Randy C Ploetz - Diseases of Tropical Fruit Crops-CABI (2003) - 96-148

4 Diseases of Banana and Plantain
Randy C. Ploetz1, John E. Thomas2 and Walter R. Slabaugh3

1University of Florida, Tropical Research and Education Center, Homestead,
Florida, USA; 2Queensland Department of Primary Industries, Queensland
Horticulture Institute, Indooroopilly, Queensland, Australia; 3Agraquest Inc.,
1050 Echo Avenue, Parma, Idaho, USA
Introduction diploid, triploid or tetraploid hybrids among

subspecies of M. acuminata, and between M.
Banana is one of the most fascinating and acuminata and M. balbisiana. No subspecies
important of all food crops. It arose in of M. balbisiana exist, but there are nine
southern Asia, and may have been one of the of M. acuminata: banksii, burmannica,
first domesticated crops. In writing of the burmannicoides, errans, malaccensis, microcarpa,
beginnings of agriculture in Southeast Asia, truncata, siamea and zebrina. Rare and unim-
Simmonds (1966) concluded, ‘It seems a portant hybrids also occur M. acuminata and
reasonable assumption that the bananas M. balbisiana, and M. schizocarpa and M. tex-
evolved along with the earliest settled tilis (Carreel, 1995). Also uncommon are the
agriculture of that area and may therefore be Fe’i bananas, which are complex hybrids
some tens of thousands of years old’. among M. lolodensis, M. maclayi and M. peeke-
Due to its origins, diversity of banana is lii. Information in this chapter focuses on
greatest in southern and Southeast Asia. bananas that are derived from M. acuminata
Dissemination outside this region occurred and M. balbisiana.
at least 2500 years ago to Africa (Mbida The haploid contributions of M. acuminata
Mindzie et al., 2001) and ~2000 years ago to and M. balbisiana to the cultivated bananas
Polynesia and tropical South America are indicated with an A and B, respectively
(Langdon, 1993). Secondary centres of (Simmonds and Shepherd, 1955). For
banana diversity developed later in the high- example, the Cavendish and East African
land and coastal areas of East Africa, and of Highland cultivars are pure triploid acumi-
the plantains in West Africa and Latin nata and, thus, referred to as AAA, whereas
America. the widespread cooking banana ‘Bluggoe’ is
a triploid hybrid and ABB. The Linnaean
species M. paradisiaca (the true plantains,
Taxonomy, Anatomy and General which are AAB) and M. sapientum (the sweet
Attributes dessert bananas, of which ‘Silk’ AAB is the
type cultivar) are no longer considered valid.
The banana family, Musaceae, is one of eight Bananas are perennial herbs that develop
in the order Zingiberales (Kress et al., 2001). from subterranean rhizomes (Purseglove,
Most edible bananas arose from two species 1985; Stover and Simmonds, 1987). Suckers
in the family, Musa acuminata and M. are sympodial shoots that develop laterally
balbisiana (Daniells et al., 2001b). They are and in a radial fashion from the base of the
© CAB International 2003. Diseases of Tropical Fruit Crops (ed. R.C. Ploetz) 73
74 R.C. Ploetz et al.
rhizome. They form a pseudostem as soon as structure. Since most cultivars are partheno-
they clear the parent plant; it is composed of carpic, pollination is not required for fruit
leaves and their fused petiole bases. Upon development. Individual fruit are called fin-
flowering, the true stem and associated api- gers, the contiguous, semicircular clusters of
cal meristem rise from within the rhizome fruit are hands, and the entire infructescence
and emerge from the top and through the is a bunch. Botanically, banana fruit are con-
centre of the pseudostem. Cold damage sidered to be berries.
(chokethroat) and the banana streak disease Banana is propagated vegetatively, with
can interrupt this sequence by causing the either suckers or rhizome pieces. In addition,
developing inflorescence to stall in, or break plantlets from meristem culture are now
through the side of, the pseudostem (Fig. used widely (Vuylsteke, 1989). They enable
4.1). As the stem emerges from the pseudo- the establishment of uniform plantings, and
stem, its growth usually becomes geotropic. have the added advantage of being free of
Flowers are arranged on the stem (peduncle) bacterial, fungal and nematode pathogens.
in nodal clusters in a radial fashion. Each Unfortunately, plants from meristem culture
flower cluster is borne on a prominence are more susceptible to Panama disease
called the crown or cushion, and is covered (Fusarium wilt), infectious chlorosis and
by a bract. Flowers in the proximal portion possibly other diseases than those from
of the inflorescence are female, those in the traditional seed pieces (Ploetz et al., 1994b;
distal portion are male, and there may be Smith et al., 1998). Moreover, meristem cul-
intervening clusters of intermediate flower turing generally does not eliminate virus
pathogens of banana. Thus, virus indexing
has become increasingly important, espe-
cially during the international exchange of
germplasm.
Banana is a climacteric fruit (Snowdon,
1990). After harvest, minute quantities of
ethylene are produced that trigger a sharp
increase in respiration. It is desirable to mini-
mize postharvest injury of fruit since injuries
are not only conspicuous upon ripening but
will also cause premature ripening and
enhance postharvest development of
anthracnose and other diseases. Premature
ripening also occurs in fruit from plants that
are affected by the Sigatoka leaf spots. The
preclimacteric life of fruit is increased by
prompt refrigeration after harvest, prevent-
ing ethylene build-up in storage areas or
ship holds with ethylene scrubbers, and ade-
quate control of the Sigatoka diseases.
Significance as Agricultural Commodity

