa

Allied Genera (Phytopathogenic Hyphomycetes) Vol. 2.
IHW-Verlag, Eching, Germany. ARUGULA
Brown, D. J. F., Kyriakopoulou, P. E., and Robertson, W. M.
1997. Frequency of transmission of artichoke Italian latent Arugula is a leafy crucifer (family Brassicaceae) grown
nepovirus by Longidorus fasciatus (Nematoda:
Longidoridae) from artichoke fields in the Iria and Kandia for salads or as a cooked vegetable. The plant is also
areas of Argolis in northeast Peloponnesus, Greece. European called roquette, rucchetta, garden rocket, and rocket
Journal of Plant Pathology 103:501–506. salad.
Cirulli, M., Ciccarese, F., and Amenduni, M. 1994. Evaluation of
Italian clones of artichoke for resistance to Verticillium
dahliae. Plant Disease 78:680–682. Albugo candida
Correll, J. C., Gordon, T. R., and Elliott, V. J. 1987. Host range, White rust
specificity, and biometrical measurements of Leveillula Signs of white rust consist of white blister-like pustules
taurica in California. Plant Disease 71:248–251.
(sori) that develop beneath the raised host epidermis on
Cragg, I. A. 1966. New or uncommon plant diseases and pests.
Itersonila perplexans on globe artichoke. Plant Pathology the underside of leaves (589). The corresponding upper
15:47. leaf surface turns yellow. If disease is severe, leaves can
Francois, L. E., Donovan, T. J., and Maas, E. V. 1991. Calcium turn chlorotic and then necrotic. Flower heads can also
deficiency of artichoke buds in relation to salinity.
HortScience 26:549–553. become infected and cause tissues to become swollen
Lipton, W. J. and Harvey, J. M. 1960. Decay of artichoke bracts and twisted. This symptom is called a staghead. For
inoculated with spores of Botrytis cinerea Fr. at various more information see the white rust section in the
constant temperatures. Plant Disease Reporter 44:837–839.
brassica chapter (page 162).
Malençon, G. 1936. Une grave maladie des artichauts au Maroc.
Revue de Mycologie NS 1:165–175.
Morton, D. J. 1961. Host range and properties of the globe Peronospora parasitica
artichoke curly dwarf virus. Phytopathology 51:731–734. (= Hyaloperonospora parasitica)
Palti, J. 1971. Biological characteristics, distribution, and control Downy mildew
of Leveillula taurica. Phytopathologia Mediterranea
10:139–153. Symptoms of downy mildew consist of small (1–4 mm
Rana, G. L., Russo, M., Gallitelli, D., and Martelli, G. P. 1980. diameter), irregular, dark brown to black speckling on
Artichoke latent virus: characterization, ultrastructure and the top and bottom sides of leaves (590, 591). Specks
geographical distribution. Annals of Applied Biology
101:279–289.
expand into tan spots 3–8 mm in diameter. The corre-
Rana, G. L., Kyriakopoulou, P. E., Gallitelli, D., Russo, M., and sponding lower leaf surfaces supports the white fungal
Martelli, G. P. 1980. Host range and properties of artichoke growth of the downy mildew (592). If sporulation is not
yellow ringspot virus. Annals of Applied Biology present, downy mildew symptoms may be mistaken for
96:177–185.
Ride, M. 1956. Sur une maladie nouvelle de l’architaut (Cynara
scolymus L.). Comptes Rendus hebdomadaires des Séances de
l’Académie des Sciences, Paris No. 243: 174–177. 589 Pustules of
589
Russo, M. and Rana, G. L. 1978. Occurrence of two legume white rust of
viruses in artichoke. Phytopathologia Mediterranea
17:212–216. arugula.
Stanghellini, M. E., Vilchez, M., Kim, D. H., Aguiar, J. L., and
Armendariz, J. 2000. First report of root rot caused by
Pythium aphanidermatum on artichoke. Plant Disease
84:811.
A RTICHOKE
590 592
590 Downy mildew lesions on arugula leaves. 592 Close-up of sporulation of downy mildew on
arugula leaf.
591 Leaf lesions of 593 Leaf spots of

591 593
downy mildew of bacterial blight of
arugula. arugula.
bacterial blight disease. The pathogen is Peronospora occasionally broccoli. For more information see the
parasitica. For more information see the downy mildew bacterial blight section in the brassica chapter (page
section in the brassica chapter (page 178). 157).
Pseudomonas syringae pv. alisalensis References

Bacterial blight Bull, C. T., Goldman, P., and Koike, S. T. 2004. Bacterial blight
Initial symptoms of bacterial blight are small (less than on arugula, a new disease caused by Pseudomonas syringae
pv. alisalensis in California. Plant Disease 88:1384.
2 mm in diameter), water-soaked spots on both fully
Koike, S. T. 1998. Downy mildew of arugula, caused by
expanded and younger leaves. As disease develops, Peronospora parasitica, in California. Plant Disease 82:1063.
lesions enlarge and become angular in shape and tan in Koike, S. T., Smith, R. F., Van Buren, A. M., and Maddox, D. A.
color (593). Older lesions become desiccated and have 1996. A new bacterial disease of arugula in California. Plant
Disease 80:464.
purple margins. Bacterial blight symptoms may be
A RUGULA
Scheck, H. J. and Koike, S. T. 1999. First occurrence of white rust

similar to those of downy mildew. The pathogen is of arugula, caused by Albugo candida. Plant Disease 83:877.
Pseudomonas syringae pv. alisalensis. It appears that
this is the same bacterium that infects broccoli raab and
Foeniculum vulgare dulce

594
FENNEL
Fennel, Florence fennel, or finochio is in the Apiaceae

family and is used as both a vegetable and herb
commodity. Fennel is eaten as a fresh and cooked
vegetable. The foliage, wide basal portions of the
petioles, and swollen above-ground stem are used.
Fennel is also produced for its seed. Fennel is distinct
from the closely related anise (Pimpinella anisum).
Cercosporidium punctum
Cercosporidium blight
594 Blighted foliage due to Cercosporidium blight of This leaf blight disease affects the older foliage of fennel
fennel. Healthy foliage on the right. but does not infect new leaves. Affected leaf tips and
stems turn brown, wither, and dry up (594). Close
595 Close-up of 595
examination of the stems and the threadlike leaves will
fennel leaves reveal the presence of tiny, discrete, dark brown to black
infected with pustules (595, 596). These pustules consist of clusters of
Cercosporidium the conidiophores and conidia of the pathogen.
punctum.
White mold
Crown and lower petiole tissues in contact with soil
develop a brown rot (597, 598). This necrotic tissue
rapidly turns into a soft rot. White mycelium and small
(0.5–3.0 mm) black sclerotia form on infected
tissues.The foliage of affected stems declines and turns
bright yellow, then brown (599). Isolates of this patho-
gen are able to infect both lettuce and fennel. The other
main white mold species, S. sclerotiorum, also infects
fennel and causes foliar blight and lower petiole decay
similar to that seen on celery.
596 Close-up of 596
fennel petiole References
infected with Cirulli, M. 1981. Cercosporidium punctum (Lacroix) Deighton
Cercosporidium su prezzemolo in Italia. Informatore Fitopatologico 3:33-37.
Koike, S. T. 1994. First report of stem rot of fennel in the United
punctum.
States caused by Sclerotinia minor. Plant Disease 78:754.
Koike, S. T., Butler, E. E., and Greathead, A. S. 1992. Occurrence
of Cercosporidium punctum on fennel in California. Plant
Disease 76:539.
Sisto, D. 1983. Cercosporidium punctum (Lacroix) Deighton su
finocchio (Foeniculum vulgare Mill. var. Azoricum Thell.) in
Italia meridionale. Informatore Fitopatologico 7-8:55-58.
F ENNEL
Helianthus tuberosus
597
JERUSALEM ARTICHOKE
Jerusalem artichoke or sunchoke (family Asteraceae) is
a native of North America and was introduced into
Europe in the 17th century. It is grown for its tubers and
is eaten as a fresh vegetable in salads, a cooked
vegetable ingredient, and as a pickled relish. In the UK,
Jerusalem artichoke is also commonly grown to provide
cover for game birds around field margins. Harvested
tubers are prone to postharvest fungal rots.
Golovinomyces orontii
Powdery mildew
597 Diseased petioles of fennel infected with Powdery mildew is a common foliar disease of
Sclerotinia minor. Jerusalem artichoke. Typical white powdery growth
develops on leaves and stems (600). Severe disease
598
results in extensive fungal growth on the foliage and
both upper and lower leaf surfaces are colonized.
Powdery mildew can cause yellowing and early death
of leaves. The pathogen is Golovinomyces orontii (pre-
viously named Erysiphe orontii). This organism
consists of various strains that differ in their respective
host ranges. Conidia are borne in long chains and are
elliptical to barrel shaped (25–45 x14–26 μm). Dark
brown cleistothecia may be produced in autumn and
have unbranched flexuous appendages up to 500 μm
long. The cleistothecia contain asci that produce two
ascospores each.
598 Fennel crown with sclerotia of Sclerotinia

minor.
599 600
J ERUSALEM A RTICHOKE
599 Chlorotic foliage of fennel infected with 600 Powdery mildew of Jerusalem artichoke.
Sclerotinia minor.

601
Sclerotinia rot/watery soft rot
Sclerotinia rot or watery soft rot is the most important
disease of Jerusalem artichoke. Both Sclerotinia minor
and S. sclerotiorum have been recorded on this host,
with the latter being more frequently reported.
Ascospores of S. sclerotiorum infect aerial parts of the
plant and cause brown petiole and stem lesions.
Subsequently, there is spread down the stem to the
tubers and formation of numerous black sclerotia on
the surface of the stem and within the pith cavity.
Affected plants wilt and die. In the case of S. minor,
soilborne sclerotia germinate to produce mycelium that
invades the stem base directly.
This disease is often associated with heavy clay soils 601 Mycelium and sclerotia of Sclerotium rolfsii
and poorly draining areas. Infected Jerusalem artichoke growing from infected Jerusalem artichoke and onto
may act as an inoculum source of S. sclerotiorum for soil surface.
other crops. In the UK, these plants are maintained as
game covers. If infected, these plantings harbor 602
602 Mycelium and
apothecia that release ascospores that are carried by spherical sclerotia
winds into oilseed rape (Brassica napus) fields. For of Sclerotium
more information see the white mold on bean section in rolfsii on Jerusalem
the legume chapter (page 262). artichoke crowns,
resulting in plant
Sclerotium rolfsii dieback.
Southern blight
Infected Jerusalem artichoke plants have foliage and
branches that turn chlorotic, wilt, and eventually
collapse. Lower stem tissue in contact with soil is the
site of infection, and the fungus causes a dry rot of these
tissues. The characteristic white mycelium and small (1-
2 mm in diameter), spherical, tan to light brown
sclerotia form on the stems and adjacent soil (601, 602).
The pathogen is Sclerotium rolfsii. For more informa-
tion see the southern blight on carrot section in the
Apiaceae chapter (page 101).
References
Laberge, C. and Sackston, W. E. 1987. Adaptability and diseases
of Jerusalem artichoke (Helianthus tuberosus) in Quebec.
Canadian Journal of Plant Science 67:349–352.
J ERUSALEM A RTICHOKE
Koike, S. T. 2004. Southern blight of Jerusalem artichoke caused

by Sclerotium rolfsii in California. Plant Disease 88:769.
McCarter, S. M. 1993. Reactions of Jerusalem artichoke
genotypes to two rusts and powdery mildew. Plant Disease
77:242–245.
McCarter, S. M. and Kays, S. J. 1984. Diseases limiting
production of Jerusalem artichokes in Georgia. Plant Disease
68:299–302.
Mentha spp.
603
MINT
Mint (family Lamiaceae) is grown as a leafy herb and

vegetable and is used in various ways in cooking. It is
also valuable as a processed commodity for oil and mint
flavoring. There are several mint types; two of the more
commonly grown species are spearmint (Mentha
spicata) and peppermint (M. x piperita).
Erysiphe biocellata, E. biocellata, E. orontii

Powdery mildew
Powdery mildew is a problem in some commercial pro- 603 Mint leaf infected with powdery mildew.
duction areas in the USA, being more severe on
spearmint than peppermint. The disease results in the 604
growth of white mycelium that is epiphytic and occurs
on both leaf surfaces (603). Conidia are produced in
chains but lack fibrosin bodies. The pathogen is
Erysiphe orontii, though the new name Golovinomyces
orontii has been suggested. In the UK, the powdery
mildew pathogen is reported as E. biocellata, which
forms cleistothecia and few conidia on M. aquatica and
M. arvensis. Older records indicate E. cichoracearum is
the pathogen.
Puccinia menthae
Rust 604 Rust pustules on mint.
Rust is probably the most important foliar disease of
mint worldwide, capable of causing reductions in both 605
yield and quality. The most obvious indication of this
problem is the presence of the rust pathogen itself. The
fungus forms discrete, dark brown uredinia pustules on
both sides of the infected leaf (604). The brown uredin-
iospores emerge in large numbers from these pustules.
If infected severely, the leaf can turn yellow and
defoliate. From late summer onwards, dark brown
teliospores are produced on leaves and stems, with telia
visible as black spots. A systemic infection of shoots in
the spring can occur if overwintering rhizomes are
infected by teliospores in soil. The systemically affected
shoots are swollen and distorted, with elongated 605 Rust aecia on eau de cologne mint.
chlorotic internodes and chlorotic leaves. Like many
rusts, the life cycle is complex and there is even a third
spore stage (aeciospores) that occurs (605).
The pathogen is Puccinia menthae, which is an host species. For example, the P. menthae isolates that
autoecious and macrocyclic rust fungus. P. menthae is infect oregano are distinct from those that infect mint.
M INT
regarded as a collective species and there are numerous Puccinia angustata is the only other rust recorded on
strains or races, which show specialization to different Mentha, on which it produces aecia.
606 One-sided
Nepeta cataria
606
leaf chlorosis CATNIP
caused by
Verticillium dahliae Catnip is a perennial shrub in the mint family
on mint. (Lamiaceae) and is probably best known as a plant that
is attractive to cats. This plant is also grown commer-
cially and used as an herb, seasoning, and tea.
Xanthomonas campestris
Xanthomonas leaf spot
Initial symptoms of Xanthomonas leaf spot consist of
small brown flecks (1–2 mm in diameter) that are
visible from both top and bottom sides of the leaves.
These flecks expand into larger leaf spots (2–8 mm
diameter) that are dark brown to black and angular in
Control mint rust by using resistant cultivars, shape (607). The pathogen is Xanthomonas campestris.
treating stolons or cuttings with hot water dips prior to Catnip strains are not able to infect carrot, cauliflower,
planting, and applying fungicides. In some cases, pepper, tomato, or the ornamental flower stock
growers use propane flamers to destroy diseased crop (Matthiola incana). Therefore, this pathogen may be a
residues in early spring. new pathovar in the X. campestris group.
Verticillium dahliae References

Verticillium wilt Koike, S. T., Azad, H. R., and Cooksey, D. A. 2001.
Verticillium wilt is a serious disease of peppermint and Xanthomonas leaf spot of catnip: a new disease caused by
a pathovar of Xanthomonas campestris. Plant Disease
other mint species. Foliage becomes chlorotic and 85:1157–1159.
shows unevenness in growth (606). The plant can be
stunted, internodes are shortened, and the plant even-
tually will die. Wilt infection also increases susceptibil-
ity to winter kill. The pathogen is Verticillium dahliae.
If plants are colonized by the lesion nematode
(Pratylenchus penetrans) the Verticillium wilt problem
can be even more severe. Spearmint is apparently
tolerant to this disease. For more information see the
Verticillium wilt section in the tomato chapter (page 607
360).
References
Hagan, R. A. and Walters, D. R. 1994. Chemical control of rust
on mint. Proceedings of the Brighton Crop Protection
Conference – Pests & Diseases 3:791–796.
Horner, C. E. 1963. Field disease cycle of peppermint rust.
Johnson, D. A. and Santo, G. S. 2001. Development of wilt
in mint in response to infection by two pathotypes of
Verticillium dahliae and co-infection by Pratylenchus
M INT, C ATNIP
penetrans. Plant Disease 85:1189–1192.

Koike, S. T. and Saenz, G. S. 1999. Powdery mildew of spearmint
caused by Erysiphe orontii in California. Plant Disease
83:399.
607 Foliar symptoms of Xanthomonas leaf spot
of catnip.
Ocimum basilicum (608, 609). Infected tissues become soft and rotted.
BASIL Gray sporulation and black, oblong sclerotia can
sometimes form. This pathogen is particularly aggres-
Basil is a widely produced herb in the mint family sive on damaged foliage and on basil stems remaining
(Lamiaceae). The plant has extensive uses as a fresh after a harvest. Gray mold can be a significant post-
leafy vegetable, cooked vegetable, spice and seasoning harvest problem, as well.
in foods, and for teas and medicinal purposes. There is
a broad range of cultivars that have green, purple, or Fusarium oxysporum f. sp. basilicum
maroon-colored leaves, flat or crinkled leaves, and Fusarium wilt
diverse flavors and fragrances. Infected basil plants show stunting, twisted and asym-
metrical growth, and foliar wilting (610). Plants can
Botrytis cinerea eventually collapse and die. Stem and crown xylem
(teleomorph = Botryotinia fuckeliana) tissues show a red-brown to almost black discoloration
Gray mold (611). The pathogen can survive in soil for extended
Gray mold disease affects all above-ground parts of periods, spread via airborne conidia, and be seedborne.
basil. If conditions of high humidity are present, the Worldwide, this disease is an important concern for
pathogen can cause brown leaf and stem lesions to form basil production.
608 610
608 Leaf infection due to gray mold of basil. 610 Wilting and collapsing of basil infected with
Fusarium wilt.
609 Gray mold 611 611 Discolored

609
stem infection of vascular tissue of
basil. Fusarium wilt of
basil.
B ASIL
612 613
621 Leaf lesions caused by Pseudomonas viridiflava on 613 Basil leaf on left is infected with Tomato spotted
basil. wilt virus. Leaf on the right is healthy.
Pseudomonas viridiflava References

Bacterial leaf spot Elmer, W. H., Wick, R. L., and Haviland, P. 1994. Vegetative
Bacterial leaf spot symptoms initially consist of angular compatibility among Fusarium oxysporum f. sp. basilicum
isolates recovered from basil seed and infected plants. Plant
water-soaked spots. These spots rapidly turn black in Disease 78:789–791.
color, but remain vein-delimited (612). Leaf spots often Gamliel, A., Katan, T., Yunis, H., and Katan, J. 1996. Fusarium
develop along the margins of the leaves. wilt and crown rot of sweet basil: involvement of soilborne
and airborne inoculum. Phytopathology 86:56–62.
Garibaldi, A., Lodovica Gullino, M., and Minuto, G. 1997.
Sclerotinia minor, S. sclerotiorum Diseases of basil and their management. Plant Disease
White mold 81:124–132.
White mold disease is caused by two pathogens. Katan, T., Gamliel, A., and Katan, J. 1996. Vegetative
compatibility of Fusarium oxysporum from sweet basil in
Sclerotinia minor causes a brown soft rot to develop on Israel. Plant Pathology 45:656–661.
the lower sections of stems that are in contact with soil. Keinath, A. P. 1994. Pathogenicity and host range of Fusarium
Such stems wilt and plants eventually collapse and rot. oxysporum from sweet basil and evaluation of disease control
White mycelium and small, irregular, black sclerotia methods. Plant Disease 78:1211–1215.
Koike, S. T. 2000. Occurrence of stem rot of basil, caused by
(3–5 mm in diameter) are observed on diseased stems. Sclerotinia sclerotiorum, in coastal California. Plant Disease
The other species, S. sclerotiorum, can cause identical 84:1342.
symptoms if the large, soilborne sclerotia directly infect Koike, S. T. and O’Brien, R. D. 1995. Basil as a host of Sclerotinia
basil stems. However, S. sclerotiorum forms apothecia minor. Plant Disease 79:859.
Little, E. L., Gilbertson, R. L., and Koike, S. T. 1994. First report
and airborne ascospores. These can land on the upper of Pseudomonas viridiflava causing a leaf necrosis on basil.
foliage of basil and cause a brown, soft decay of leaves Plant Disease 78:831.
and upper stems. Infected foliage will also develop Reuveni. R., Dudai, N., Putievsky, E., Elmer, W. H., and Wick, R.
white mycelium and large (5–10 mm) black sclerotia. L. 1997. Evaluation and identification of basil germ plasm for
resistance to Fusarium oxysporum f. sp. basilicum. Plant
For more information see the white mold on bean Disease 81:1077–1081.
section in the legume chapter (page 262). Sharabani, G., Shtienberg, D., Elad, Y., and Dinoor, A. 1999.
Epidemiology of Botrytis cinerea in sweet basil and
Tomato spotted wilt virus (TSWV) implications for disease management. Plant Disease
83:554–560.
Tomato spotted wilt
TSWV causes basil leaves to develop a light green to
yellow mottle, mosaic, and blotches (613). Symptom-
atic leaves can be buckled. TSWV is vectored by thrips.
B ASIL
See also the tomato spotted wilt section in the tomato

chapter (page 364).
Origanum majorana/O. vulgare Physalis ixocarpa

MARJORAM, OREGANO TOMATILLO
Oregano (Origanum vulgare) and sweet marjoram Tomatillo, or tomate verde, is native to Mexico and is a
(Origanum majorana) are two closely related herbs in member of the Solanaceae family. This annual plant is
the mint family (Lamiaceae). Both plants are used for a grown for its relatively small (3–6 cm in diameter)
variety of purposes in cooking. The two species have spherical, light green to yellow fruit that resembles a
similar flavor, with marjoram tending to be milder than small immature tomato. However, the tomatillo fruit is
oregano. noticeably sticky and is encased in an enlarged, papery
sheath or husk (which is a modified calyx). The fruit is
Puccinia menthae used in sauces, salsa, and many other foods.
Rust
Both herbs are susceptible to the same rust pathogen. Fusarium oxysporum
Symptoms on both plants are similar and mostly consist Fusarium wilt
of small (2–5 mm diameter), circular, brown, necrotic Plants affected with Fusarium wilt grow poorly. Foliage
leaf spots that develop cinnamon-brown pustules in the turns chlorotic, and later wilts (615). In advanced stages
center of the spot or in concentric groups around the the foliage turns brown and falls off the plant. The
spot periphery (614). Pustules sometimes develop vascular tissue in lower stems turns brown (616).
without spots. On sweet marjoram, leaf spots can be
surrounded by a chlorotic halo. Ellipsoidal uredin-
iospores measure 22–25 μm x 19–22 μm and contain 615
two to three germ pores in an equatorial configuration.
The pathogen, Puccinia menthae, is regarded as a col-
lective species, and there are numerous strains or races
which show specialization to different host species. For
example, the P. menthae isolates that infect mint are
distinct from those that infect oregano and marjoram.
References
Koike, S. T., Subbarao, K. V., Roelfs, A. P., Hennen, J. F., and
Tjosvold, S. A. 1998. Rust disease of oregano and sweet
marjoram in California. Plant Disease 82:1172.
615 Declining tomatillo infected with Fusarium wilt.
614 616
616 Discolored
vascular tissue of M ARJORAM , O REGANO , T OMATILLO
Fusarium wilt of
tomatillo.
614 Rust pustules on oregano.

Rheum rhubarbarum
617
RHUBARB
Rhubarb is a perennial plant in the Polygonaceae family

that is grown mostly for its thick, edible stalks or stems.
The roots of some rhubarb selections are used for
medicinal purposes. However, the rhubarb leaves are
toxic.
Ascochyta rhei
Ascochyta leaf spot
This disease is common in North America. Symptoms
are small, green-yellow spots that turn brown within a
few days. Spots are variable in size and often have a pale
center, a red margin, and are surrounded by a gray-
617 Tomatillo foliage infected with Turnip mosaic virus. green zone. The centers of individual or coalesced
Healthy foliage on the right. lesions tend to fall out and leave ragged holes. Dark
pycnidia are produced but can be difficult to observe in
618
the lesions. The pathogen is Ascochyta rhei.
Botrytis cinerea
(teleomorph = Botryotinia fuckeliana)
Gray mold
Gray mold is common in forcing sheds where the
humidity is high and soft new growth is easily damaged.
On outdoor crops gray mold can develop after frost
damage on new growth, and after wind damage to
mature foliage. The pathogen is Botrytis cinerea. The
perfect stage, Botryotinia fuckeliana, is rarely observed
628 Tomatillo fruit infected with Turnip mosaic virus. on the crop.
Colletotrichum erumpens
Turnip mosaic virus (TuMV) Anthracnose
Turnip mosaic Anthracnose is caused by Colletotrichum erumpens.
The foliage of affected plants becomes extremely The disease produces small, oval watery spots on
deformed, twisted, and chlorotic (617). Stem internodes petioles. These spots increase in size and number par-
are shortened, giving the leaves a bunched up look. ticularly under warm, humid conditions. Foliage later
Fruit appear blotchy with white and green patterns collapses and there can be postharvest rots of the
(618). TuMV is vectored by aphids. petioles and stems. The diagnostic dark acervuli are
produced abundantly in lesions.
Erwinia carotovora, Pseudomonas marginalis

Bacterial soft rot
Two bacterial pathogens cause water-soaked, slimy rots
T OMATILLO
on rhubarb stalks. Severely affected stems can collapse.

This disease occurs both in the field and in postharvest
storage situations. Bacterial soft rot is caused by
Erwinia carotovora and Pseudomonas marginalis.
Puccinia phragmitis
619
Rust
Rust is caused by the fungus Puccinia phragmitis and is
occasionally reported on rhubarb, causing red or deep
purple leaf spots that measure 5–15 mm in diameter
(620, 621). Dense clusters of the aecidial stage are
produced at the center of the leaf spots; aeciospores
measure 16–26 μm and appear white on the leaf. The
urediniospores and teliospores are formed on the
alternate host, water reed (Phragmites communis).
Pythium spp., Phytophthora spp.

Root rot diseases
Various root rots have been recorded on rhubarb,
notably those caused by Pythium and Phytophthora
619 Discolored rhubarb crown tissue caused by Erwinia species when sites are poorly drained. Violet root rot
crown rot. (Helicobasidium brebissonii), Armillaria root rot
(Armillaria mellea), and southern blight (Sclerotium
rolfsii) are occasionally detected.
Erwinia rhapontici
620
Crown rot
Crown rot is caused by the bacterium Erwinia rhapon-
tici, which results in a rot of the terminal bud. The rot
may extend into the central pith (619), where a dark
brown soft rot develops and then breaks down to form
cavities. Side shoots can grow from infected plants, but
these shoots often wilt and rot. In wet weather, older
leaves can develop rot. Infection is thought to be asso-
ciated with wounds, and the stem and bulb nematode
(Ditylenchus dipsaci) may spread the pathogen.
Peronospora jaapiana 620 Rust disease on rhubarb leaf.

Downy mildew
Severe attacks of downy mildew, caused by Perono-
621
spora jaapiana, have occurred in eastern England in
recent years. Downy mildew is a destructive disease on
seedlings but also affects crops at any stage. Symptoms
are large, brown leaf lesions that bear a purple-white
fungal growth on the undersurface. Small spots often
disintegrate and cause foliage to have a tattered appear-
ance. Severe infection results in leaf death, reducing
yield in the following year.
R HUBARB
621 Underside of rhubarb leaf infected by rust.

Rorippa nasturtium-aquaticum
622
WATERCRESS
Watercress is a crucifer plant (family Brassicaceae) that

is usually started as a transplant and then later placed in
specially constructed beds with shallow water (10–15
cm deep). There is slow movement of water through the
bed (usually from an underground source and at a
constant temperature of 10–12º C), so waterborne
problems are a significant threat to production.
622 Circular to oval tan leaf spots on rhubarb caused by Peronospora parasitica
Ramularia rhei. (= Hyaloperonospora parasitica), Septoria sisymbrii
Downy mildew, Septoria leaf spot
There are several minor foliar diseases of watercress
Ramularia rhei including downy mildew (Peronospora parasitica) and
Ramularia rot Septoria leaf spot (Septoria sisymbrii). Downy mildew
Ramularia rot occurs in Europe, North America, and causes yellow blotches on leaves (623) with white
New Zealand. The disease causes oval sunken lesions sporulation on the leaf underside. It is most often found
on leaf stalks and leaves (622). It can cause crop loss in autumn and spring when humidity is high and there
and hence justifies a program of fungicide sprays when is poor air circulation. See also the downy mildew
infection occurs early in the season. The pathogen is section in the brassica chapter (page 178).
Ramularia rhei. Septoria sisymbrii develops on the lower leaves as
small (5–10 mm) pale brown or yellowish spots con-
Virus diseases taining prominent dark pycnidia (624). Spread occurs
Rhubarb is affected by a number of viruses. Turnip by splashing water. Septoria may originate from
mosaic virus (TuMV) is the most important, but Arabis infected debris, wild hosts, or be seedborne.
mosaic virus (ArMV), Cucumber mosaic virus (CMV),
Cherry leaf roll virus (CLRV), and Strawberry latent Spongospora nasturtii
ringspot virus (SLRSV) have been reported. Aphids are Crook root
the vectors for TuMV and CMV. ArMV, CLRV, and Crook root was first recorded in Wiltshire, England, in
SLRSV have nematode vectors while ArMV and CLRV 1947. It is a serious threat to commercial production in
may be seedborne. Combinations of different viruses parts of Europe and the USA and also occurs on wild
may occur in the same plant, producing leaf mosaic and watercress. It is caused by Spongospora nasturtii, which
ring spot symptoms. Foliar growth may be stunted. is now classified as a protozoan (like the clubroot
pathogen of crucifers) rather than as a fungus. This
References pathogen causes stunting and chlorosis of the foliage.
Ormrod, D. J., Sweeney, M. E., and MacDonald, L. S. 1985. Diseased roots are swollen and brittle with a character-
Effect of fungicides on Ramularia leaf and stalk spot of istic curved or crook-like appearance. The roots decay
rhubarb in coastal British Columbia. Canadian Plant Disease
Survey 65:29–30. and plants may float away. Symptoms are most pro-
Sellwood, J. E. and Lelliot, R. A. 1978. Internal browning of nounced when temperatures are low, appearing from
hyacinth caused by Erwinia rhapontici. Plant Pathology October through to April under UK conditions.
27:120–124.
Symptoms often appear first near the water outlet and
Tomlinson, J. A. and Walkey, D. G. A. 1967. The isolation and
identification of rhubarb viruses in Britain. Annals of Applied spread back up the bed towards the water inlet. Plants
Biology 59:415–427. show some recovery as temperatures rise in the spring.
R HUBARB
Walkey, D. G. A., Creed, C., Delaney, H., and Whitwell, J. D. In addition, S. nasturtii is the vector of two viruses
1982. Studies on re-infection and yield of virus-tested and
commercial stocks of rhubarb cv. Timperley Early. Plant
affecting watercress: Watercress yellow spot virus and
Pathology 31:253–260 Watercress chlorotic leaf spot viroid.
Virus diseases 623

Watercress is susceptible to several virus pathogens.
Turnip mosaic virus (TuMV) is synonymous with
Watercress mosaic virus. The symptoms include green
and yellow mottling, yellowish spotting, leaf distortion,
and mosaics. Affected plants are usually stunted. It is
common in Europe, where it is spread by aphids, par-
ticularly Myzus persicae and Brevicoryne brassicae.
Turnip yellow mosaic virus is also common in water-
cress and is transmitted by the mustard beetle (Phaedon
cochleariae) and flea beetles (Phyllotreta spp.).
Watercress chlorotic leaf spot viroid (WCLVd)
initially causes small (3–5 mm), bright yellow or golden 623 Downy mildew of watercress.
spots to appear on leaves (625), followed by more
numerous spots, many of which are chlorotic and 624 Septoria leaf 624
measure 3–9 mm in diameter. Badly affected plants are spot of watercress.
unmarketable. Symptoms appear when temperatures
are low (less than 10º C) and fade when plants are
grown at 10–15º C. The affected plants often have
crook root symptoms because the crook root pathogen
(Spongospora nasturtii) is the vector of WCLVd.
Initially thought to be a virus, WCLVd is a viriod and
consists of an RNA genome that lacks a protein coat.
Watercress yellow spot virus (WYSV) has been
reported in France since 1962 and southern England
since 1983. It causes bright yellow spots, irregularly
shaped yellow blotches, and sometimes ringspots. The
vector is the crook root fungus Spongospora nasturtii.
The virus has isometric particles that are reported to be
27 nm in diameter in French isolates and 37–38 nm in
isolates from England.
625 Watercress 625
References chlorotic leaf spot
Claxton, J. R., Arnold, D. L., Blakeley, D., and Clarkson, J. M. viroid on water-
1995. The effects of temperature on zoospores of the crook cress.
root fungus Spongospora subterranea f. sp. nasturtii. Plant
Down, G. J. and Clarkson, J. M. 2002. Development of a PCR-
based diagnostic test for Spongospora subterranea f. sp.
nasturtii, the causal agent of crook root of watercress
(Rorippa nasturtium-aquaticum). Plant Pathology
51:275–280.
Gungoosingh, A., Beni Madhu, S. P., and Dumur, D. 2001. First
report of turnip mosaic virus in watercress in Mauritius. Plant
Disease 85:919.
Hashimoto, T., Kimura, T., and Katsuki, S .1987. [Leaf spot
disease of watercress (Rorippa nasturtium-aquaticum Hayek)
WATERCRESS
caused by Cercospora nasturtii Passerini.] Scientific Report of

the Miyagi Agricultural College No. 35:77–79.
Stevens, C. P. 1983. ADAS/MAFF Reference Book 136.
Watercress: Production of the cultivated crop. Grower Books,
London, 56 pp.
Strandberg, J. O. and Tucker, C. A. 1968. Diseases of watercress

in Florida. Proceedings of Florida State Horticultural Society 626
81:194–196.
Tomlinson, J. A. 1958. Crook root of watercress. I. Field
assessment of the disease and the role of calcium bicarbonate.
Tomlinson, J. A. 1958. Crook root of watercress. III. The causal
organism Spongospora subterranea (Wallr.) Lagerh. f. sp.
nasturtii f. sp. nov. Transactions of the British Mycological
Society 41:491–498.
Tomlinson, J. A. and Hunt, J. 1987. Studies on watercress
chlorotic leaf spot virus and on the control of the fungus
vector (Spongospora subterranea) with zinc. Annals of
Tomlinson, J. A. and Hunt, J. 1987. Studies on watercress
chlorotic leaf spot virus and control of the fungal vector
(Spongospora subterranea) with zinc. Annals of Applied
Biology 110:75–88.
Walsh, J. A, Clay, C. M., and Miller, A. 1989. A new virus disease 626 Sage crown and roots infected with Phytophthora
of watercress in England. EPPO Bulletin 19:463-470.
cryptogea.
Walsh, J. A. and Phelps, K. 1991. Development and evaluation of
a technique for screening watercress (Rorippa nasturtium-
aquaticum) for resistance to watercress yellow spot virus and
crook-root fungus (Spongospora subterranea f. sp. nasturtii). 627
Salvia officinalis
SAGE
Sage is a commonly grown herb from the mint family
(Lamiaceae). It is widely used as a seasoning and ingre-
dient in cooking. There are numerous varieties having
different leaf shapes and colors.
Powdery mildew
Typical white growth of powdery mildew develops on
the mature foliage of sage. Under favorable warm, dry
conditions, there can be active development on young
leaves. As plants are often cropped for several years,
powdery mildew can survive by overwintering on the
lower stems. The pathogen is Golovinomyces cicho- 627 Seedling sage infected with Phytophthora
racearum (previously named Erysiphe cichoracearum). cryptogea. Healthy plant on right.
Phytophthora cryptogea
Phytophthora root rot References
Phytophthora root rot causes roots to turn necrotic and Koike, S. T., Henderson, D. M., MacDonald, J. D., and Ali-
black (626). Crowns and lower stems also turn black. Shtayeh, M. S. 1997. Phytophthora root and crown rot of
sage caused by Phytophthora cryptogea in California. Plant
S AGE
Affected plants can wither and die (627). The pathogen Disease 81:959.
is Phytophthora cryptogea.
Tragopogon porrifolius, Scorzonera hispanica

628
SALSIFY, SCORZONERA
Salsify (Tragopogon porrifolius) and black salsify or

scorzonera (Scorzonera hispanica) are members of the
Asteraceae and are grown for their edible taproots.
Both commodities are steamed or otherwise cooked
prior to eating.
Albugo tragopogonis
White rust
White rust is the most common and important disease
on salsify and black salsify. The pathogen affects closely
related wild and ornamental species including Gerbera
and sunflower. The characteristic small white blisters
occur on leaves (628) and stems (629) and develop after
initial chlorotic spotting. Severe infection can cause
death of plants.
Puccinia hysterium, P. jackyana

Rust
There are occasional problems with the autoecious rust
Puccinia hysterium infecting salisfy. In the spring this 628 White rust on salsify leaf.
rust produces aecia that deform the new growth.
Aecidiospores are produced and measure 20–30 x 629
18–24 μm; however, this species does not have uredin-
iospores. Brown teliospores are uniseptate, variable in
size, and mostly measure 30–44 x 22–30 μm.
Teliospores are produced on the stems. On black salsify,
the rust pathogen is P. jackyana, which produces aecia
and uredinia. Puccinia scorzonerae is a form of
P. jackyana which does not produce aecia.
S ALSIFY, S CORZONERA
629 White rust on salsify stem.