and Food Source
Banana is now grown in almost all areas

Fig. 4.1. Symptoms of chokethroat on ‘Dwarf between 30°N and S latitude that have suffi-
Cavendish’ AAA at ~1000 m above sea level in cient water. After citrus, it has the highest
Malawi. This disorder develops when temperatures gross production of any fruit (97.7 Mt in
of <15°C occur during bunch emergence (photo: 2001), and it is the most important fruit in
R.C. Ploetz, UF). world trade; in 2000, world commerce in
Diseases of Banana and Plantain 75
banana was valued at US$4.8 billion can be grown with minimal care. For exam-
(Anonymous, 2001). Although a handful of ple, a kilogram, 1000 calories or a hectare of
countries are responsible for most export these fruit can be produced more cheaply
production (Table 4.1), production in other than any other important source of carbohy-
countries is also significant. For example, drates in West Africa.
bananas accounted for one-third of the total
export revenues for Honduras, and about
one-half of those for the Windward Islands, Impact of Banana Diseases
Guadeloupe and Martinique in 1982 (Stover
and Simmonds, 1987). Diseases are major production constraints
Despite their importance, exported wherever banana is grown, and are the key
bananas represented only 17% of the total reasons for the creation of the banana-breed-
annual production of this crop in 2000 ing programmes (Buddenhagen, 1993). For
(Anonymous, 2001). Non-exported fruit are example, Panama disease is considered one of
grown by diverse producers and are impor- the most destructive plant diseases in modern
tant commercial products, staple foods and times (Stover, 1962; Simmonds, 1966).
dietary supplements. The latter bananas have Currently, black Sigatoka is the most impor-
diverse genomes, and are eaten raw; are tant disease on this crop. Export production of
baked, fried or boiled; or are brewed for beer. the Cavendish cultivars would not be possible
These include: AA (e.g. ‘Pisang Mas’) and AB without expensive and intensive applications
(e.g. ‘Ney Poovan’) dessert bananas; AAA of fungicides, and smallholder production of
dessert bananas, e.g. members of the plantains and several other types of banana
Cavendish subgroup and ‘Gros Michel’; AAA can be reduced by 50% or more.
highland cooking bananas that are endemic In this chapter, we summarize current
to East Africa; diverse AAB plantains that are information on the most important diseases
most significant in Latin America and West of this crop. They are listed alphabetically
Africa; AAB dessert bananas, of which ‘Silk’ according to the causal agents and the organ
and ‘Pome’ are prominent members; and of the plant that is affected. Minor diseases
ABB cooking bananas, including ‘Bluggoe’, that could not be covered in the chapter are
‘Cardaba’ and ‘Pelipita’. In this chapter, all listed in Table 4.2. More thorough coverage
will be referred to as bananas. on diseases of this crop is found in Diseases of
Banana is a most important crop for mil- Banana, Abacá and Enset (Jones, 2000).
lions of the world’s poorest people. The fruit
are nutritional and those of most cultivars
are good sources of carbohydrates, potas- DISEASES THAT ARE CAUSED BY
sium, calcium, phosphorus and vitamin C; in BACTERIA
lower concentrations they also contain vita-
mins A, thiamine, riboflavin and niacin Bacteria cause serious diseases of the fruit,
(Stover and Simmonds, 1987). Banana is rhizome and pseudostem of banana.
prized in the developing world because it Although they are not usually as important
as the major fungal diseases, they can cause
Table 4.1. The major exporters of banana in 2000. considerable losses when insects vector the
Gross exports causal agents, and in export monocultures if
Country (1000 t) adequate control measures are not used.
Ecuador 4095
Costa Rica 2096 Diseases of Fruit
Colombia 1710
Philippines 1600
Bugtok
Guatemala 857
Panama 490
This disease, which is also known as
Data are from FAO, http://www.fao.org/default.htm tapurok, occurs in the Philippines. It was
Table 4.2. Non-infectious disorders and diseases of minor importance or unknown aetiology.
Disorder/disease Cause
Alligator skin Light abrasions on fruit peel caused by leaves or bracts