Valerianella locusta, V. olitoria

630
CORN SALAD
Corn salad is a leafy vegetable that is also known as

lamb’s lettuce, field salad, and fetticus. The plant is in
the Valerianaceae family. The term ‘mache’ is a market
term applied to corn salad. The plant is grown for its
succulent leaves that are used in salads or as cooked
greens.
Golovinomyces orontii
Powdery mildew
On corn salad, powdery mildew forms white mycelium
and conidia on both sides on leaves (630), causes slight 630 White fungal growth of powdery mildew on
twisting of foliage, and results in quality loss of the corn salad.
harvested product. Severely affected leaves turn necrotic
and collapse, and such plants are not harvested. 631
Conidia are cylindric to doliform, measure 27–32 x
15–17 μm, and lack fibrosin bodies. Conidial length-to-
width ratios are usually less than, or equal to, 2.0.
Conidia germinate at the ends (cichoracearum-type).
No cleistothecia have been observed. The pathogen is
Golovinomyces orontii (previously named Erysiphe
orontii).
Sclerotinia minor
White mold
White mold infections cause a gray-brown soft rot to
develop on crowns and lower sections of stems.
Affected stems wilt and plants eventually collapse and
rot (631). White mycelium and small, irregular, black 631 Diseased corn salad crowns infected with
sclerotia (3–5 mm in diameter) are observed on infected Sclerotinia minor.
stems and crowns. The pathogen is Sclerotinia minor.
For more information see the white mold on bean
section in the legume chapter (page 262).
References
Koike, S. T. and Saenz, G. S. 2005. First report of powdery
mildew caused by Golovinomyces orontii on corn-salad in
Koike, S. T. 2003. Sclerotinia stem and crown rot of corn-salad
caused by Sclerotinia minor in California. Plant Disease
87:1264.
C ORN S ALAD
Zea mays var. saccharata 632 Stalk rot of 632

SWEETCORN sweetcorn caused
by Fusarium verti-
Sweetcorn or sugar corn is a variety of maize, Zea mays cillioides (syn.
var. saccharata (family Poaceae). Baby corn refers to F. moniliforme).
standard corn cultivars that are harvested when the ears
are very small and before they develop the silk.
Fusarium spp.
Stalk rot
Root, stem, and ear diseases of sweetcorn are caused by
various Fusarium species. These Fusarium diseases are
of particular concern because some of these pathogens
produce mycotoxins such as fumonisin, zearalenone,
and trichothene. Stalk rot produces a gray coloration in
the foliage of mature plants. This discoloration is often
followed by wilting and yellowing as the plant senesces
prematurely. Plants break off at the basal internode 633 Smut galls on
633
(632), resulting in considerable crop lodging. The stem cob of sweetcorn.
base has red-brown internal discoloration and rotting
of the internodes and pith. There are several species of
Fusarium involved, and laboratory isolation is required
to identify them: F. avenaceum, F. culmorum, F. gramin-
earum, F. poae, F. verticillioides (= F. moniliforme).
Ustilago maydis
Maize smut
This disease occurs worldwide and is both seedborne
and soilborne. Affected cobs are unmarketable, but
losses are usually limited except where sweetcorn is
grown continuously or in short rotations. Symptoms
occur at any growth stage but are often only noticed
close to harvest when cobs are examined. The most
obvious symptoms consist of conspicuously swollen,
white to gray galls on the cobs or on other aerial parts
of the plant (633). The galls vary in size from a few mil-
limeters to several centimeters in diameter. At maturity
the galls break open and release a dark brown or black
mass of chlamydospores (also known as brand spores
or smut spores). These spores are globose to elliptical, References
have blunt spines, and measure 8–12 μm in diameter. Banuett, F. 1992. Ustilago maydis, the delightful blight. Trends in
Spores are dispersed by wind or insects such as frit fly Genetics 8:174–180.
Magan, N., Marin, S., Ramos, A. J., Sanchis, V. 1997. Impact of
(Oscinella frit). Infection often occurs in young meris-
ecological factors on germination, growth, fumonisin
tematic tissues or through wounds. The pathogen production by F. moniliforme and F. proliferatum and their
S WEETCORN
(Ustilago maydis) remains localized and does not interactions with other common maize fungi. Cereal Research
Communications 25:643–646.
become systemic. In Mexico and the USA, the young
Pataky, J. K. and Chandler, M. A. 2003. Production of
galls are considered a delicacy and are eaten before the huitlacoche, Ustilago maydis: timing inoculation and
spores form and mature. controlling pollination. Mycologia 95:1261–1270.
422
Glossary
Abiotic Pertaining to nonliving factors. Agonomycetes One of three subgroups Anastomosis The fusion of one fungal
Abiotic problems of plants are often of mitosporic fungi (the other two hypha with another. This fusion usually
caused by environmental factors. groups are hyphomycetes and results in combination and exchange of
coelomycetes). Mitosporic fungi (also genetic material. For some fungi, such as
Abscission The physiological process known as deuteromycetes or fungi Rhizoctonia species, anastomosis
in which leaves, petioles, flowers, and imperfecti) do not have sexually groups are used to classify and differen-
fruits fall off the plant, either as a produced spores. Agonomycetes are tiate isolates (the method is called vege-
natural part of plant senescence or as the asexual fungi that are sterile and do not tative compatibility pairing).
result of infection and disease. make any spores at all. An example of
an agonomycete is Rhizoctonia solani. Antagonism The interaction between
Acervulus A small, saucer-shaped, microorganisms in which one species
fungal fruiting body that produces Alga A primitive, non-vascular plant inhibits, competes with, or kills a second
asexual conidia. Acervuli are embedded ranging from microscopic single-celled species. The antagonist accomplishes
within plant host tissue. Some dark species to large, multicelled species such this inhibition through competition for
acervuli can be seen as small dark specks as seaweed. Most algae are aquatic. A resources, parasitism, predation, or the
or dots within symptomatic tissue, while few algae (an example is Cephaleuros production of toxic substances.
others are colorless. An example of a virescens, a green alga) are pathogens of
fungus that produces dark acervuli is higher vascular plants. Recent Antheridium Specialized male
Colletotrichum. taxonomic research indicates that the structure for fungi that have sexual
oomycete group, an important group of phases. Antheridia form male sexual
Actinomycete A microorganism that pathogens, is closely related to algae. cells (gametes).
forms branching filaments which later
break into fragments that look like indi- Allele One of two or more alternate Anthocyanin Water-soluble, flavonoid
vidual bacterial cells. Actinomycetes are forms of a gene. Corresponding alleles plant pigments that are blue, purple, or
classified as a type of Gram-positive are located at the same place on a partic- red in color. In some plant species, the
bacterium and are often found in soil. ular chromosome. development of anthocyanins in plant
An example of an actinomycete is tissue indicates that the plant is
Streptomyces. Alternate host One of two distinct damaged, diseased, or under stress.
kinds of plants that serve as hosts for
Aeciospore One of the several different some pathogenic fungi. Some rust Anthracnose The common name used
types of rust fungi spores. Aeciospores species, for example, require alternate for some foliar plant diseases that are
are borne in and on aecia and germinate hosts to complete its life cycle. caused by fungi (acervular
to form dikaryotic mycelium. Some ref- coelomycetes) that produce acervuli. An
erences call these spores aecidiospores. Anaerobic Referring to environmental example of this kind of fungus is
See also urediniospore, teliospore, and conditions, usually in the soil, in which Colletotrichum.
basidiospore. oxygen levels are not sufficient for
normal physiological growth of most Antibiotic A chemical that is produced
Aecium The fruiting structure of rust organisms. Under such conditions, only by one microorganism and which can
fungi that produces aeciospores. specialized organisms such as anaerobic inhibit or kill other microorganisms.
bacteria can survive.
Aerobic Referring to environmental Antibody A protein that is produced by
conditions, usually in the soil, in which Anamorph The asexual stage of a the lymphatic system of warm-blooded
oxygen levels are sufficient for normal fungus. Spores and propagules animals in response to the presence of a
physiological growth of most produced in this stage do not involve foreign protein or substance. The
organisms, including plants. sexual recombination or processes. This foreign substance is called an antigen.
form of fungi is also called the imperfect The antibody reacts to the antigen,
Agar A gelatinous substance that is stage. Anamorphs are placed in a binds with it, and causes the antigen to
extracted and purified from algae. Agar category that uses one of the following become inactive. This antibody–antigen
is an ingredient in semi-solid culture synonymous names: mitosporic fungi, interaction is the basis for serology and
media that are used for culturing deuteromycetes, fungi imperfecti. pathogen detection techniques such as
bacteria and fungi. ELISA.
G LOSSARY 423
Antigen A substance, usually a protein, Aseptate Referring to fungal hyphae Basidium The specialized cell, usually
that is foreign to the body of warm- that do not have cross walls. A synonym club shaped, that produces and bears
blooded animals. Scientists intentionally for aseptate is coenocytic. The aseptate externally formed basidiospores. Fungi
inject plant pathogen antigens into nature of certain fungi is used in classifi- that produce basidia are placed in the
animals so that antibodies are produced. cation systems. basidiomycete group.
The resulting antibodies can be used in
serological tests to detect the presence of Aseptic Free of living microorganisms. Binucleate Referring to a cell that
the plant pathogen. contains two nuclei.
Asexual Reproduction that does not
Antiserum The serum part of a warm- involve gamete union and meiosis. Bioassay A test that uses a living
blooded animal’s blood that contains Fungi that do not reproduce sexually are organism to measure that organism’s
antibodies to introduced antigens of called imperfect or anamorphic fungi. sensitivity to a chemical substance or
plant pathogens. Various antisera are susceptibility to a pathogen.
used in serological tests such as ELISA. Autoecious fungus A pathogenic
fungus that completes its entire life cycle Biological control The control or man-
Aphid Small, soft bodied insect in the on one host plant. Rust fungi are good agement of a pathogen or pest by means
order Homoptera. Aphids cause examples of this life cycle. Compare of another living organism. The biologi-
problems by direct feeding on plant with heteroecious. cal control agent can act in various
tissues, producing honeydew that causes ways: predator, parasite, competitor.
plant surfaces to be sticky and discol- Avirulent Referring to an organism
ored, and vectoring virus pathogens. that is nonpathogenic and unable to Biotechnology The study, design, and
cause disease. use of genetically modified organisms
Apical Referring to the end or upper (GMOs). Also, the modern techniques
part of a structure. Bacillus (such as sequencing and inserting genes)
A bacterium that is rod-shaped. used in manipulating DNA and other
Apothecium Fruiting body of genetic material.
ascomycete fungi that is a cup or vase Bactericide
shaped structure that usually forms on A chemical or substance that kills Biotic Pertaining to living organisms.
top of a stalk. The fertile layer of the bacteria. Biotic problems of plants are usually
apothecium is lined with ascospore- Bacterium A microscopic, single-celled called diseases and are caused by fungi,
producing asci. organism, usually but not always bacteria, viruses, and other micro-
enclosed in a rigid cell wall. Bacteria do organisms.
Appressorium A fungal cell that is not have membrane-bound nuclei and
often enlarged and which attaches the are therefore classified as prokaryotes. Biotype A subgroup or subdivision of a
fungus to the plant host surface. The science and study of bacteria is bac- species or race. The individual
teriology. organisms making up the biotype share
Ascocarp The fruiting body of common features and genetics. Similar
ascomycete fungi. The different shapes Bar Unit of pressure that expresses to physiologic race and strain.
(apothecium, cleistothecium, peri- water potential, with 1.013 bar = 1
thecium, pseudothecium) all have asci atmosphere. Bitunicate ascus An ascus having a
that contain ascospores. double wall. Bitunicate asci are charac-
Basal Referring to the base or bottom teristic of certain groups of ascomycetes.
Ascomycete One of the major divisions part of a structure.
of fungi having a perfect or sexual stage. Blast The plant disease symptom of
All ascomycetes have sexual spores Basidiomycete One of the major death of buds, flowers, or young fruit.
(ascospores) that are produced within a divisions of fungi having a perfect or
sac-like or club-shaped structure (ascus). sexual stage. All basidiomycetes have Bleached The plant disease symptom
sexual spores (basidiospores) that are of light- colored to white tissue, particu-
Ascospore The sexually produced spore produced and borne on pegs (sterigma) larly of the foliage.
that is formed within the ascus of that extend from a specialized cell called
ascomycete fungi. the basidium. Blight The plant disease symptom of
extensive withering and dying of leaves,
Ascus The sac-like or club-shaped Basidiospore The sexually produced flowers, shoots, fruit, or the entire
structure in which ascospores are spore that is produced on the club above-ground portion of the plant.
formed. Asci are contained within shaped structure, the basidium, of
various ascocarp forms. Asci-producing basidiomycete fungi. Basidiospores are Blotch The plant disease symptom of
fungi are placed in the ascomycete usually haploid. large, irregular, necrotic spots or areas
group. on foliage.
424 G LOSSARY
Bordeaux mixture One of the first Chlorophyll The green, light-sensitive Clone A population of organisms or
fungicides, consisting of copper sulfate pigment found in the chloroplasts of cells that is genetically identical and was
and lime. leaves and other green organs of plants. produced asexually from one such
Chlorophyll uses light energy to convert organism or cell.
Bract A modified leaf that is associated water and carbon dioxide into food via
with a flower structure. photosynthesis. Plant diseases can Coalesce Merging or growing together
interfere with this process. Some through growth and expansion. For
Broadcast The act of spreading seed, pathogens prevent the normal some disease symptoms, such as leaf
fertilizers, pesticides, or other amend- formation of chlorophyll. spots, continued growth of adjacent
ments evenly over the soil surface and spots can result in a merging together, or
not in lines. Chlorosis The plant disease symptom coalescence.
of fading, yellowing, and whitening of
Canker A diseased area that has well green leaves, stems, and other foliage. Coelomycetes One of three subgroups
defined edges, is localized, and occurs Chlorosis occurs when plant chloro- of mitosporic fungi (the other two
on stems, twigs, branches, or trunks of phyll fades, is degraded, or does not groups are hyphomycetes and agono-
plants. Cankers are usually necrotic and form. Yellowing is generally considered mycetes). Mitosporic fungi (also known
sunken in appearance. a synonym of chlorosis. as deuteromycetes or fungi imperfecti)
do not have sexually produced spores.
Capsid The protein coat of viruses that Chromista The name of the taxonomic Coelomycetes are asexual fungi that
forms the outer shell of the virus kingdom that some taxonomists believe produce spores in pycnidia, acervuli, or
genome. should contain the important oomycete other similar structures.
Carotenoid A plant compound that is pathogen group. Kingdom Chromista is
usually yellow or red in color. Examples distinct from fungi and contains certain Coenocytic Referring to fungal hyphae
of carotenoids are carotenes and xan- types of primitive golden algae, diatoms, that do not have cross walls. A synonym
thophylls. and giant kelp. However, other for coenocytic is aseptate. The coenocyt-
researchers believe the appropriate ic nature of certain fungi is used in clas-
Catenulate Referring to the develop- name for this group should be Kingdom sification systems.
ment of objects in chains or attached Straminipila.
end-to-end. Powdery mildew spores Colonize To grow and become estab-
often grow in sequential chains and are Circulative virus Referring to a plant lished on either a host plant or in
therefore catenulate. pathogenic virus that is acquired by an culture.
insect vector, accumulates internally in
Causal agent The organism that is the insect, then is transmitted to plants. Colony Growth of a microscopic
responsible for causing the disease in organism, usually on culture media, to
question. Causal agents include Cirrus A small mass of spores exuded the degree that the growth is visible with
bacteria, fungi, phytoplasmas, from fungal fruiting bodies called the unaided eye.
nematodes, viruses, and viroids. pycnidia. Cirri are curled, tendril-like,
and held together by a slimy matrix Complex (as in disease complex)
Certification A registration procedure material. Also called a tendril. Referring to the situation in which a
in which an official agency declares plant disease is caused by more than one
plant material to be acceptably free of Clamp connection A hyphal pathogen or factor.
pathogenic organisms, weeds, and pests. outgrowth that occurs on the hyphae of
Plant material can also be certified to be some basidiomycete fungi. During cell Compost A mixture of plant residues
true-to-type and therefore representa- division the clamp connection makes a and other organic materials that has
tive of the cultivar name. Certification link between the two resulting cells. been incubated and managed to allow
procedures are based upon tests and for decomposition and aging. Composts
inspections of the plant material. Clavate A club-shaped structure. The are used as soil amendments for plants,
base of the structure is narrower than and in some circumstances may have
Chlamydospore Usually a single- the apex. Some fungal structures are possible disease suppressing effects.
celled, thick-walled asexual spore described as being clavate in shape.
produced within a hypha by a fungus. Concentric spot The plant disease
Chlamydospores enable the fungus to Cleistothecium Fruiting body of symptom where multiple circles (which
survive unfavorable conditions. ascomycete fungi that is an entirely usually are alternating in appearance
enclosed, spherical structure. The inner between dark and light colors) form
cavity of cleistothecia contains within one larger circle or lesion. All the
ascospore producing asci. circles share the same center. This
symptom is also called ring spot.
G LOSSARY 425
Conical A cone-shaped structure. Some Cull The unusable or unmarketable Defoliate The plant disease symptom
fungal structures are conical in shape. portion of the harvest that is left in the of the dropping of leaves from a plant.
field or is discarded after harvest. For perennial deciduous plants, defolia-
Conidiogenous cell Any fungus cell tion is a normal process of senescence.
that directly produces one or more Cultivar (abbreviation: cv.) A cultivat-
conidia ed variety of plant. All individuals of a Dematiaceous Referring to fungal
particular cultivar share characteristic spores and structures that are darkly
Conidiophore The specialized hypha features. Cultivar is generally used syn- colored.
that bears one or more conidiogenous onymously with variety.
cell. Deuteromycetes Fungi (also known as
Culture (V.) to grow microorganisms mitosporic fungi or fungi imperfecti)
Conidium An asexually produced, or plant cells on prepared media and that do not have sexually produced
non-motile spore, primarily from under controlled, artificial conditions. spores. This is an artificially created
deuteromycete fungi (also called (N.) the growth and colonies of group and is not an official taxonomic
mitosporic fungi or fungi imperfecti). microorganisms or plant cells on category. Deuteromycetes can be further
Conidia form from, and externally to, a prepared media and under controlled organized based on the way that spores
conidiogenous cell. Conidia do not conditions. are made (see hyphomycetes, agono-
develop as a result of the division of mycetes, coelomycetes). While a
cytoplasm within a specialized structure Cylindrical Round in cross section and deuteromycete fungus does not produce
(see sporangiospore). Conidia are of equal width throughout the length. any sexual spore, some deuteromycetes
released from the conidiogenous cells Some fungal structures are cylindrical in can enter a phase of development in
and serve to disperse the organism. shape. which it becomes associated with a
sexual form (an ascomycete or a basid-
Contaminant A substance or organism Cyst In fungi and oomycetes, a resting iomycete teleomorph). In such situa-
that makes an otherwise pure culture or spore or propagule that usually is tions, the deuteromycete is called the
system impure, unfit, and unclean. enclosed in a protective, thick cell wall. anamorph form of that teleomorph.
Such encysted cells can survive during
Coremium A reproductive structure of unfavorable conditions. In nematodes, Diagnosis The systematic, problem-
asexual fungi. See synnema. the resilient, hardened outer body of solving process of identifying the cause
non-viable females in the genera of a plant problem or disease.
Cotyledon The first leaf (monocot Heterodera and Globodera. These cysts
plants) or a leaf of the first leaf pair enclose and protect eggs of these Dieback The plant disease symptom of
(dicot plants) developed by the embryo nematodes. a progressive decline and death of plant
of a seed plant. parts. Dieback usually begins at the tip
Damping-off A disease affecting seeds of the roots or branches, then progresses
Cover crop Plants that are seeded, and young seedlings, caused by towards the main part of the host.
grown, and used to add organic matter soilborne pathogens. The disease has
to fields, improve soil conditions, reduce different aspects. Planted seeds can be Differential hosts A series of different
erosion, retain nutrients in soil profiles, infected and die. Seeds may germinate, cultivars or lines of a particular plant
and provide a rotation for agronomic but the resulting seedling may become species, each line of which varies in sus-
cash crops. infected and die prior to emerging above ceptibility to a given pathogen.
ground (pre-emergence damping-off). Inoculating such a series of differential
Crop rotation In a given field, the Seedlings may emerge above ground but hosts can help identify pathogen races.
practice of not growing the same crop later become infected and die (post-
consecutively or too frequently in emergence damping-off). Diploid The genetic condition in which
sequence. Crop rotation strategies use an organism has twice the number of
diverse crops from different plant Decay The plant disease symptom of chromosomes (2n) as the haploid (1n)
groups and families. Poor crop rotation decomposition and rotting of plant condition.
can increase problems with soilborne tissue.
pathogens. Disease Any abnormality in a plant’s
Decline The plant disease symptom of growth, development, functioning,
Crown Typically the lower base of a reduced plant vigor and deterioration of value, or appearance due to the activity
plant from which both the main root a plant’s condition and growth. of a pathogenic, biotic agent. A disease
and above ground stems or trunk arise. results in symptoms caused by the
The crown is the tissue that serves as the Decomposition Breakdown and pathogens. Injury or effect from an
root-stem junction. Note that for trees, rotting of plant tissue, usually caused by abiotic agent is usually considered a
the crown refers to the upper part, from microorganisms. disorder.
which the foliage emerges.
426 G LOSSARY
Disease cycle The sequence of events Echinulate Having sharply pointed Enzyme A complex protein that
that takes place during disease spines. This term is used to describe catalyzes a specific biochemical reaction
development, appearance of disease spiny textures on fungal spores, conidio- but which is not changed or degraded
symptoms, and growth and develop- phores, and other structures. during the reaction. Some plant
ment of the pathogen. A synonym is echinate. pathogens release enzymes that break
down plant tissues.
Disease triangle The pathology Ecology The study of the interrelation-
concept in which all plant diseases can ships between organisms and their envi- Epidemic Widespread and rapidly
be analyzed and understood in terms of ronments. developing outbreak of an infectious
three components: host, pathogen, and disease. This term is commonly used for
environment. Electron microscope A specialized diseases of all organisms, including
microscope that uses a focused beam of plants. Such an outbreak in plants can
Disinfectant A chemical or treatment electrons to create images of tiny, sub- also be called an epiphytotic.
(such as steam or heat) that kills or inac- cellular structures and entities. For
tivates microorganisms once such agents example, electron microscopy is the Epidemiology The science and study of
have infected a plant. only means of seeing virus particles. the factors influencing disease develop-
ment, outbreak, and spread.
Disinfestant A chemical or treatment ELISA Enzyme-linked immunosorbent
(such as steam or heat) that kills or assay. A serological method that uses Epidermis The outer layer of cells that
removes microorganisms from the antibodies to recognize and detect target line the surfaces of plant tissues.
surfaces of plants, seeds, tools, working antigens of pathogens and other
surfaces, and other objects. organisms. The ELISA method uses Epinasty The plant disease symptom of
polystyrene microtiter plates and abnormal downward twisting, curling,
Disorder Any abnormality in a plant’s registers a positive test by a color change or bending of leaves and other above-
growth, development, functioning, in the reaction liquid. ground parts.
value, or appearance due to the effects
of an abiotic factor. A disorder results in Ellipsoidal Elliptical or oval in shape. Epiphyte An organism that is present
symptoms caused by these nonliving Some fungal spores are ellipsoidal. and growing on the surface of a plant,
factors and is not infectious. Injury or but which has not infected the plant.
effect from a biotic agent is usually con- Emergence Appearance of plant struc-
sidered a disease. tures, primarily shoots, above the soil Epiphytotic Widespread and rapidly
surface following germination of seeds developing outbreak of an infectious
DNA Deoxyribonucleic acid. DNA is and below-ground growth of the disease of plants. Such an outbreak in
any of various nucleic acids that occur in seedling. plants can also be called an epidemic.
nuclei (for eukaryotes) or cell contents
(for prokaryotes) of living organisms. Enation Typically small, malformed Eradicant A chemical substance that
DNA molecules are composed of tissue and swellings that occur on leaves can stop the growth of a pathogen even
repeating sub-units of deoxyribose (a and other organs of plants. if the pathogen has already infected the
five-carbon sugar), phosphoric acid, and host plant.
four nitrogenous bases (adenine, Encyst When fungi or oomycete spores
cytosine, guanine, and thymine). form a cyst. Eradicate To control plant pathogens
by completely eliminating them from
Dolipore septum A complex septum Endemic Native or naturally occurring plant tissue or planted area. Complete
found in hyphae of some basidiomycete to a region or area. eradication is rarely possible.
fungi. This septum has a barrel-shaped
structure in the middle of the septum. Endophyte An organism, particularly a Erumpent The act of breaking through
fungus, that lives inside a plant but to the outside of a surface. This term is
Dominant gene A gene that is fully produces no external signs of infection. often used for pathogenic fungi that
expressed and completely dominates the colonize plant tissues and later form
phenotype of the organism. When Environment The complete surround- erumpent fruiting bodies that break
paired with a corresponding gene or ings, conditions, and forces that through the plant epidermis.
allele, the dominant gene will be the one influence living organisms. For a suscep-
that is expressed. tible plant host to become infected by a Escape The situation that exists when a
virulent pathogen, environmental condi- susceptible plant avoids infection and
tions favorable for disease development subsequent disease due some feature of
must occur. the plant or because the plant is located
where there are no pathogens.
G LOSSARY 427
Etiology The science of the causes of Flagellum The flexible whip-like or Free-living Referring to an organism
diseases, including the study of the hair-like filament that is found on the that is able to survive in the environment
responsible agents and their interactions cells of zoospores and some bacteria. without dependence on a host
with the host. The twisting of the flagella enables these organism.
cells to swim through water and be
Eukaryote An organism that has a motile. Fruiting body A multicellular structure
membrane-bound nucleus. of fungi that produces and contains
Fleck The plant disease symptom of reproductive spores.
Exclusion A disease control step in small, white to tan lesions.
which pathogens, pathogen- Fumigant A volatile gas that is used to
contaminated materials, and infected Flexuous Referring to the edge or kill pathogens and other pests in soil,
plants are not allowed into a particular shape of an object that is serpentine, agricultural products, and structures.
field or area. wavy, or sinuate. The practice of applying a fumigant is
fumigation.
Exudate A liquid or slimy substance Floret One individual flower that is a
that is released by diseased or damaged part of a flower cluster or compact Fungicide A chemical substance used
plant tissue. In culture, some fungi also group of florets. to kill or inhibit fungi.
produce exudates.
Fluorescent The visible reaction, in the Fungi imperfecti Fungi (also known as
Facultative parasite An organism that form of a glow of light, when a mitosporic fungi or deuteromycetes)
is normally saprophytic (non- substance or organism is placed under that do not have sexually produced
pathogenic) but under certain condi- ultraviolet radiation. spores. This is an artificially created
tions can act as a parasite or pathogen. group and is not an official taxonomic
Foliar Referring to leaves and other category. Fungi imperfecti can be further
Facultative saprophyte or saprobe An parts of the above-ground portion of organized based on the way that spores
organism that is normally pathogenic plants. are made (see hyphomycetes, agono-
but under certain conditions can act as a mycetes, coelomycetes). While a fungus
saprophyte (non-pathogen). Foot cell A structure found in fungi in the fungi imperfecti does not produce
that is used to identify and classify fungi any sexual spore, some fungi imperfecti
Fallow Referring to land that is not to species. For powdery mildews, the can enter a phase of development in
planted with crops and is uncultivated. foot cell is the bottom cell of the conid- which it becomes associated with a
Leaving land fallow is one aspect of con- iophore that connects the conidiophore sexual form (an ascomycete or a basid-
trolling soilborne pathogens. to supporting hyphae. For Fusarium iomycete teleomorph). In such situa-
species, the foot cell is the bent basal cell tions, the fungi imperfecti species is
Family A taxonomic group of of the conidium. called the anamorph form of that teleo-
organisms that is one category above a morph.
genus and below an order. Foot rot The plant disease symptom of
a decay of the lower stem, hypocotyl, or Fungus An organism that lacks chloro-
Fasciation The plant disease symptom upper root. phyll, is usually multicelled, and usually
of striking distortion in which multiple has a vegetative body consisting of
stems are flattened and appear fused Forma specialis Abbreviated f. sp., microscopic tube-like structures
together. refers to a ‘special form’ or biotype of a (hyphae) that grow and become
pathogen species. A particular forma organized into branched systems
Fatty acid An organic fat compound specialis differs from other forms in its (mycelium). Fungi usually reproduce via
consisting of carbon, hydrogen, oxygen, ability to infect certain plant species. For spores.
and glycerol. The fatty acid profile of example, the pathogen Fusarium
bacteria and other organisms is used to oxysporum f. sp. apii infects only celery. Fusiform Spindle-shaped, with the ends
identify and classify these organisms. This term is used primarily for fungi. A narrower than the middle. Some fungal
similar designation for bacteria is spores are fusiform.
Filamentous Thread-like in shape. pathovar.
A synonym is filiform. Some pathogenic Gall The plant disease symptom of
fungi have filamentous spores. Formulation The nature and form of a abnormal plant growths that are
pesticide or fertilizer preparation. localized, swollen, and usually spherical.
Flagellate Having one or more flagella Formulations influence how chemicals Galls are caused by a number of
or whiplike structures. Bacteria and function and are handled. Examples of pathogens and other pests.
zoospores that move in water are flagel- formulations are wettable powders,
lates. granules, dry flowable granules, emulsi-
fiable concentrates, and liquids.
428 G LOSSARY
Gametangium A fungal cell that Haploid The genetic condition in Hybrid The resulting offspring from a
contains gametes. Gametangia fuse which an organism has half the number cross between two species or genotypes.
together and enable sexual reproduction of chromosomes (1n) as the diploid (2n)
and meiosis to take place. condition. Hydathodes Glands in the edges of
leaves, from which water collects and is
Gamete A male or female reproductive Haustorium A specialized hyphal discharged via guttation.
cell on fungal gametangia. branch that absorbs nutrients for the
fungus. Haustoria sometimes penetrate Hydroponics The growing of plants in
Gene A discrete, linear segment of a and grow into host cells. an aerated water solution instead of soil
chromosome which codes for one or or solid rooting media. The water
more genetic traits. A gene is the Heteroecious Pertaining to a pathogen- solutions include nutrients necessary for
smallest functioning unit of genetic ic fungus that needs two distinct kinds plant growth.
material in an organism’s genome. of hosts to complete its life cycle. Many
rust fungi are heteroecious. Hyperplasia An abnormal increase in
Geniculate Referring to structures that plant cell division due to the influence of
are bent. Heterothallic Referring to fungi that a pathogen. Galls, enations, and
produce male or female organs and witches’ broom symptoms are caused by
Genome The genetic material of an gametes on different individuals. Sexual hyperplasia.
organism. reproduction between isolates is
therefore possible only if each mating Hypersensitive reaction (HR) Ultra-
Genotype The genetic constitution of type is present. sensitivity of a plant and its cells to
an organism that dictates its physical invasion by pathogens. When cells are
characteristics (phenotype). Holomorph The mycological concept infected, the cells rapidly die and
of the ‘whole fungus.’ The holomorph prevent the pathogen from spreading
Genus A taxonomic group of includes the whole fungus in both its beyond the dead cells. Synonymous
organisms that is one category above a teleomorph (sexual or perfect) and with hypersensitivity.
species and below a family. anamorph (asexual or imperfect) stages.
Hypertrophy An abnormal increase in
Germ theory The idea that contagious Homothallic Referring to fungi that plant cell size due to the influence of a
diseases are caused by infectious produce male and female organs and pathogen.
microorganisms. gametes on the same individual. Sexual
reproduction therefore does not require Hypha The microscopic tube-like
Germ tube The initial growth of the presence of two distinct mating filament or thread that comprises the
mycelium made when a fungal spore types or individuals. basic vegetative body of a fungus.
germinates. Hyphae grow and are organized into
Horizontal resistance Partial resistance extensive branched systems (mycelium).
Globose Spherical or globe-shaped. in plants that is effective against most or
Some fungal spores are globose. all distinct races of a pathogen. In Hyphomycetes One of three subgroups
contrast to vertical resistance, this type of mitosporic fungi (the other two
Gram stain A microbiological of resistance is usually determined by groups are coelomycetes and agono-
technique in which bacteria are stained multiple genes. mycetes). Mitosporic fungi (also known
with various solutions. The resulting as deuteromycetes or fungi imperfecti)
violet (Gram-positive) or red (Gram- Host The susceptible plant that is do not have sexually produced spores.
negative) coloration helps distinguish subject to infection and colonization by Hyphomycetes are asexual fungi that
bacterial groups based on differing cell a virulent agent, the pathogen. For produce spores on individual or
wall features. disease to develop on the host, condi- multiple hyphae. Such conidia-bearing
tions favorable for the pathogen–host hyphae, however, are not contained
Guttation The collection and interaction must be present. within other structures or fruiting
exudation of water from plant leaves, bodies.
especially from glands (hydathodes) in Host range A documented range of
the edges of leaves. plant species or cultivars that is suscepti- Hypocotyl The part of a plant embryo
ble to a particular pathogen. or seedling that is below the point of
Halo A plant disease symptom in cotyledon attachment. The tissue
which a ring of discolored, necrotic, or Hyaline Clear or colorless. This term is between the stem and the root. In some
otherwise symptomatic tissue surrounds often used to describe fungal structures plants, such as radish, the hypocotyl is
a lesion or spot. (spores, mycelium, conidiophores) that extremely swollen.
are clear in appearance.
G LOSSARY 429
Imbibition The taking up and absorp- Infestation Occurs when a pathogen or Isolate (V.) to recover and separate a
tion of water by solid materials, such as pest is present on and contaminates pathogen from the infected tissue of its
plant seeds. surfaces, fields, soil, plant material, and host plant. Once recovered, the isolation
other objects. If a plant is infested, procedure usually includes purifying the
Immune Not subject to infection by a however, it may not be actually infected. pathogen so it is a pure culture. (N.) a
particular pathogen. An immune plant pure, viable culture of a pathogen. Such
does not become infected. Immunity is Inoculation The intentional act of a culture is obtained by isolating the
an extreme form of resistance. introducing a pathogen to a host plant pathogen from host tissue, and is
so that infection will take place followed usually followed by obtaining one
Imperfect fungus A fungus that does by the development of disease. distinct individual by growing out a
not produce sexual spores. See fungi Inoculations are important steps in single spore or hypal tip.
imperfecti or anamorph. proving pathogenicity of an organism
(see Koch’s postulates). Koch’s postulates The underlying
Incidence The frequency of a disease principle that is used to identify the
within a plant population. Incidence is Inoculum The propagules or parts of a causal agent of a disease. The suspected
often expressed as the percentage of pathogen that initiate disease in a host. pathogen must be present in all disease
plants that are affected. Inocula are often the parts of pathogens cases, be isolated and grown in culture,
that are dispersed and spread in the cause disease when inoculated into
Incipient Referring to the beginning, environment. Examples of inocula are healthy plants, and be re-isolated from
initial phase of infection and disease the spores of fungi, cells of bacteria, and the test plant.
development. particles of viruses.
Latent To be hidden. To be present but
Inclusion bodies Various structures, Insensitive Often referring to not visible.
crystals, and bodies that form in plant pathogens that have adapted and
cells as a result of virus infections. changed so that the insensitive isolate is Latent infection An infection in a plant
Inclusion bodies are visible with the no longer killed by and susceptible to a that does not yet show visual symptoms.
compound microscope and can be used pesticide or other control chemical. For
to diagnose some virus diseases. example, an insensitive fungal pathogen Latent period In virology, referring to
is not controlled by a particular the period of time between when an
Incubate To maintain in a controlled fungicide, and an insensitive bacterial insect vector acquires a plant pathogenic
environment with a given set of condi- pathogen is not controlled by a particu- virus and when it can transmit the virus
tions (temperature, humidity, light, etc.). lar antibiotic. Some pathologists to a plant host. For fungi, the latent
consider insensitive to be synonymous period is the period of time between
Incubation period The time between with resistant. infection and the initial appearance of
initial infection by the pathogen and fungal signs (mycelium or spores).
expression of disease symptoms by the Integrated pest management (IPM)
host. Incubation period can also refer to The use of all available methods (biolog- Leaf spot The plant disease symptom
the length of time that plants are kept at ical, chemical, genetic, physical, and of a well defined, localized, diseased
controlled environments (see incubate). cultural) to manage plant diseases and lesion on a leaf.
pests for maximum control, while mini-
Indexing Examining and testing plant mizing damage to the environment. Lesion The plant disease symptom of a
materials for the presence of pathogens. Examples of IPM components are the well defined, localized area of diseased
following: resistant plants, exclusion, tissue.
Indicator plant A plant that reacts to pesticides, crop rotations, sanitation,
virus infections by developing diagnos- environmental manipulation, and other Localized Related to the restricted
tic and characteristic symptoms. cultural practices. movement of a chemical, pathogen, or
Indicator plants can therefore be used to infection that in plants only spreads in a
detect and confirm some virus In vitro Referring to the growing and small area of cells and tissues. In
pathogens. culturing of organisms in artificial envi- contrast to systemic.
ronments or culture. A pathogen being
Infection The invasion, penetration, grown in vitro (Latin ‘in glass’) is not Lunate Crescent-shaped like a new
and establishment of a pathogen within living inside its natural host. moon. Some fungal spores are lunate.
a host. Distinguished from infestation,
in which the pathogen is present on the In vivo Referring to the growing of
host but has not yet infected it. organisms in natural environments.
A pathogen being grown in vivo (Latin
‘in living’) is living inside its natural
host.
430 G LOSSARY
Macronutrients Major chemical Mitosporic fungi Fungi (also known as Mucilaginous A viscous, slimy, or
elements, needed in relatively large fungi imperfecti or deuteromycetes) that sticky substance or surface.
amounts, that allow for normal plant do not have sexually produced spores.
growth. There are three macronutrients: This is an artificially created group and Mulch In agriculture, a substance or
nitrogen (N), phosphorus (P), and is not an official taxonomic category. material that is placed in a layer on the
potassium (K). Mitosporic fungi can be further soil surface. Mulches are used to catch
organized based on the way that spores water, reduce soil moisture loss, prevent
Mechanical injury Physical damage to are made (see hyphomycetes, agono- weed growth, regulate soil tempera-
a plant organ by abrasion, crushing, or mycetes, coelomycetes). While a fungus tures, keep plants clean from splashing
other wounding factor. in the mitosporic group does not soil, and other purposes. Mulch
produce any sexual spore, some material include straw or hay, dried
Mechanical transmission Referring to mitosporic fungi can enter a phase of leaves, compost, plastic films, and other
the successful introduction and estab- development in which it becomes associ- materials.
lishment of a pathogen into a host by ated with a sexual form (an ascomycete
means of a physical action. In the field, or a basidiomycete teleomorph). In such Multinucleate Having more than one
the rubbing of an infected leaf against a situations, the mitosporic species is nucleus per cell.
healthy leaf can result in mechanical called the anamorph form of that teleo-
transmission of the pathogen. morph. Mutant An individual organism that
Mechanical transmission is used in virus has a novel inheritable feature or trait as
research by taking virus laden plant sap Mollicute Prokaryotic microorganisms a result of undergoing a mutation.
and rubbing it onto leaves so that the that are single-celled, lack a cell wall,
virus can become established in the test but are bounded by flexible cell Mutation A permanent change in the
plant. membranes. In plant pathology, phyto- genetic material of an organism. The
plasmas and spiroplasmas are molli- resulting organism, or mutant, will have
Medium The artificial food or cutes. some new trait or character.
substrate that is prepared and used to
grow and culture microorganisms. Monoclonal antibody A homogeneous Mycelium The collection or mass of
antibody made from a single clone of hyphae of a fungus.
Meristem Layer or zone of undifferen- antibody producing cells. Such antibod-
tiated plant cells that functions ies react with only one of the antigens of Mycology The science and study of
primarily in cell division and is thus a pathogen or protein. Monoclonal fungi.
responsible for the first phase of plant antibodies are important components of
growth. serological detection methods such as Mycoplasma A bacterium-like
ELISA. organism that is prokaryotic, usually
Micronutrients Minor chemical single- celled, and not having a rigid cell
elements, needed in relatively small Monocyclic Having only one cycle per wall. Mycoplasmas belong in the class
amounts, that allow for normal plant season or host crop. mollicutes.
growth. There are many micronutrients,
such as boron, chlorine, copper, iron, Morphology The science and study of Mycoplasma-like organism (MLO)
manganese, molybdenum, and zinc. the form and structure of organisms. Obsolete term for a microorganism that
has the characteristics of mycoplasmas,
Microorganism An organism that Mosaic The plant disease symptom of but which has not been proven to be a
usually is so small that it is not visible foliage, particularly leaves, showing mycoplasma. MLOs live in the phloem
without microscopes. A synonym is abnormal, irregular patterns and tissue of their plant hosts. These
microbe. Microorganisms include actin- patches of light green, dark green, pathogens are now called phytoplasmas
omycetes, algae, bacteria, fungi, proto- yellow, and other colors. Many virus (non-helical species) and spiroplasmas
zoans, and viruses. The science and pathogens cause leaves to show mosaic (helical species).
study of microorganisms is microbiolo- patterns. Similar to mottle.
gy. Mycorrhiza A fungus that survives in
Motile Able to move about and be the soil and lives in association with
Midrib The main, central, thickened mobile. Bacteria and zoospores with plant roots. This type of fungus has a
vein of a leaf. flagella are motile and can swim in symbiotic relationship with the plant.
water. Mycorrhizae probably assist plants by
helping in the uptake of nutrients.
Mottle The plant disease symptom of
irregular patterns of indistinct light and
dark areas. Similar to mosaic.
G LOSSARY 431
Mycotoxins Poisonous, toxic sub- Obligate parasite A parasite that can Pathogen A virulent agent that is able
stances produced by certain fungi. If grow and multiply only on or in living to infect plants. For disease to develop
toxigenic fungi are present on materials tissue and that cannot be cultured on an on the susceptible host, conditions
such as animal feed, grains, and other artificial medium. favorable for the pathogen–host interac-
foods, the mycotoxins can cause disease tion must be present.
and death to the animal or person eating Oogonium The female gametangium
the contaminated food. of oomycete organisms. Oogonia each Pathogenicity The ability of a pathogen
contain one or more female gametes. to cause disease. The state of being path-
Myxomycetes True slime molds, which ogenic.
are not pathogenic to plants. Oomycete An important group of
plant pathogens that includes the downy Pathovar Abbreviated pv., refers to a
Necrosis The plant disease symptom of mildews, Aphanomyces, Phytophthora, ‘special form’ or biotype of a bacterial
darkened, brown to black tissue, usually Pythium, and others. These organisms pathogen species. A particular pathovar
consisting of dead cells. lack chitin in their cell walls, usually differs from other pathogens in its
have zoospores with heterokont flagella ability to infect certain plant species.
Nematicide A chemical pesticide used (one whiplash, one tinsel type), and For example, the pathogen
to kill or inhibit nematodes. possess other features that separate Xanthomonas campestris pv. campestris
them from the true fungi and align them infects only Brassica plants. A similar
Nematode An unsegmented, usually more closely with certain types of designation for fungi is forma specialis.
microscopic, roundworm in the phylum primitive golden algae, diatoms, and
Nematoda. Different nematode species giant kelp in Kingdom Chromista or Pedicel The plant stalk that supports
are parasitic on plants or animals or are Kingdom Straminipila. and bears flowers.
free-living in soil, soil organic matter, or
water. Some plant parasitic nematodes Oospore A sexual spore produced by Perfect fungus A fungus that produces
form disease complexes with pathogenic the union of two morphologically sexual spores. See teleomorph.
fungi. The science and study of different gametangia (oogonium and
nematodes is nematology. antheridium). Oospores are resting Perithecium Fruiting body of
spores that can survive during unfavor- ascomycete fungi that is a spherical to
Node On a plant the enlarged joint on able conditions. flask-shaped structure. The inner cavity
a stem, usually located where leaves are of perithecia contains ascospore
attached. Ostiole A pore-like opening in some producing asci. Ascospores are released
fungal fruiting bodies (perithecia, through ostioles in the perithecia.
Non-circulative virus Referring to a pycnidia) through which spores leave
plant pathogenic virus that is borne on the fruiting body. Persistent A feature of the relationship
the stylet of its insect vector and which between a plant virus and its arthropod
does not accumulate internally in the Paraphysis A sterile hypha that is vector in which the virus remains on or
insect. present in some fungal fruiting bodies. in the vector indefinitely. The vector can
The presence or absence of paraphyses, transmit the virus throughout its life.
Nonpathogenic Not able to cause and their morphology if present, are
disease. used to help identify fungal species. Phenotype The physical characteristics
of an organism as dictated by its genetic
Nonpersistent A feature of the rela- Parasite An organism that lives in or on constitution (genotype).
tionship between a plant virus and its another living organism (the host). The
arthropod vector in which the virus does parasite obtains its food and sustenance Phycomycete An obsolete term previ-
not remain on or in the vector indefinite- from the host. ously used to describe the ‘lower fungi’
ly. The vector eventually loses the virus, such as zygomycetes and oomycetes.
often within a few hours. Parasitism The association where one
organism (parasite) grows at the Phyllody A plant disease symptom in
Nucleic acid Genetic material that expense of another organism (the host). which flower petals and other floral
consists of DNA or RNA. organs are transformed into green, leaf-
Pascal (Pa) A metric unit of pressure like structures. Phyllody can be caused
Nucleus The cellular organelle of equivalent to 0.00014504 lb/in2; 1 kPa by certain pathogens, insects, mites, and
eukaryotic organisms that contains the = 0.14504 lb/in2; 100 kPa = 1 bar. genetic mutations.
chromosomes. Nuclei are bounded by a
membrane. Phylloplane The surface of plant
leaves.
432 G LOSSARY
Phylogenetic tree A diagram that Pleomorphic Referring to an organism Prokaryote An organism that lacks a
consists of branches that indicate evolu- that exists in various shapes and sizes. membrane-bound nucleus.
tionary relationships between members For example, phytoplasmas have no
of the tree. rigid cell wall, so their shapes vary and Propagule A discrete, separate unit of
are therefore pleomorphic. an organism that is able to grow and
Phylogeny The science and study of propagate the organism.
changes and evolution of organisms Polyclonal antibodies The natural mix
over time. The evolutionary history of of diverse antibodies present in the Protectant A chemical substance that
an organism. blood serum of an animal that had been protects the plant against infection by a
injected with a pathogen or protein. pathogen only if the pathogen has not
Phylum A taxonomic group of Polyclonal antibodies are components yet infected and established itself in the
organisms that is one category above a of serological detection methods. plant. Compare eradicants.
class and below a kingdom.
Polycyclic Having more than one cycle Protozoan An organism in the phylum
Physiologic race A subgroup or subdi- per season or host crop. In fungi, this Protozoa. Protozoans are single-celled,
vision of a species. The individual occurs when the pathogen produces mostly motile, and include a few plant
organisms making up a physiologic race additional generations of spores that pathogens such as the plasmodio-
share common features and genetics. spread within the same crop and cause phoromycetes (example clubroot of
Similar to biotype and strain. new infections. crucifers) and flagellate protozoans.
Physiology The science and study of Polygenic A character or trait that is Pseudothecium Fruiting body of
the functions of living organisms or their controlled by many genes. ascomycete fungi that consists of a mass
parts, and organic processes that take of hyphae (stroma) and hollow cavities
place in organisms. Polymerase chain reaction (PCR) that develop within the stroma. The
A technique in molecular biology in ascospore-bearing asci are formed
Phytoplasma A plant pathogenic which a specific DNA fragment is within these cavities. Ascomycetes that
microorganism that has the characteris- greatly amplified. The technique uses make pseudothecia are called loculo-
tics of mycoplasmas, but which has not specially designed primers that ascomycetes.
been proven to be a mycoplasma. hybridize with the target DNA.
Phytoplasmas are nonhelical in shape Temperature changes in the PCR Pustule Small, raised, blister-like
and live in the phloem tissue of their protocol allow for the rapid multiplica- structure that forms on a leaf infected by
plant hosts. These pathogens were tion of the DNA fragment. fungi such as rusts. Pustules initially are
formerly called mycoplasma-like covered by the leaf epidermis, but the
organisms. The helical species are called Post-emergence The period of time plant tissue later ruptures and allows
spiroplasmas. after the appearance of plant structures release of spores.
above the soil surface following germi-
Phytotoxicity The damage or death nation of seeds and below-ground Pycnidium A small, flask-shaped to
that plants sustain due to exposure to growth of the seedling. spherical, fungal fruiting body that
injurious factors, primarily chemicals produces asexual conidia. Pycnidia are
such as pesticides and fertilizers. Predispose To make susceptible to either embedded within or form on the
Symptoms of phytotoxicity include infection, or to increase susceptibility to outside of host tissue. Conidia develop
burning or scorching, chlorosis, defor- infection. Some environmental stresses within pycnidia and are later released
mities, inhibited growth and develop- and factors can predispose plants to through pores in the structure (ostiole)
ment, and plant death. infection by pathogens. or when the pycnidia rupture.
Pith The soft, spongy, thin-walled Pre-emergence The period of time Pyriform Pear-shaped. Some fungal
cellular tissue found most often in the prior to the appearance of plant struc- spores are pyriform.
central core of plant stems and roots. tures above the soil surface following
germination of seeds and below-ground Quarantine Temporary holding of
Plasmid A small piece of circular DNA growth of the seedling. imported plants or plant materials in
that is not part of a cell’s chromosomes, isolation so that the materials can be
is self-replicating, and is found in certain Primary inoculum The inoculum, or determined to be free from diseases and
bacteria and fungi. pathogen propagule, that first infects the pests. Quarantines are regulatory
host and causes initial disease. Infection requirements designed to exclude
caused by primary inoculum usually pathogens.
takes place following an overwintering
period.
G LOSSARY 433
Race A subgroup or subdivision of a Rhizomorph An aggregation or bundle Saprobe An organism, usually a