Armillaria corm rot Armillaria mellea and A. tabescens
Banana dieback Banana dieback virus
Black root rot Rosellinia bunodes
Blue disease Magnesium deficiency
Brown blotch Pestalotiopsis leprogena
Ceratocystis fruit rot Ceratocystis paradoxa (anamorph: Chalara paradoxa)
Choke Low winter temperatures
Cladosporium speckle Cladosporium musae
Corm dry rot Junghuhnia vincta
Damping-off Deightoniella torulosa
Dwarf Cavendish tip-rot Fusicoccum mangiferum
Dwarfism Genetic mutation
Elephantiasis Unknown
Finger tip rot (gumming) Pseudomonas spp.
Fruit chimera Genetic mutation
Fruit rot Botryosphaeria ribis (anamorph: Fusicoccum parvum)
Fungal root-rot Haematonectria haematococca (anamorph: Fusarium solani )
Fusarium oxysporum
Rhizoctonia spp.
Fungal scald Colletotrichum musae
Fused fingers Genetic defect
Giantism Genetic mutation
Heart leaf unfurling disorder Unknown
High mat Unknown
Javanese vascular wilt Pseudomonas sp. (reports of this disease may actually have been of
Fusarium wilt)
Leaf edge chlorosis Unknown
Leaf spot Curvularia eragrostidis
Leaf spot Drechslera musae-sapientum
Leaf spot Leptosphaeria musarum
Leaf spot Pestalotiopsis disseminata
Leaf spot Pestalotiopsis palmarum
Main stalk rot Ceratocystis paradoxa (anamorph: Chalara paradoxa)
Maturity bronzing High rainfall, humidity and temperature coupled with excessive fruit caliper
Peduncle rot Botryosphaeria rhodina (anamorph: Diplodia theobromae)
Fusarium pallidoroseum
Fusarium oxysporum
Verticillium theobromae
Pseudostem wet rot Erwinia chrysanthemi
Rayadilla Zinc deficiency
Rhizome and pseudostem Erwinia sp.?
soft rot
Root-knot Meloidogyne arenaria, M. incognita and M. javanica
Rosetting Nitrogen deficiency
Roxana Unknown
Sclerotinia fruit rot Sclerotinia sclerotiorum
Sheath rot Nectria foliicola
Spike leaf Low winter temperatures
Split peel Rapid filling of pulp of fruit
Stem-end rot Colletotrichum musae
Taiwan marginal scorch Unknown
Trachysphaera finger rot Trachysphaera frutigena
Underpeel discoloration Chilling injury to fruit
Continued
Table 4.2. Continued.
Disorder/disease Cause
Verticillium tip rot Verticillium theobromae

Yellow mat Adverse soil conditions
Yellow pulp Delay in fruit filling, drought, excessive shading, magnesium deficiency,
poor nutrition
Yellows Lack of water, flooding, nutritional disorders
Major portions of this list are from the list of common names for banana diseases that was compiled by
D.R. Jones (http://www.scisoc.org/resources/common/names/banana.htm). Additional entries are from
Jones (2000).
first recorded in 1965, but may have been zomes either do not germinate or, in older
present long before this report (Roperos, plants, decay can be so extensive that the
1965). Bugtok affects ‘Cardaba’, ‘Saba’ and pseudostem breaks off from the rhizome.
other ABB cooking bananas and has no There are few, if any, conspicuous external
impact on export production of Cavendish symptoms, but internally affected tissues
cultivars. are yellow to brownish water-soaked areas
Infection appears to occur initially via the with black borders. These necrotic areas
male bud (Jones, 2000). The causal bacterium eventually blacken and can develop into
can ooze from and blacken bracts, and extensive cavities that resemble those
peduncles may shrivel. Bugtok causes grey caused by the weevil borer, Cosmopolites sor-
to reddish yellow internal rot of fingers, and didus (Fig. 4.2).
all or only a few fingers in a bunch may be Both Erwinia carotovora ssp. carotovora
affected. Unlike other bacterial diseases that and E. chrysanthemi have been indicted as
affect fruit (e.g. blood disease and Moko), causes of this disease (Jones, 2000). They are
symptoms do not develop in the pseu- facultatively anaerobic, peritrichously fla-
dostem’s vascular system. gellated Gram-negative rods. These pec-
Bugtok is caused by Ralstonia solana- tolytic species are closely related, but can be
cearum (general characteristics for the species separated using biochemical tests (Schaad et
are listed in the section on Moko disease). al., 2001).
Based on different phenotypic, genetic and The pathogens are presumed to be oppor-
pathogenicity studies, strains of the bugtok tunistic residents of banana soils that enter
bacterium are indistinguishable from those the rhizome through wounds (Jones, 2000).
that cause Moko disease (Schaad et al., 2001). The disease is most prevalent in wet, humid
The pathogen is thought to be vectored areas. It is seldom a major problem but,
by thrips and is not moved in planting mate- where it is important, large, high quality
rial (Jones, 2000). Covering inflorescences rhizomes should be selected for planting
with bags or nets controls the disease, but purposes. In addition, knives that are used to
removing the male bud or managing the prepare seed pieces should be disinfested
putative thrips vectors do not. frequently and the cut surfaces on rhizomes
or rhizome pieces should be allowed to
suberize thoroughly before planting.
Diseases of the Rhizome and Pseudostem
Rhizome rot Vascular Wilts
This is the most important of the rhizome Blood disease