species. The individual organisms of hyphal strands that appears root-like. microbe, that colonizes, feeds on, and
making up a physiologic race share Rhizomorphs function as a means of decomposes dead organic matter. A true
common features and genetics. Similar spreading the fungus and as an aid to saprobe is not pathogenic to plants.
to biotype and strain. survival. However, some pathogens can function
as saprobes. A synonym is saprophyte.
Recessive gene A gene that is not fully Rhizosphere The soil environment
expressed when paired with a corre- near and around the roots of plants. Scab The plant disease symptom where
sponding dominant gene or allele. affected plant surfaces are rough, crusty,
Ring spot The plant disease symptom and dry.
Relative humidity (RH) A standard where multiple circles (which usually
weather measurement of the ratio of the are alternating in appearance between Sclerotium A compact mass of fungal
amount of water vapor actually in the dark and light colors) form within one growth that enables the organism to
air to the greatest amount of water larger circle or lesion. All the circles survive unfavorable conditions.
vapor that air can hold at that same share the same center. This symptom is Sclerotia are mostly dark-colored, hard,
temperature. RH is often important in also called a concentric spot. with smooth and rounded surfaces, and
the germination and survival of spores having a distinct outer rind (as for
of pathogenic fungi RNA Ribonucleic acid. RNA is any of Sclerotinia and Sclerotium species). For
various nucleic acids that occur in nuclei some fungi, such as Rhizoctonia solani,
Replication The process in which a (for eukaryotic organisms) and cell sclerotia are made up of closely inter-
virus pathogen reproduces by inducing contents (eukaryotic and prokaryotic woven hyphae and lack the rind layer.
the host cell to make more virus entities. organisms) of living organisms. RNA
In molecular biology, the process in molecules are composed of repeating Scorch The plant disease or damage
which a nucleic acid (DNA or RNA) is sub-units of ribose (a five-carbon sugar), symptom that resembles the effects of
copied. phosphoric acid, and four nitrogenous burning on a leaf or other plant part.
bases (adenine, cytosine, guanine, and Scorch can be caused by pathogens,
Resistant (regarding host plants) uracil). RNA is involved with protein nutrient deficiencies, or various abiotic
The genetically based ability of a plant synthesis. RNA is the only nucleic acid factors such as chemical damage, high
to not become infected, or when a plant in some viruses. salt content in soil and water, or weather
minimizes the effect of a pathogen. extremes.
Related to immune. Rogue The act of removing undesirable
plants from a field or planting. Plants Secondary inoculum The inoculum, or
Resistant (regarding pesticides) are rogued because they may show pathogen propagule, that develops
Often referring to pathogens that have symptoms of disease, exhibit abnormal following initial disease development.
adapted and changed so that the growth, or not conform (off-types) to Secondary inoculum is produced after
resistant isolate is no longer killed by the desired cultivar. the primary inoculum already incited
and susceptible to a pesticide or other disease on the host.
control chemical. For example, a Rosette The plant disease symptom
resistant fungal pathogen is not con- where plant growth is short and stunted, Secondary organism An organism that
trolled by a particular fungicide, and a and leaves and stems are bunched colonizes and multiplies in already
resistant bacterial pathogen is not con- together and compressed. diseased tissue. Secondary organisms do
trolled by a particular antibiotic. Some not cause disease on their own.
pathologists consider resistant to be syn- Rot The plant disease symptom of soft,
onymous with insensitive. mushy, and discolored tissue. Rots Seed transmission Passage of inoculum
usually involve the disintegration of from an infected or infested seed to the
Resting spore Any spore that is able to plant tissues due to release of enzymes germinating plant that grows from that
survive despite unfavorable conditions and other factors by the pathogen. seed.
such as drying, high temperatures, and
lack of a host. An example of a resting Sanitation The removal and disposal of Seed treatment Chemical or other
spore is the thick walled, sexual oospore diseased plants and other contaminated treatment used to reduce or eliminate
of oomycetes. material. Also, the cleansing or deconta- the presence of pathogens on seeds.
mination of production equipment, Also, the application of fungicides to
Rhizoid Fungal filaments and hyphae tools, hands, and other objects that seeds so that when seeds are planted
that grow root-like towards nutrients might be sources of pathogen inoculum. they are protected against damping-off
and substrates. pathogens.
434 G LOSSARY
Seedborne The situation in which a Sinuate Referring to the edge or shape Sporangium A fungal reproductive
disease, pathogen, or pathogen of an object that is serpentine, wavy, or structure that encloses cytoplasm and
inoculum is present on or in seed. flexuous. cell contents that later differentiate into
individual spores (sporangiospores).
Selection In agriculture, the process of Soil inhabitant A microorganism that The cell walls of the spores are distinct
choosing certain plants, having desired is able to survive in the soil for many and not derived from the sporangium.
traits, for use in growing and breeding years or indefinitely. Soil inhabitants In some cases the cytoplasm does not
crops. Also, selection is the biological that are pathogenic to plants usually differentiate, and the sporangium itself
process where certain microorganisms, have a saprophytic ability as well. can function as a spore (hence can be
having survival traits such as resistance called a conidium in this situation). If
to pesticides or the ability to overcome Soil invader A microorganism that is the sporangiospores are motile and
plant host resistance, are able to survive not able to survive and persist in the soil swim in water, the sporangium can also
in greater numbers than individuals that for more than a relatively short time of be called a zoosporangium.
do not possess the same trait. one or two years. A synonym is soil
transient. Spore The reproductive unit of fungi,
Senescence The natural aging process some bacteria, and other micro-
of plant tissues as tissues mature, then Soilborne pathogen A pathogen that is organisms.
decline. Senescence can also be induced present in soil, is usually a soil inhabi-
by diseases. tant, and which survives by inoculum Sporodochium A reproductive
that is present in soil. structure of asexual fungi that consists
Septate Referring to the presence of of a raised cushion-shaped mass of
cross walls (septa) between cells. Solarization The use of solar radiation hyphae. The sporodochia then support
to treat soil and reduce populations of short conidiophores.
Septum The cross wall that divides soilborne pathogens. Solarization
fungal hyphae or spores into separate usually involves the placement of clear Sporulate The action of forming and
cells. The presence or absence of septa plastic tarps on the soil surface, then releasing spores.
characterizes some fungal groups. allowing the sun to heat the soil for a
number of days or weeks. Sterile For an organism, the state of
Serology The science and study of being infertile. Also, the condition of
antigen and antibody interactions. Sorus A compact mass of spores in a being free from living microorganisms
Serological methods are critical for the fruiting structure. This term is used and contaminants.
identification of protein antigens of especially for rust and smut fungi.
plant pathogens, and are the basis for Strain A subgroup or subdivision of a
detection methods such as ELISA. Species The smallest formal classifica- species. The individual organisms
tion unit in taxonomy. Species is one making up a strain share common
Seta In fungi, a sterile, hair-like category below genus. features and genetics. Similar to biotype
structure. and race. Also, in bacteriology and
Spiroplasma A plant pathogenic virology a group or collection of
Sexual Reproduction that involves the microorganism that has the characteris- clonally related individuals derived from
union of gametes and meiosis. Fungi tics of mycoplasmas, but which has not one isolation and maintained as a pure
that reproduce sexually are called been proven to be a mycoplasma. culture.
perfect or teleomorphic fungi. Spiroplasmas are helical in shape and
live in the phloem tissue of their plant Straminipila The name of the
Shot-hole The plant disease symptom hosts. These pathogens were formerly taxonomic kingdom that some taxono-
of small, often circular or oval leaf spots called mycoplasma-like organisms. The mists believe should contain the
that later become necrotic. The necrotic nonhelical species are called phyto- important oomycete pathogen group.
tissue will dry up and fall out of the leaf, plasmas. Kingdom Straminipila is distinct from
leaving a hole. fungi and contains certain types of
Sporangiophore The specialized hypha primitive golden algae, diatoms, and
Sign The visible presence of the that bears one or more sporangia. giant kelp. However, other researchers
pathogen on host tissue. Signs usually believe the appropriate name for this
are limited to fungal growth, spores, Sporangiospore The asexual spore that group should be Kingdom Chromista.
and other structures, and bacterial ooze differentiates within and is released
and accumulation. Signs are distinct from a sporangium. If the sporangio- Stroma A mass of hyphae of fungi. The
from symptoms. spores are motile and swim in water, stromata themselves do not produce
they can also be called zoospores. spores and are therefore vegetative in
nature. Stromata can contain or support
the reproductive structures.
G LOSSARY 435
Stylet The long, slender, hollow mouth Teleomorph The sexual stage of a Tylosis Balloon-like growth that
structure of piercing and sucking insects fungus. Spores and propagules develops and blocks vascular cells in the
such as aphids and leafhoppers. produced in this stage involve sexual xylem of plants. Tyloses sometimes
Viruliferous aphids insert their stylets recombination or processes. This form form in reaction to infection by vascular
into plant tissues and transmit virus of fungi is also called the perfect stage. pathogens such as Verticillium dahliae.
particles. Also, the spear-like structure Teleomorph fungi include ascomycetes,
of plant parasitic nematodes that basidiomycetes, and zygomycetes. Umbel A type of flower structure in
enables these nematodes to feed on which flowers are borne on pedicels that
plants. Teliospore One of the several different arise from a common attachment. The
types of rust fungi spores. Teliospores result is a cluster of flowers having a
Stylet-borne virus Referring to a non- are borne in and on telia and often are rounded or flat top. Umbels are charac-
circulative virus that is borne on the the overwintering spore stage. teristic of plants in the Apiaceae family.
stylet of its insect vector. Teliospores germinate to form basidia
and basidiospores. See also aeciospore, Urediniospore One of the several
Substrate The surface or medium upon urediniospore, and basidiospore. different types of rust fungi spores.
which a microorganism grows. Urediniospores are borne in and on
Telium The fruiting structure of rust uredinia, windborne, and responsible
Suppressive soil A soil in which some fungi that produces teliospores. for widespread distribution of
soilborne diseases are reduced in inoculum. See also aeciospore,
severity or incidence. The mechanisms Tendril (of fungi) A small, linear mass teliospore, and basidiospore.
of suppressive soils are not well under- of spores exuded from fungal fruiting
stood, but probably involve the activity bodies called pycnidia. Tendrils are Uredinium The fruiting structure of
of antagonistic and beneficial microor- curled and held together by a slimy rust fungi that produces urediniospores.
ganisms. matrix material. Also called a cirrus.
Variability The phenomenon in which
Susceptible Subject to infection. Tolerance Ability of a plant to endure a some organisms have slightly different
disease without sustaining serious traits even though they are of the same
Symptom The visual manifestation of damage or yield loss. Related to and species.
disease (or abiotic disorder). The sometimes considered synonymous with
reaction of the host to infection. resistance. Variety In agriculture and horticulture,
Symptoms do not include the actual a cultivated variety of plant. All individ-
physical presence of the pathogen (see Toxin A non-enzymic metabolite uals of a particular variety share charac-
sign). produced by one organism that is teristic features. Variety is generally used
damaging or inhibitory to another synonymously with cultivar.
Synnema A reproductive structure of organism. Mycotoxins are toxins that
asexual fungi that consists of a column are produced by fungi, which are Vascular pathogen A pathogen that is
of compacted, erect, fused conidio- therefore considered to be mycotoxi- able to colonize and move about in the
phores. On synnemata, conidia are genic species. vascular tissue of plants.
produced only on the outer surfaces of
these columns. The term coremium is Transformation The change of a cell Vascular tissue The conductive tissue
also used. through uptake and expression of addi- (xylem and phloem) of plants.
tional genetic material.
Systemic Related to the movement of a Vector An organism that can acquire
chemical, pathogen, or infection that Transgenic Referring to organisms that and subsequently transmit a pathogen
spreads internally through the plant’s have been altered by the insertion of (mostly viruses but also fungi and
vascular system (primarily the xylem). genes via modern molecular techniques. bacteria) to plants. Primary vectors
In contrast to localized. include insects, mites, nematodes, and
Transmission The transfer or spread of primitive soil fungi.
Taproot The main, central root of a pathogens, especially viruses, from plant
plant from which secondary or lateral to plant, seed to plant, or from vector to Vegetative compatibility The ability of
roots arise. plant. vegetative (non-reproductive) hyphae to
fuse together (anastomose). This fusion
Taxonomy The science and study of Transverse section Viewing plant tissue usually results in combination and
systematic naming, ordering, and classi- that has been cut or dissected crosswise, exchange of genetic material. For some
fying of organisms on the basis of their at right angles to the longitudinal axis. fungi, pairing of vegetatively compatible
natural relationships, characteristics, isolates assists in the classification and
and genetics. Trichome A hair-like cell projection on identification of groups within a species.
the epidermis of plants.
436 G LOSSARY
Verrucose Having a surface with small, Water-soaked The plant disease

rounded structures or warts. symptom where succulent tissue
appears wet, greasy or dark due to the
Verruculose Delicately or minutely activity of a pathogen. Water-soaked
verrucose. symptoms are often the initial
symptoms of bacterial or fungal infec-
Vertical resistance Complete resistance tions of leaves and shoots.
in plants that provides resistance to
some races of a pathogen but not to Wilt or wilting The plant disease
others. In contrast to horizontal resist- symptom where leaves, shoots, and
ance, this type of resistance is often foliage in general will droop and sag.
determined by a single gene. Wilting is often caused by insufficient
water in the plant as a result of damaged
Verticillate In fungi, having phialides or roots or plugged vascular systems.
other structures that arise from a
common point. Structures occurring in Witches’-broom The plant disease
whorls. symptom where shoots are abnormally
clustered into a tight brush-like mass.
Vesicle A balloon-like structure that These witches’-broom shoots result
expands from sporangia of Pythium from a proliferation of buds from one
organisms and in which the zoospores section of the plant.
differentiate and are released. Vesicles
also refer to other mycology structures, Yellows The plant disease category
such as swellings in Aspergillus conidio- characterized by yellowing of plant
phores. foliage and sometimes stunting of the
diseased plant. The yellowing symptom
Virescence The plant disease symptom can also be called chlorosis.
in which normally white or non-green
tissue becomes green. Zonation The plant disease symptom
where multiple circles (usually alter-
Virion The complete virus particle that nating in appearance between dark and
consists of a nucleic acid (RNA or light colors) form within one larger
DNA) and a surrounding protein coat. circle or lesion. All the circles share the
same center. This symptom is also called
Viroid A type of pathogen that consists a concentric spot or ring spot.
only of a single-stranded RNA. Viroids
do not have an enclosing protein coat, Zoosporangium A sporangium which
as is the case with viruses. produces and releases swimming
zoospores.
Virulence The degree or severity of
pathogenicity. Zoospore An asexual sporangiospore
that is motile and can swim in water.
Virulent Referring to something that is
pathogenic. Zygomycete A group of fungi that
produce sexual zygospores. Zygo-
Viruliferous Referring to a vector that mycetes lack cross walls (septa) in their
has acquired a virus and is able to vegetative hyphae and produce asexual
transmit it. sporangiospores.
Virus A submicroscopic pathogen that Zygospore The sexual or resting spore

consists of a nucleic acid (RNA or of zygomycetes. Zygospores are
DNA) and an enclosing protein coat. produced by the fusion of two
The science and study of virus and virus- morphologically similar gametangia.
like organisms is virology.
437
Index
Note: Page numbers in italic refer to Alternaria leaf spot Cucumber mosaic virus 93–4
tables in the text brassicas/mustards 164–6 damping-off/Pythium root rot 87–8,
endive/escarole 391–2 126–7
A Alternaria petroselini 96 downy mildew 122–3
abiotic factors 24, 33 Alternaria porri 56–7 Fusarium yellows 85–6
ammonium toxicity 325 Alternaria radicina 98–9 late blight 90–1
calcium deficiency 94, 370, 395, Alternaria raphani 165 licorice rot 107
400 Alternaria smyrnii 96 Phoma crown/root rot 86–7
Acalymma trivittatum 249 Alternaria solani 338–9 pink rot 88–9
Acalymma vittatum 223 Alternaria tomatophila 339 powdery mildew 103–4
Aceria tulipae 78 ammonium toxicity (lettuce) 325 rust 115–16
acibenzolar-S-methyl 47, 331 Anasa tristis 225 scab 112–13
Acidovorax avenae subsp. citrulli 220–1 Anethum graveolens (dill) 385 violet root rot 105–6
Acremonium cucurbitacearum 226–8 angular leaf spot (cucurbits) 224–5 viral disease 92–4, 116–17, 124–5
Acyrosiphum pisi 267, 268 anthracnose disease white mold 111–12, 127
Acyrothosiphon pisum 283, 285, 286 beans (Phaseolus) 260–2 see also carrot; celery; parsley;
Albugo candida 163, 383, 390, 391, cucurbits 238–9 parsnip
404 lettuce 308–9 Apion vorax 295
Albugo occidentalis 369–70, 373 pepper 204 Apium graveolens see celery
Albugo tragopogonis 419 rhubarb 414 Arabis mosaic virus 416
alfalfa 114, 225, 271, 277, 286 spinach 373 artichoke
Alfalfa mosaic virus 361 tomato 343–4 globe 26, 41, 268, 398–403
algae 18 Anthriscus cerefolium (chervil) 385 Jerusalem 28, 407–8
Alliaceae 26 Anthriscus sylvestris 93, 117, 124 world production trends 13
bacterial blight 54–5 Anthriscus yellows virus 124 Artichoke curly dwarf virus 398
black mold 58–9 antibiotics 39 Artichoke Italian latent virus/Artichoke
Cladosporium leaf blotch 64–5 Aphanomyces spp. yellow ringspot virus 398
downy mildew 67–8 control 43 Artichoke latent virus 398
Fusarium basal plate rot 63–4 pea 270–1 arugula 26, 157, 404–5
neck rot 61–2 Aphanomyces cochlioides 139, 371 Aschochyta blight (pea) 278–9
penicillium blue mold 66–7 Aphanomyces euteiches 139, 256, Aschochyta hortorum 398
pink root 69–70 270–1, 273, 287 Ascochyta leaf spot (rhubarb) 414
purple blotch 56–7 aphids 50, 93, 318 Aschochyta pinodella see Phoma
rust 72–4 green peach 79, 137, 150, 151, 153, medicaginis var. pinodella
seedborne pathogens 40 154, 196, 197, 198, 267, 268, Aschochyta pinodes 278
smut 77 283, 286, 317, 318, 363, 380, 417 Ascochyta pisi 274
southern blight 74, 76 lettuce 318 Ascochyta rhei 414
viral diseases 78–9 pea 267, 268, 283, 285, 286 Aschochyta rot (artichoke) 398
white rot 47, 74–6 shallot 79 Ascomycete fungi 22, 23
white tip 70–1 willow carrot 117, 124 asparagus (Asparagus officinalis) 26, 41
world production trends 13 Aphis craccivora 283 Cercospora blight 129
Alternaria alternata 336 Aphis fabae 151, 154, 267, 268 Fusarium crown/root rot 130–1
Alternaria alternata f. sp. lycopersici Apiaceae 14, 80 Phytophthora spear/crown rot 133
337–8 aster yellows 80–1 purple spot 134–5
Alternaria brassicae 164–6, 390 black mold 114 root rots 105, 132
Alternaria brassicicola 164, 166 blackheart 89, 94 rust 135–6
Alternaria cichorii 391–2 cavity spot 108–9 seedborne pathogens 40
Alternaria dauci 96–7 Celery mosaic virus 92–3 violet root rot 105–6
Alternaria leaf blight (carrot) 96–7 crater spot 91–2 viral disease 131, 137
crown and root rot 113–14 world production trends 13
438 I NDEX
Asparagus viruses 1, 2, 3 137 beans (Phaseolus spp.) 26, 252–68 biological control 47, 264, 315
Aspergillus spp. 336 anthracnose 260–2 black canker (parsnip) 118–19
Aspergillus niger 58–9 bacterial brown spot 253 black leg
aster leafhopper 38–9, 81, 297 common bacterial blight 254–5 beet 143–4
aster yellows Fusarium wilt/yellows 260 brassicas 171–4
Apiaceae 80–1 gray mold 258–9 black mold
disease cycle 38–9, 81, 297 halo blight 252–4 Alliacea 58–9
lettuce 296–7 powdery mildew 259 Apiaceae 114–15
Asteraceae 14 root/foot rot complex 256–7 tomato 336
Asteromella brassicae 175 rust 265–6 black root rot (beet) 138–9
Athelia arachnoidea 100 seedborne pathogens 40 black rot 14
Athelia rolfsii 101, 202, 340 viral diseases 267–8 artichoke 399
Atriplex spp. 140 white mold 262–5 brassicas 39, 159–61, 169
aubergine see eggplant world production trends 13 carrot 98–9
beet (Beta vulgaris) 26, 138 cucurbits (gummy stem blight)
B black leg 143–4 230–1
bacteria 18–19 Cercospora leaf spot 140 horseradish 384
dispersal 19 damping-off/black root rot 138–9 black salsify 419
isolation 36 downy mildew 142–3 blackheart 89, 94
bacterial blight fodder 147 blossom end rot (tomato) 367
Alliaceae 54–5 powdery mildew 141–2 blue mold
arugula 405 Ramularia leaf spot 145 penicillium (Alliaceae) 66–7
beans 254–5 rhizomania 151–2 spinach 375–6
brassicas 157, 389 rust 147 bok choy 162, 164, 165, 176–7, 181,
pea 269–70 scab 146 192, 194, 198
bacterial canker (tomato) 327–8 seedborne pathogens 40 BOTCAST 60
bacterial crown rot (artichoke) 399 time of planting 43 Botryotinia squamosa 59–60
bacterial fruit blotch (cucurbits) 220–1 viral diseases 148–54 Botrytis allii (B. aclada) 61–2
bacterial head/spear rot (broccoli) Beet chlorosis virus 150, 153, 380 Botrytis byssoidea 62
155–6 Beet curly top virus 148, 214, 362, Botrytis cinerea 44, 47, 60, 167, 275–6
bacterial leaf blight (carrot) 95 379–80, 386 artichoke 399–400
bacterial leaf spot Beet leaf curl virus 149 basil 411
basil 412 Beet mild curly top virus 148, 214, 362, beans 258–9
brassicas 158 380 brassicas 167
catnip 410 Beet mild yellowing virus 150, 153, 380 lettuce 304–5, 310, 326
celery 82–3 Beet mosaic virus 151 pepper 202–3
cilantro 397 Beet necrotic yellow vein virus rhubarb 414
Italian dandelion 393 (rhizomania) 43, 151–2 tomato 341–2
lettuce 301–2 Beet pseudo-yellows virus 152 Botrytis fabae 288–9
spinach 368–9 Beet severe curly top virus 148, 214, Botrytis fuckeliana 167, 203, 258, 276,
Swiss chard 388 362, 380 304, 342
bacterial soft rot Beet western yellows virus 153, 196, Botrytis leaf blight (botrytis blast)
endive/escarole 392, 393 317, 380–1, 392 59–60
rhubarb 414 Beet yellows virus 154 Botrytis porri 62
bacterial speck (tomato) 330–1 beetles Botrytis squamosa 62
bacterial spot flea 417 bottom rot
pepper 199–200 mustard 417 brassicas 191–3
tomato 332–4 spotted cucumber 249 lettuce 311–12
bacterial wilt (cucurbits) 222–3 striped cucumber 223 Brassica napus see oilseed rape
Basidiomycete fungi 22, 23 western striped cucumber 249 Brassica rapa subsp. rapa (broccoli
basil 26, 40, 411–12 beetroot see table beet raab) 27, 40, 389–90
Bean common mosaic virus 267 Bemisia tabaci 248, 366 brassicas 14, 155, 389–91
Bean leaf roll virus 283 benzimidazoles 46, 264 Alternaria leaf spot/head rot 164–6,
Bean yellow mosaic virus 268 Beta maritima (sea beet) 141, 142, 147 390–1
bicarbonate-based fungicides 49 bacterial blight 157, 389
big vein disease (lettuce) 321–2 bacterial head/spear rot 155–6
I NDEX 439
bacterial leaf spot 158 C Carrot mottle virus 116

black leg 171–4 cabbage Carrot red leaf virus 116
black rot 159–61, 169 bacterial leaf spot 158 catnip 27, 410
clubroot 24, 41, 43, 181–3 black rot 159–61 cauliflower
downy mildew 178–80 Chinese 162, 164, 177, 183, 184, Alternaria leaf spot 164–6
Fusarium yellows/wilt 169–71 192, 194, 197 bacteria leaf spot 158
gray mold 167 gray mold 167 black leg 171–4
light leaf spot 186–8 Phytopthora diseases 184–6 black rot 159–61
Phytophthora root rot 71, 185–6 powdery mildew 168–9 clubroot 181–3
Phytophthora storage rot 184–5 ring spot 174–6 downy mildew 178–80
powdery mildew 168–9 root/bottom rot 191–3 gray mold 167
ring spot 174–6 savoy 184 light leaf spot 186–8
Sclerotinia disease/white mold Sclerotinia disease 189–90 Phytophthora root rot 185–6
189–90 Verticillium wilt 194–5 powdery mildew 168–9
Verticillium wilt 169, 194–5 viral disease 196–8 Rhizoctonia diseases 191–3
viral diseases 196–8 white 167, 184 ring spot 174–6
white leaf spot 176–7 world production trends 13 Sclerotinia disease 189
white rust/white blister 162–3 ‘caida’ see damping-off, beet Verticillium wilt 41, 194–5
see also named species of brassicas calabrese see broccoli viral disease 196, 197
Bremia lactucae 302–4 calcium white rust/white blister 162–3
Brevicoryne brassicae 197, 198, 417 plant deficiency 94, 370, 395, 400 world production trends 13
Broad bean stain virus 295 soil amendments 42–3, 182 Cauliflower mosaic virus 197
Broad bean true mosaic virus 295 calcium hypochlorite 200 Cavariella aegopodii 117, 124
broad bean (Vicia faba) 28, 40, 260 canker cavity spot (Apiaceae) 108–10
chocolate spot 288–90 Alternaria stem (tomato) 337–8 celeriac 86, 90, 92, 105
downy mildew 291–2 bacterial (tomato) 327–8 celery (Apium graveolens) 27, 39, 42,
leaf and pod spot 290–1 Itersonilia/black canker (parsnip) 80–94, 122
root rots 287–8 118–19 bacterial leaf spot 82–3
rust 293–5 Phoma (parsnip) 121–2 blackheart 89, 94
viral disease 295 cantaloupe 220, 225, 231, 240, 241–2 crater spot 91–2
white mold/Sclerotinia rot 292–3 Capsella bursa-pastoris 183, 316 damping-off/Pythium root rot 87–8
world production trends 13 Capsicum spp. see pepper disease resistance 41
broccoli captan 281 early blight 83–4
Alternaria leaf spot/head rot 164–6 caraway 99, 107 Fusarium yellows 85–6
bacterial blight 157 carrot (Daucus carota) 27, 92, 95–117 late blight 90–1
bacterial head/spear rot 155–6 Alternaria leaf blight 96–7 Phoma crown/root rot 86–7
downy mildew 178–80 bacterial leaf blight 95 pink rot 88–9
as rotation crop 42 black mold 114–15 seedborne pathogens 40
white mold Sclerotinia) 190 black rot 98–9 southern blight 101
white rust 162–3 cavity spot 108–10 viral diseases 42, 91–3
broccoli raab 27, 40, 157, 389–90 Cercospora leaf blight 102–3 Celery mosaic virus 42, 92–3
Brussel sprouts 158, 164, 165, 168, crater rot 100 Cephaleuros virescens 18
169, 179 crown and root rot 113–14 Cercospora amoraciae 383
black leg 171–3 licorice rot 107 Cercospora apii 84
light leaf spot 186–8 motley dwarf 42, 116–17 Cercospora asparagi 129
ring spot 174–6 powdery mildew 103–4 Cercospora beticola 140, 387
Verticillium wilt 194–5 rust 115–16 Cercospora blight (asparagus) 129
viral disease 197 scab 112–13 Cercospora carotae 102–3
buckeye rot 350 seed treatments 39 Cercospora leaf blight (carrot) 101–2
bugs seedborne pathogens 40 Cercospora leaf spot
beet lace 149 southern blight 101 beet 140
squash 225, 226 violet root rot 105–6 horseradish 383
butternut squash 231 viral diseases 116–17, 124–5 Swiss chard 387
white mold (cottony rot) 111–12 Cercosporidium blight (fennel) 406, 407
wild 117 Cercosporidium punctum 406
world production trends 13 Ceutorhynchus pleurostigma 181
440 I NDEX
Chalara elegans see Thielaviopsis Colletotrichum gloeosporioides 204, crown rot

basicola 343–4 artichoke 399
Chalaropsis thielavioides 114 Colletotrichum lagenarium see rhubarb 414
charcoal rot (cucurbits) 240 Colletotrichum orbiculare crown/root rot
Cheiranthus cheiri 160 Colletotrichum orbiculare 238 Fusarium 130–1, 236–7, 346–7
Chenopodiaceae 14, 138 composting 76 Phoma 86–7
Chenopodium spp. 137, 138, 140, 369, composts 42–3 Phytophthora 243–4
375, 379 conditioners 47 Rhizoctonia 113–14
Cherry leaf roll virus 416 conidia 22 crucifers 27
chervil 122, 385–6 conidiophores 22 black rot 14, 39
chickpea (garbanzo bean) 272, 276, Coniothyrium minitans 47, 264, 314 seed treatments 39
277, 286 Conium maculatum 93 seedborne pathogens 40
chickweed 94 control of disease see also brassicas
chicory, red see radicchio biological 47, 264, 314 cucumber 248
Chinese cabbage 162, 164, 176–7, 183, challenges 16 angular leaf spot 224–5
184, 192, 194, 197 checklist of options 48 downy mildew 244–5
Chinese parsley see cilantro criteria for 38 Fusarium wilt 235
Chinese winter melon 246 cultural practices 42–3 gummy stem blight/black rot 230–1
chives 72, 73 exclusion 39–41 Phytophthora crown/root rot 243–4
chloropicrin 75 forecasting 47, 60, 68, 142, 154, powdery mildew 232–3
chlorothalonil 135, 163, 176, 290 230, 339, 344, 354 scab 228–9
chocolate spot (broad bean) 288–90 integrated disease management Verticillium wilt 246–7
Cicer arietinum (chickpea/garbanzo 49–50 viral disease 247–51
bean) spp. 272, 276, 277, 286 organic systems 49 world production trends 13
Cichorium endivia (endive/escarole) postharvest handling 49 cucumber beetle
391–5 resistant plants and cultivars 41–2, spotted 223
Cichorium intybus 393 50 striped 223
Ciculifer tenellus 386 sanitation 43–4 western striped 249
cilantro 27, 40, 82, 92, 116, 396–7 site selection 38–9 Cucumber mosaic virus 93–4, 215, 247,
Cilantro yellow blotch virus 396 copper treatments 49, 95, 158, 200, 363, 381, 416
Circulifer opacipennis 148, 214 220, 225, 253–4, 299, 302, 329, Cucurbitaceae 14, 28, 220
Circulifer tenellus 148, 214, 379 331, 333 angular leaf spot 224–5
Cladosporium spp. 336 Coriandrum sativum (cilantro) 27, 40, anthracnose 238–9
Cladosporium allii-cepae 64–5 92, 116, 396–7 bacterial fruit blotch 220–1
Cladosporium cucumerinum 228 corky root disease bacterial wilt 222–3
Cladosporium leaf blotch (Alliaceae) lettuce 41, 299–300 charcoal rot 240
64–5 tomato 356–7 damping-off/root rots 226–8
Cladosporium leaf spot (spinach) 371–2 corn see sweetcorn downy mildew 244–5
Cladosporium tenuissimum 228–9 corn salad 27, 420 Fusarium crown/foot rot 236–7
Cladosporium variabile 371–2 Corticum rolfsii see Sclerotium rolfsii Fusarium wilt 44, 234–5
Clavibacter michiganensis subsp. Corynebacterium michiganense see genetic modification 42
michiganensis 328 Clavibacter michiganensis subsp. gummy stem blight/black rot 230–1
clovers 268, 271, 293 michiganensis Monosporascus root rot/vine
club-rush 115 cotton 225, 228 decline 241–2
clubroot (brassicas) 24, 41, 43, 181–3 cottony rot see white mold Phytophthora crown/root rot 243–4
collards 158 cover crops 42, 114, 264, 314 powdery mildew 232–3
Collectotrichum lindemuthianum 261 cow parsley 93, 117, 124 scab 228–9
Colletotrichum capsici 204 cow parsnip 121 seed treatments 39
Colletotrichum circinans 77 cowpea 260 seedborne pathogens 40
Colletotrichum coccodes 204, 343–4, crater rot (carrot) 100 Verticillium wilt 246–7
357 crater spot (celery/parlsey) 91–2 viral diseases 247–51
Colletotrichum dematium 343–4 crook root (watercress) 24, 416 world production trends 13
Colletotrichum dematium f. sp. crop breeding programs 15 yellow vine disease 225–6
spinaciae 373 crop residues 42, 264, 314 cultural practices 42–3
Colletotrichum erumpens 414 crop rotations 42 Curculifer opacipennis 379
I NDEX 441
Cylindrosporium concentricum 188 E fungi 22–3

Cymbopogon citratus (lemongrass) 397 early blight disease diagnosis 36
Cynara scolymus (artichoke) 399–404 celery 83–4 taxonomy 22
tomato 338–9 fungi imperfecta 23, 56, 194
D eggplant (aubergine) 13, 243, 328, 339, fungicides 15, 44–7
damping-off 357 categories 46
Apiaceae 87–8, 126–7 endive/escarole 28, 300, 391–5 choice of agent 46
beet 138–9 environmental factors 39 foliage applied 46
brassicas 191–3 environmental manipulation 44 mode of action 46
cucurbits 226–8 enzyme-linked immunosorbent assay organic systems 49
pea 282–3 (ELISA) 35 resistance to 46–7, 230, 276, 303,
peppers 208–9 Eruca sativa (arugula) 26, 157, 404–5 305, 353–4
prevention 44 Erwinia spp. 19, 393 safety 15–16
spinach 370–1 Erwinia carotovora 334, 414 seed treatment 39–41
Swiss chard 388 Erwinia carotovora subsp. carotovora specialty crops 46, 382
tomato 355–6 95, 156 fungus-like pathogens 23–4, 36
dandelion, Italian 393 Erwinia chrysanthemi 95, 399 Fusarium spp., sweetcorn 421
Daucus carota see carrot Erwinia rhapontici 415 Fusarium avenaceum 287, 421
dazomet 75 Erwinia tracheiphila 222–3 Fusarium basal plate rot (Alliaceae)
demethylation inhibitors (DMIs) 46 Erysiphe betae 141–2 63–4
Diabrotica undecimpunctata 223, 249 Erysiphe biocellata 409 Fusarium crown/root rot
diagnosis of disease 31 Erysiphe cichoracearum see asparagus 130–1
digitally assisted 36 Golovinomyces cichoracearum cucurbits 236–7
fungal/fungal-like disease 36 Erysiphe cruciferarum 168–9 tomato 346–7
laboratory tests 35–6 Erysiphe heraclei 103–4, 118, 126, 385 Fusarium culmorum 63, 130, 287, 421
strategy 31–5 Erysiphe orontii see Golovinomyces Fusarium equiseti 227
viral disease 36 orontii Fusarium graminearum 287, 421
diallyl disulfide (DADS) 47, 75 Erysiphe pisi 276 Fusarium oxysporum 287, 371, 413–14
dicarboximides 75, 264, 276, 305 Erysiphe polygoni 259, 387 Fusarium oxysporum f. sp. apii 85–6
dichlofluanid 342 exclusion 39–41 Fusarium oxysporum f. sp. asparagi 130
Didymella bryoniae 230 Fusarium oxysporum f. sp. basilicum
dieback disease (lettuce) 320–1 F 411
digitally assisted diagnosis (DAD) 36 faba bean see broad bean Fusarium oxysporum f. sp. cepae 63
dill 28, 92, 99, 116, 385 Fabaceae 13, 14, 252 Fusarium oxysporum f. sp. ciceris 277
disease forecasting 47, 60, 68, 142, 154, see also beans; broad bean; pea Fusarium oxysporum f. sp. conglutinans
230, 339, 344, 354 fat hen 137, 375 170
disease resistance 41–2, 50 fennel 28, 86, 88, 115, 122, 406–7 Fusarium oxysporum f. sp. corianderii
Ditylenchus dipsaci 415 fenpropimorph 173 396
downy mildew 24 fertilizers 42–3, 163 Fusarium oxysporum f. sp.
Alliaceae 67–8 finochio see fennel cucumerinum 235
Apiaceae 122–3 flagellates 18 Fusarium oxysporum f. sp. lactucae 306
arugula 404, 405 flooding 76 Fusarium oxysporum f. sp. lycopersici
beet 142–3 Foeniculum vulgare dulce (fennel) 345
brassicas 163, 178–80 406–7 Fusarium oxysporum f. sp. melonis 44,
broad bean 291–2 food safety 15–16 235
control 39 foot rot disease Fusarium oxysporum f. sp. niveum 235
cucurbits 244–5 beans (Phaseolus) 256–7 Fusarium oxysporum f. sp. phaseoli 260
horseradish 383–4 pea 272–3 Fusarium oxysporum f. sp. pisi 277
lettuce 41, 302–4 forecasting see disease forecsting Fusarium oxysporum f. sp. radicis-
pea 280–2 fosetyl aluminium 133, 303 cucumerinum 235
rhubarb 415 Frankliniella fusca 218 Fusarium oxysporum f. sp. radicis-
spinach 41, 375–6 Frankliniella occidentalis 137, 218, 323 lycopersici 346–7
Swiss chard 387 fruit blotch, bacterial (cucurbits) 220–1 Fusarium oxysporum f. sp. raphani 170
watercress 416–17 fruit rots (tomato) 350–1, 355–6 Fusarium oxysporum f. sp. spinaciae
dry rot (black leg) 171–3 fumigants, pre-plant 44 371, 374
Fusarium poae 421
442 I NDEX
Fusarium proliferatum 63, 130 lettuce 304–5 I

Fusarium redolens f. sp. asparagi 130 pea 275–6 infection indices 97
Fusarium root rot (broad bean) 287–8 pepper 202–3 integrated disease management 49–50,
Fusarium solani 227, 287, 384 rhubarb 414 382
Fusarium solani f. sp. cucurbitae 236–7 tomato 341–3 interactions 131
Fusarium solani f. sp. fabae 287 ‘gray stem’ 177 iprodione 166, 173
Fusarium solani f. sp. phaseoli 256 greenhouse environment 44 irrigation of crops 43, 44
Fusarium solani f. sp. pisi 273 ground cherry 200, 333 Italion dandelion 393
Fusarium verticilloides (F. moniliforme) groundsel 316 Itersonilia blight (dill) 385
421 ‘gummosis’ 228 Itersonilia canker (parsnip) 118–19
Fusarium wilt gummy stem blight (cucurbits) 230–1 Itersonilia pastinaceae 118–19
basil 411 Itersonilia perplexans 118–19, 385
beans (Phaseolus) 260 H
cilantro 396 halo blight, beans 252–4 J
control 44 head rot Jerusalem artichoke 28, 407–8
cucurbits 44, 234–5 Alternaria 164–6
lettuce 306–7 bacterial (brocolli) 155–6 K
resistance to 41 Helianthus tuberosus (Jerusalem ketchup (tomato) 14
spinach 374 artichoke) 407–8
tomatillo 413–14 Helicobasidium brebissonii 105–6, 132 L
tomato 344–6 Helicobasidium compactum 106 laboratory tests 35–6
Fusarium yellows/wilt 41, 85–6, Helicobasidium mompa 106 lace bug, beet 149
169–71 hemlock 93 Lactuca sativa see lettuce
Heracleum lanatum 121 Lactuca serriola 300, 308
G Heracleum sphondylium 120, 124 Lamiaceae 14
garbanzo bean (chickpea) 272, 276, herbs late blight 24
277, 286 fungicides 46, 382 Phytophora (tomato) 24, 41, 352–5
garlic seedborne pathogens 40 Septoria (Apiaceae) 90–1
black mold 58 see also named herbs Lathyrus spp. 269, 278
Penicillium mold 66–7 Heterosporium allii see Mycosphaerella leaf blight
rust 72–4 allii Alternaria (carrot) 96–7
viral disease 78 Heterosporium allii-cepae see bacterial (carrot) 96
white rot 74–5 Mycosphaerella allii-cepae Cercospora 102–3
world production trends 13 Heterosporium variabile see Cercosporidium 406
Garlic mosaic virus 78 Cladosporium variabile leaf and pod spot
Garlic yellow streak virus 78 higher plant pathogens 18 broad bean 290–1
Garlic yellow stripe virus 78 hogweed 120, 124 pea 274–5
Gazania spp. 39, 50, 318 horsenettle 339 leaf spot
genetic modification 42 horseradish 28, 160, 194, 383–4 Alternaria 164–6, 390–1
gherkin, world production 13 host plants Ascochyta 414
gibberellic acid 97 specificity 14 bacterial
gladiolus 268 weeds 38–9, 115 angular 224–5
Glomerella lagenarium 238 host-free period 42, 50 basil 413
Glomerella lindemuthiana 261 hot water seed treatment 39, 144, 200, brassicas 158
Glycine max (soyabean) 269, 290 372, 377, 379 celery 82–3
Golovinomyces cichoracearum 232–3, human health 12, 15–16 cilantro 397
307–8, 392, 393, 400–1, 418 Hyaloperonospora parasitica see Italian dandelion 393
Golovinomyces orontii 407, 420 Peronospora parasitica lettuce 301–2
gourd family see Cucurbitaceae hybridization nodules 181 spinach 368–9
grass hosts 115 hydrochloric acid 200 Swiss chard 388
gray leaf spot (pepper) 211–12 hymexazol 139 Xanthomonas 332–4, 410
gray mold 44, 60 Cercospora 140, 383, 387
artichoke 399–400 gray (pepper) 211–12
basil 411 light (brassicas) 186–8
beans (Phaseolus) 258–9 Phloeospora (parsnip) 120
brassicas 167 Phoma/black leg (brassicas) 171–3
I NDEX 443
Ramularia 123, 145, 383–4, 402 M Myzus persicae 79, 137, 150, 151, 153,
Septoria 416–17 Macrophomina phaseolina 240 154, 196, 197, 198, 267, 268, 283,
Stemphylium (spinach) 376–7 Macrosiphum euphorbiae 268, 286 286, 317, 318, 363, 380, 417
leafhoppers 38–9, 297 Macrosteles fascifrons 81
aster 38–9, 81, 297 Macrosteles quadrilineatus 297 N
beet 148, 214, 379, 386 maize smut 421 Nasonovia ribis-nigri 318
leek maneb fungicides 331, 333 neck rot (Alliaceae) 61–2
bacterial blight 54–5 mangold 142, 147 Nectria haematococca 236
Cladosporium leaf blotch 65 manures 41 nematodes 18, 44, 249, 284, 345, 410,
Fusarium basal plate rot 63–4 marjoram 29, 413 415, 416
purple blotch 56–7 Marssonina panattoniana see Nepeta cataria (catnip) 410
rust 72–3 Microdochium panattonianum Nicotiana glutinosa 328
world production trends 13 Matthiola spp. 160 nightshade
Yellow stripe virus 78 Melica spp. 115 black 200, 328, 333, 339
legumes 114, 225, 273 Meloidogyne spp. 345 cutleaf 328
lemongrass 28, 397 melon hairy 316, 353
Lens culinaris 276, 286 bacterial wilt 222–3 perennial 328
lentils 276, 286 citron 220 nutritional value of vegetables 12
Leptosphaeria biglobosa 173 damping-off 226–8
Leptosphaeria maculans 171–3 Fusarium wilt 44, 235 O
lettuce honeydew 220 Ocimum basilicum (basil) 411–12
prickly 300 powdery mildew 233 Oidiopsis spp. 104
wild 300, 308 Mentha spp. (mint) 29, 409–10 Oidiopsis neolycopersici 348–9
lettuce (Lactuca sativa) 28 metalaxyl 110, 184, 303, 353–4, 370, Oidiopsis taurica 205, 232, 348, 349
ammonium toxicity 325 371 Oidium spp. 348–9
anthracnose disease 308–9 metam sodium 75 oilseed rape (Brassica napus) 166, 171,
aster yellows 296–7 methyl bromide 75 178, 186–8, 196, 384, 408
bacterial leaf spot 301–2 Mexican parsley see cilantro okra, world production trends 13
bottom rot 311–12 Microdochium spp. 397 Olpidium brassicae 322
corky root 299–300 Microdochium panattonianum 308–9 Onion yellow dwarf virus 79
downy mildew 41, 302–4 mildew see downy mildew; powdery onions
Fusarium wilt 306–7 mildew bacterial blight 55
gray mold 304–5 milk thistle 308 black mold 58–9
Phoma basal rot 310–11 mint 29, 409–10 Cladosporium leaf blotch 65
powdery mildew 307–8 Mirafiori lettuce virus 322 downy mildew 67–8
seedborne pathogens 40 mite-borne disease 78 green 77
tipburn 326 mold see black mold; blue mold; gray neck rot 61–2
varnish spot 41, 298–9 mold; white mold Penicillium mold 66–7
Verticillium wilt 315–16 molecular technology 42 pink root 69–70
viral diseases 20, 41, 43, 317–24 mollicutes 19, 81, 297–8 rust 72–3
white mold (lettuce drop) 43–4, Monosporascus cannonballus 241–2 salad 59–60
313–15 morpholine fungicides 169 sweet 54–5
world production trends 13 motley dwarf (carrot) 42, 116–17 white rot 74–5
Lettuce mosaic virus 39, 41, 42, 49–50, mushrooms 13 world production trends 13
318–19 muskmelon 220, 227, 235 see also Alliaceae
Lettuce necrotic stunt virus 20, 41, 43, mustards 29, 162, 390–1 Onobrychis vicifolia 225
320–1, 322 Mycocentrospora acerina 107 oomycetes 24, 36
Leveillula lanuginosa 103–4, 126 Mycosphaerella allii 64–5 see also named species and genera
Leveillula taurica 103–4, 205–6, 233, Mycosphaerella allii-cepae 64–5 oregano 29, 413–14
348, 400 Mycosphaerella brassicicola 175–6 organic growing 49
licorice rot (Apiaceae) 107 Mycosphaerella capsellae 176–7 Origanum vulgare/majorana
light leaf spot (brassicas) 186–8 Mycosphaerella melonis see Didymella (oregano/marjoram) 413
lime applications 42–3, 182 bryoniae Oscinella frit 421
Mycosphaerella pinodes 274, 278–9 oxtongue, bristly 318
mycotoxins 421
Myzus ascalonicus 79
444 I NDEX
P pepper (Capsicum spp.) 29, 199 Phragmites communis 415

pak-choi see bok choy anthracnose 204 Phyllotreta spp. 417
Papaya ringspot virus type W 248 bacterial spot 199–200 Physalis ixocarpa (tomatillo) 413–14
Paratrichodorus spp. 284 damping-off/root rot 208–9 Physalis minima 200, 333
parsley (Petroselinum crispum) 29, 122 gray leaf spot 211–12 physiological disorders
crater spot 91–2 gray mold 202–3 blackheart 89, 94
powdery mildew 126 Phytophthora blight/root and blossom end rot 367
root rot 88, 126–7 crown rots 206–8 tipburn 326, 395
seedborne pathogens 40 powdery mildew 205–6 Phytophthora spp.
Septoria blight 128 seedborne pathogens 40 asparagus 133
southern blight 101 southern blight 201–2 brassicas 71, 184–6
viral diseases 92–3, 116–17 Verticillium wilt 212–13 cucurbits 227–8, 243–4
white mold 127 viral diseases 214–19 disease cycle 133
parsnip (Pastinaca sativa) 29, 112, white mold (Sclerotinia rot) 210–11 parsley 126–7
118–25 world production trends 13 pepper 206–9
black (Itersonilia) canker 118–19 Pepper mild mottle virus 216 rhubarb 415
black rot 97 Peronospora destructor 67–8 sage 418
cavity spot 108–10 Peronospora effusa see Peronospora tomato 350–1, 355–6
downy mildew 122–3 farinosa f.sp. spinaciae Phytophthora brassicae 71, 184
licorice rot 107 Peronospora farinosa f. sp. betae 142–3, Phytophthora cactorum 133, 185
Phloeospora leaf spot 120 387 Phytophthora capsici 43, 206–8, 243–4,
Phoma canker 121–2 Peronospora farinosa f. sp. spinaciae 350–1, 356
powdery mildew 118 41, 375–6 Phytophthora cryptogea 133, 350, 371,
Ramularia leaf spot 123 Peronospora jaapiana 415 418
seedborne pathogens 40 Peronospora parasitica 163, 178–80, Phytophthora drechsleri 185, 227, 244,
southern blight 101 383, 404, 416 350
viral diseases 92–3, 124–5 Peronospora viciae 280–1, 291–2 Phytophthora erythroseptica var. pisi
wild 93 Peronospora viciae f. sp. pisi 280 288
Parsnip yellow fleck virus 124–5 pesticide resistance 46–7, 230, 276, Phytophthora infestans 24, 354–6
Pastinaca sativa see parsnip 303, 305, 353–4 Phytophthora megasperma 133, 185–6,
Pea (bean) leaf roll virus 283 pesticides 44–7 287–8
Pea early browning virus 284 safety 51–6 Phytophthora parasitica 350, 351, 356
Pea enation mosaic virus 285 see also fungicides Phytophthora porri 70–1
pea (Pisum sativum) 29, 269–87 Petunia spp. 353 Phytophthora primulae 126–7
Aphanomyces/common root rot pH, soil 110, 182 Phytophthora richardiae 133
270–1 Phaedon cochleariae 417 phytoplasmas 19, 81
Ascochyta blight 278–9 Phaseolus spp. see beans aster yellows 38–9, 80–1, 296–7
bacterial blight 269–70 Phaseolus coccineus 260 Picris echioides 318
bean leaf roll 284 phenylamides 46, 133, 163, 281, 303 Piesma quadratum 149
downy mildew 280–2 Phloeospora herclei 120 pigeon pea 276
foot rot complex 272–3 Phoma apiicola 86–7 pink root (Alliaceae) 69–70
Fusarium wilt 277–8 Phoma basal rot, lettuce 310–11 pink rot (Apiaceae) 88–9
gray mold 275–6 Phoma betae 144 Pisum sativum see pea
leaf and pod spot 274–5 Phoma canker (parsnip) 121–2 pith necrosis (tomato) 334–5
powdery mildew 276–7 Phoma complanata 86, 121–2 plant stimulants 47
Pythium root rot/damping-off 282 Phoma crown/root rot (Apiaceae) 86–7 planting, timing of 43
seed treatments 39 Phoma cucurbitacearum 230 Plasmidiophoromycota 23–4
viral diseases 283–6 Phoma diachenii 121 Plasmodiophora brassicae 24, 181–3
white mold 283 Phoma exigua 310–11 Plasmopara lactucae-radicis 303
world production 13 Phoma leaf spot/canker (black leg) Plasmopara umbelliferarum 122
Pea seedborne mosaic virus 286 171–3 Pleospora bjoerlingii 139, 143–4
Pea streak virus 286 Phoma lingam 172–3 Pleospora herbarum 134–5, 377
penicillium blue mold 66–7 Phoma medicaginis var. pinodella 256, Poaceae 14
Penicillium hirsuitum (P. corymbiferum) 272–3, 278, 279 Podosphaera xanthii/P. fusca
66–7 Phoma rostrupii 86 (Sphaerotheca fuliginea/S.fusca)
Phoma terrestris 69–70 232–3, 259
I NDEX 445
Polygonaceae 14 Pseudomonas syringae pv. spinaciae R

Polymyxa betae 152 368–9 radicchio 29, 391–5
postharvest handling 15, 49 Pseudomonas syringae pv. syringae 200, radish 29, 158
potato 105, 339, 353–4 224, 253 Alternaria leaf spot 164–6
Potato virus Y 217, 363 Pseudomonas syringae pv. tomato 330–1 black leg 171–2
powdery mildew Pseudomonas viridiflava 54–5, 95, 156, downy mildew 178–80
Apiaceae 103–4 334, 412 Fusarium wilt 169–70
artichoke 400–1 Pseudoperonospora cubensis 244–5 Rhizoctonia root rot 192–3
beans (Phaseolus) 259 Puccinia allii 14, 72–3 white rust/white blister 162–3
beet 141–2 Puccinia angelicae 115 Ralstonia solanacearum 399
brassicas 168–9 Puccinia angustata 409 Ramularia amoraciae 383–4
chervil 385 Puccinia apii 115 Ramularia beticola 145
corn salad 420 Puccinia asparagi 135–6 Ramularia cynarae 402
cucurbits 232–3 Puccinia hieracii 393 Ramularia leaf spot
dill 385 Puccinia hysterium 419 artichoke 402
endive and radicchio 392, 393 Puccinia jackyana 419 beet 145
Jerusalem artichoke 407 Puccinia menthae 409, 413 horseradish 383–4
lettuce 307–8 Puccinia nakanishikii/cymbopogonis parsnip 123
mint 409 397 Ramularia pastinaceae 123
parsley 126 Puccinia nitida 115 Ramularia rhei 416
parsnip 118 Puccinia phragmitis 415 Ramularia rot (rhubarb) 416
pepper 205–6 Puccinia pimpinellae 115 rappini 162
sage 418 pumpkin 13, 220, 225, 236–7, 243, 248 red chicory see radicchio
Swiss chard 387 purple blotch (Alliaceae) 56–7 research 15
tomato 348–9 purple spot (asparagus) 134–5 resistance see disease resistance;
Pratylenchus penetrans 410 Pyrenochaeta lycopersici 357 pesticide resistance
production practices 34 Pyrenochaeta terrestris see Phoma Resseliella spp. 287
protozoa 181–3, 416 terrestris Rheum rhubarbarum 414–16
Pseudocercosporella capsellae 176, 390 Pyrenopeziza brassicae 188 Rhizoctonia carotae 101
Pseudomonas spp. 55, 392 Pythium spp. Rhizoctonia crocorum 106, 132
Pseudomonas cepacia 54 Apiaceae 87–8, 126 Rhizoctonia solani
Pseudomonas cichorii 41, 43, 298–9 artichoke 401 anastomosis groups 114, 192, 193,
Pseudomonas corrugata 334–5 beans 256, 257 273, 312
Pseudomonas fluorescens 156, 334 beet 139 Apiaceae 92, 113
Pseudomonas gladioli pv. alliicola 54 broad bean 287 brassicas 191–3
Pseudomonas marginalis 95, 156, 414 control 44 broad bean 288
Pseudomonas pseudoalcaligenes subsp. cucurbits 226–8 Chenopodiaceae 139
citrulli see Acidovorax avenae pea 272, 273, 282 control 193
subsp. citrulli pepper 208–9 cucurbits 227
Pseudomonas syringae 18–19, 393 rhubarb 415 description and disease cycle 114,
Pseudomonas syringae pv. alisalensis spinach 370–1 193, 356
157, 389, 405 Swiss chard 388 endive/escarole 394
Pseudomonas syringae pv. apii 82 tomato 355–6 foliar blight 192
Pseudomonas syringae pv. aptata 224, Pythium aphanidermatum 209, 227, legumes 114, 256, 273
388 228, 282, 356, 371, 401 lettuce 311–12
Pseudomonas syringae pv. coriandricola Pythium arrhenomanes 356 pepper 209
82, 397 Pythium artotrogus 87 Swiss chard 388
Pseudomonas syringae pv. lachrymans Pythium debaryanum 87, 282, 356 tomato 356
224–5 Pythium irregulare 87, 227, 371 rhizomania 43, 151–2
Pseudomonas syringae pv. maculicola Pythium mastophorum 87 Rhizomonas suberifaciens 41, 299–300
158 Pythium myriotylum 209, 227, 228, rhubarb 198, 414–16
Pseudomonas syringae pv. phaseolicola 356 rice 225, 226
252–4 Pythium paroecandrum 87, 126 ring spot
Pseudomonas syringae pv. pisi 269 Pythium sulcatum 109 brassicas 174–6
Pseudomonas syringae pv. porri 19, Pythium ultimum 87, 227, 282, 356 lettuce 308–9
54–5 Pythium violae 109–10 rocket see arugula
446 I NDEX
roguing 43 Scirpus spp. 115 Sitona lineatus 295

root rots Sclerotinia diseases slippery skin disease 54
Aphanomyces (pea) 270–1 Apiaceae 88–9, 111–12 Smith periods 354
Apiaceae 87, 126–7 beans (Phaseolus) 262–5 smudge disease 77
artichoke 401 brassicas 189–90 smut
asparagus 132 broad bean 292–3 alliums 77
beet 138–9 control 44, 47, 211 maize 421
brassicas (Phytophthora) 185–6 disease cycle 264 sodium hypochlorite 39, 372, 377, 379
brassicas (Rhizoctonia) 191–3 lettuce 313–15 soft rot
broad bean 287–8 pea 283 bacterial 55, 392, 393
cucurbits 226–8, 241–2 pepper 210–11 watery (Sclerotinia) 111–12,
Monosporascus 241–2 specialty/herb crops 386, 394, 406, 189–90, 408
peppers 206–9 407, 408, 412, 420 soilborne disease 44
rhubarb 415 tomato 358–9 soils 34, 42–3, 44
sage 418 Sclerotinia minor 111, 210–11, 262–4, pH 110, 182
spinach 370–1 293, 420 Solanaceae 14
tomato 350–1, 355–6 Apiaceae 88–9, 111–12 Solanum carolinense 339
violet (carrot) 105–6 brassicas 189–90 Solanum douglasii 328
rooting material, and disease diagnosis lettuce 313–15 Solanum lycopersicum see tomato
34 specialty/herb crops 394, 406–7, Solanum nigrum 328, 339
Rorippa nasturtium-aquaticum 412, 420 Solanum physalifolium 353
(watercress) 416–18 tomato 358–9 Solanum sarrachoides 316, 353
runner bean Sclerotinia sclerotiorum 94, 111, 127, Solanum triflorum 328
common 252 210–11, 283, 292–3 solarization 44, 76
scarlet 252, 260 Apiaceae 88–9, 111–12, 127 Sonchus spp. 300, 316
rust 14 beans 262–4 sour skin (Alliaceae) 54
Alliaceae 72–4 brassicas 189–90 southern blight
Apiaceae 115–16 lettuce 313–15 Alliaceae 74, 76
asparagus 135–6 specialty/herb crops 386, 408, 412 Apiaceae 101
autecious 115 tomato 358–9 Jerusalem artichoke 408
beet 147 Sclerotinia trifoliorum 263, 283, 292–3 pepper 201–2
broad bean 293–5 Sclerotium cepivorum 47, 74–5 tomato 340–1
endive/escarole 393 Sclerotium rolfsii 74, 101, 202, 340–1, sowthistle 300, 316
heteroecious 115 408 soyabean 269, 290
lemongrass 397 Sclerotium stem rot see southern blight spear rot, bacterial (broccoli) 155–6
mint 409–10 Scorzonera hispanica (black salsify) 419 specialty crops 382
oregano/marjoram 413 sea beet, wild 141, 142, 147 disease resistance 41
Phaseolus spp. 265–6 seed health 39–40 fungicides 46, 382
rhubarb 415 seed treatments 14–15, 39–41, 44, 144, range 382
salsify 419 176, 200, 220, 372, 377, 379 seedborne pathogens 40
Swiss chard 388–9 seedborne pathogens 39, 40 see also named crops
weed hosts 115 Senecio vulgaris 316 Sphaerotheca fuliginea (Podosphaera
see also white rust Septoria apiicola 90–1 xanthii/P. fusca) 232–3, 259
Septoria blight (parsley) 128 Spinach curly top virus 148, 214, 362,
S Septoria leaf spot (watercress) 416–17 380
sage 418 Septoria petroselini 128 spinach (Spinacia oleracea) 368
sainfoin 225 Septoria siyimbrii 416 anthracnose 373
Salinas Valley, California 42, 49–50 serological tests 35 bacterial leaf spot 368–9
salsify 419 Serratia marcescens 225–6 Cladosporium leaf spot 371–2
Salvia officinalis (sage) 418 shallot 13 damping-off/root rots 370–1
sanitation 43–4, 193 Shallot latent virus 79 disease control 44
scab shepherd’s purse 183, 316 downy mildew/blue mold 41, 375–6
Apiaceae 112–13 shot hole see anthracnose disease Fusarium wilt 374
beet 146 signs 33 seedborne pathogens 40
cucurbits 228–9 Sinaloa tomato leaf curl virus 217 Stemphylium leaf spot 376–7
scientific names 14 site selection 38–9, 50 Verticillium wilt 378–9
I NDEX 447
viral disease 151, 153, 379–81 sweetcorn 13, 40, 421 Tomato spotted wilt virus 218, 323,
white rust 369–70 Swiss chard 40, 138, 142, 147, 153, 364–5, 384, 394, 395, 412
world production trends 13 386–9 tomato verde see tomatillo
Spinacia oleracea see spinach systemic acquired resistance (SAR) 47 Tomato yellow leaf curl virus 366
spiroplasmas 19 TOMCAST 339, 344
Spongospora nasturtii 416 T Tragopogon porrifolius (salsify) 419
sporangiospores 22 table beet (beetroot) 138, 142, 147, transplants 15, 41, 54
sprouts 179 154, 386 Trialeurodes vaporariorum 152
see also Brussel sprouts tah tsai 390 triazoles 75, 118, 136, 142, 166, 169,
squash 220, 225 taxonomy 14 264, 266, 290
anthracnose 238–9 technological advances 14–15 Trichodorus spp. 284
bacterial wilt 222–3 temperature manipulation 44 Trifolium spp. 268, 269, 273, 293
downy mildew 244–5 Thanatephorus cucumeris 91–2, 114, trisodium phosphate 39, 364
Fusarium crown/root rot 236–7 192, 227, 288, 312, 394 Tuberculina spp. 106
hard 243 Thielaviopsis basicola (Chalara elegans) turnip 158, 162, 164, 168–9
Papaya ringspot virus 248 114–15, 256–7, 273 dry rot (black leg) 171–3
Phytophthora crown/root rot 243–4 thiram 144, 173, 176, 281 white leaf spot 176–7
powdery mildew 232–3 thrips 218, 323, 364, 413 turnip gall weevil 181
scab 228–9 tobacco (Thrips tabaci) 137, 218, Turnip mosaic virus 198, 324, 384, 414,
spaghetti 237 323 416, 417
summer 42, 235, 244 western flower 137, 218, 323 Turnip yellow mosaic virus 417
world production trends 13 tipburn 326, 395
zucchini 229 Tobacco etch virus 217 U
squash bug 225, 226 Tobacco mosaic virus 218, 364 Umbelliferae see Apiaceae
Squash leaf curl virus 248–9 Tobacco ringspot virus 249 Urocystis cepulae 77
Squash mosaic virus 249 Tobacco streak virus 137 Urocystis colchici 77
stalk rot (sweetcorn) 421 tomatillo (Physalis ixocarpa) 413–14 Uromyces appendiculatus 265–6
Stellaria media 94 Tomato bushy stunt virus 20, 320 Uromyces betae 147, 388–9
stem blight, gummy (cucurbits) 230–1 tomato ketchup 14 Uromyces graminis 115
stem canker, Alternaria (tomato) 337–8 Tomato mosaic virus 39, 218, 364 Uromyces lineolatus 115
stem rot, Sclerotium (southern blight) tomato (Solanum lycopersicum) 327 Uromyces vicia-fabae (U. fabae) 294
74, 76, 101, 201–2, 340–1, 408 Alternaria stem canker 337–8 Ustilago maydis 421
Stemphylium spp. 67, 336 anthracnose 343–4
Stemphylium botryosum 211–12, bacterial canker 327–9 V
376–7 bacterial speck 330–1 Valerianaceae 14
Stemphylium floridanum 211–12 bacterial spot 332–4 Valerianella locusta/olitoria (corn salad)
Stemphylium leaf spot (spinach) 376–7 black mold 336 27, 420
Stemphylium lycopersici 211–12 blossom end rot 367 varnish spot (lettuce) 41, 298–9
Stemphylium solani 211–12 corky root rot 356–7 vectors of disease 20, 44
Stemphylium vesicarium 56, 57, 134 damping-off/fruit rots 355–6 see also named vectors e.g. aphids
storage disease defined as vegetable or fruit? 14 vegetable production
brassicas 184–5 disease resistance 41 challenges 15–16
carrot 100, 111 early blight 338–9 technological advances 14–15
Strawberry latent ringspot virus 416 Fusarium crown/root rot 346–7 world trends 12, 13
streak and bulb rot, bacterial 54–5 Fusarium wilt 344–6 Verticillium dahliae, host range 212–13
Streptomyces spp. 18, 146 gray mold 341–3 Verticillium longisporum 194, 384
Streptomyces scabies 112–13, 146 late blight 41, 352–5 Verticillium wilt (V. dahliae) 41, 43
strobilurins 46, 163, 166, 176, 230, Phytophthora root rot 350–1 artichoke 403
264, 276, 290 pith necrosis 334–5 brassicas 169, 194–5
sugar beet 105, 138, 142, 147 powdery mildew 348–9 cucurbits 246–7
Beet yellows virus 154 seedborne pathogens 40 horseradish 384
seed treatments 144 southern blight 340–1 lettuce 315–16
sulfur 49, 118, 142, 169, 266 Verticillium wilt 360–1 mint 410
swede 168, 169, 176–7 viral diseases 361–6 pepper 212–13
dry rot (black leg) 171–3 white mold/Sclerotinia rot 358–9 spinach 378–9
storage rot 185 world production trends 13 tomato 360–1
448 I NDEX
Vicia spp. (wild vetches) 268, 269, 276, pea 283

278, 286, 290 pepper 210–11
Vicia faba see broad bean specialty/herb crops 406, 407, 412
Vigna unguiculata (cowpea) 260 tomato 358–9
vine decline (cucurbits) 241–2 white rot (Alliaceae) 41, 74–5
violet root rot 105–6, 132 white rust 24
viral diseases arugula 404
Alliaceae 78–9 horseradish 383
Apiaceae 92–4, 116–17, 124–5 salsify 419
asparagus 131, 137 spinach 369–70
beans (Phaseolus) 267–8 white rust (white blister), brassicas
beet 148–54 162–3
brassicas 196–8 white tip 70–1
broad bean 295 whiteflies 152, 249, 366
cucurbits 247–51 wilt see bacterial wilt; Fusarium wilt;
diagnosis 36 Verticillium wilt
helper viruses 124 wirestem (Rhizoctonia disease),
pathogen dispersal 20–2 brassicas 191–3
pea 283–6
pepper 214–19 X
rhubarb 416 Xanthomonas spp. 18, 55, 399
spinach 151, 153, 379–81 biology 332–3
tomato 361–6 control 14, 333
watercress 417–18 Xanthomonas campestris 169, 410
Xanthomonas campestris pv. amoraciae
W 160, 384
wallflower 160 Xanthomonas campestris pv. campestris
water reed 415 39, 160, 169
water supply 34, 41 Xanthomonas campestris pv. carotae 95
watercress 24, 40, 198, 416–18 Xanthomonas campestris pv. phaseoli
Watercress chlorotic leaf spot viroid 254–5
417 Xanthomonas campestris pv. phaseoli
Watercress yellow spot virus 417 var. fuscans 255
watering methods 44 Xanthomonas campestris pv. vesicatoria
watermelon 220–1, 225, 227–8, 235, 199–200, 332–3
244, 246 Xanthomonas campestris pv. vititans
Watermelon mosaic virus 250 301–2
Watermelon mosaic virus I see papaya Xiphinema americanum 249
ringspot virus type W Xyella 18
watery soft rot (Sclerotinia rot)111-12
189–90, 408 Y
weed hosts 38–9, 115 Yellow fleck virus, parsnip 124–5
see also named weeds/wild species yellow vine disease (cucurbits) 225–6
weevils 181, 295
Whetzelinia see Sclerotinia spp. Z
white leaf spot (brassica spp.) 176–7, Zea mays var. saccharata (sweetcorn)
390–1 421
white mold Zopfia rhizophila 132
Apiaceae 111–12, 127 zucchini squash 229
beans (Phaseolus) 262–4 Zucchini yellow mosaic virus 250–1
brassicas 189–90 Zygomycetes 22, 23
broad bean 292–3
control 295
corn salad 420
endive/escarole/radicchio 394
lettuce (lettuce drop) 313–15

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What is the book about?

What is the book about?

What are some of the major vegetable diseases discussed in the book?

What are some of the major vegetable diseases discussed in the book?

Vegetable

Copyright © 2007 Manson Publishing Ltd

Commissioning editor: Jill Northcott

Plant Protection Handbooks Series

Mycocentrospora acerina ASPARAGUS OFFICINALIS BRASSICACEAE

CAPSICUM (pepper) CUCURBITACEAE FABACEAE (pea family)

Mycosphaerella pinodes LACTUCA SATIVA (lettuce) SOLANUM

MAY THE WINDS blow sweetly,

. . . IF THERE IS FAMINE in the land, if there is pestilence,

TABLE 1 Thirty-year trends for world production of major vegetable crops

Vegetable crop 1972 1982 1992 2002

Units = million metric tonnes [ million MT]

Technological advances stock sources, placement of seed increase plantings in

The challenge of plant diseases

Diseases caused by biotic agents BACTERIA

VIRUSES now grouped into families of closely related virus

TABLE 4 Common viruses that cause diseases of vegetables

Ilavirus Asparagus virus 2 Tobamovirus Pepper mild mottle virus

Ophiovirus Mirafiori lettuce virus Tospovirus Tomato spotted wilt virus

Polerovirus Beet chlorosis virus Umbravirus Carrot mottle virus

FUNGUS-LIKE PATHOGENS TABLE 6 Selected physiological and abiotic

TABLE 7 Vegetable diseases discussed and illustrated in this book

CROP BACTERIAL DISEASES FUNGAL DISEASES VIRAL DISEASES

Alliums Bacterial blight Black mold Garlic mosaic

Artichoke Bacterial crown rot Ascochyta rot Artichoke curly dwarf

Arugula Bacterial blight Downy mildew

Asparagus Cercospora blight Asparagus virus 1

Basil Bacterial leaf spot Fusarium wilt Tomato spotted wilt

Bean Common bacterial blight Anthracnose Bean common mosaic

Beet Bacterial leaf spot Black leg Beet chlorosis

TABLE 7 Vegetable diseases discussed and illustrated in this book (continued)

CROP BACTERIAL DISEASES FUNGAL DISEASES VIRAL DISEASES

Brassicas Bacterial blight Alternaria head rot Beet western yellows

Broad bean Chocolate spot Bean leaf roll

Broccoli raab Bacterial blight Alternaria leaf spot

Catnip Bacterial leaf spot

Celery Aster yellows Crater spot Celery mosaic

TABLE 7 Vegetable diseases discussed and illustrated in this book (continued)

CROP BACTERIAL DISEASES FUNGAL DISEASES VIRAL DISEASES

Celery continued... Powdery mildew

Chervil Powdery mildew

Cilantro Bacterial leaf spot Fusarium wilt Cilantro yellow blotch

Corn salad Powdery mildew

Cucurbit Angular leaf spot Anthracnose Cucumber mosaic

Dill Itersonilia canker

Fennel Bacterial leaf spot Cercosporidium blight

Horseradish Black rot Cercospora leaf spot Turnip mosaic

Jerusalem artichoke Powdery mildew

Lettuce Aster yellows Anthracnose Beet western yellows

TABLE 7 Vegetable diseases discussed and illustrated in this book (continued)

CROP BACTERIAL DISEASES FUNGAL DISEASES VIRAL DISEASES

Mint Powdery mildew

Mustards Alternaria leaf spot

Parsley Powdery mildew

Parsnip Downy mildew Celery mosaic

Chemical group Name Date Chemical group Name Date