and pseudostem diseases that are caused by
bacteria (Stover, 1972; Jones, 2000). New Blood disease is a lethal problem on dessert
plantings of AA and AAA cultivars are and cooking bananas, as well as wild Musa
affected most often. Newly planted rhi- taxa (Jones, 2000). ‘Penyakit Darah’, as it is
Fig. 4.2. Extensive decay in the rhizome and pseudostem of a young ‘Silk’ AAB sucker caused by Erwinia sp.
Note its resemblance to damage caused by the weevil borer, Cosmopolites sordidus (photo: R.C. Ploetz, UF).
known locally, was first reported from terium exudes from severed vascular tissues
Sulawesi in 1906 where it destroyed new as a cream to blackish ooze.
plantations of dessert banana. It was pre-
sumed to be an anomalous occurrence of CAUSAL AGENT Gäumann named the blood
Moko disease until work in the late 1980s disease bacterium Pseudomonas celebensis
demonstrated that an outbreak of blood dis- (Jones, 2000). None of his isolates remain and
ease on Java was caused by a bacterium that the name he used is no longer valid, but
differed from that causing Moko (Eden- because his descriptions of the bacterium
Green and Sastraatmadja, 1990). agree with more recent results he clearly
Blood disease continues to spread and worked on this disease.
recently has been reported from Sumatra, Biochemical, genetic and physiological
Kalimantan, the Moluccan Islands and Irian tests indicate that the pathogen is closely
Jaya. It has not been reported outside the related to Ralstonia solanacearum. For exam-
Indonesian archipelago. ple, restriction fragment length polymor-
phism (RFLP) and 16S rRNA sequence data
SYMPTOMS Leaves become chlorotic, place the pathogen firmly in the R.
necrotic and buckle, usually close to the solanacearum species complex (Cook and
pseudostem (Jones, 2000). Although the Sequeira, 1994; Taghavi et al., 1996).
inflorescence may appear unaffected exter- Recently, it was suggested that the bac-
nally, it often develops the blackened shriv- terium should be considered a separate
elled symptoms that occur when plants are species or a subspecies of Ralstonia (Thwaites
affected by the SFR insect-vectored strain of et al., 1999; Jones, 2000). Although random
the Moko pathogen (Ploetz et al., 1994b). amplified polymorphic DNA (RAPD) and
Internally, the fruit and vascular system polymerase chain reaction (PCR) analyses
become a reddish brown. Infection is sys- clearly distinguish isolates of the pathogen
temic, and can extend into the rhizome and from isolates of R. solanacearum that cause
connected suckers in a mat. The causal bac- bugtok and Moko disease, the blood disease
bacterium has not been described formally and was first recorded in the 1890s on
as a new taxon. Trinidad. In the western hemisphere, Moko
disease is now recognized in an area extend-
EPIDEMIOLOGY Despite the importance of ing from the Amazon Basin to Guatemala
blood disease, not much is known about the and southern Mexico, as well as on Grenada
disease’s epidemiology (Ploetz et al., 1994b). and Trinidad. Although the disease has been
The pathogen can reside in soil and in reported in India and several countries in
infested host tissue for more than a year, and Africa, the only verified occurrence in the
in apparently healthy seed pieces and fruit. eastern hemisphere is in the Philippines
The latter traits enable long-distance spread (Ploetz et al., 1994b). Infested planting
of the pathogen; for example, its movement material from Honduras is thought to be
from Sulawesi to Java may have resulted responsible for the latter outbreak.
from the movement of infected fruit. A rate Moko is a classic ‘new encounter’ disease
of spread of 25 km yearⳮ1 was been reported (Buddenhagen, 1960; French and Sequeira,
recently, and this rapid movement is proba- 1970). Species of Heliconia are common
bly due, at least in part, to insect dissemina- understorey plants in rainforests in tropical
tion of the pathogen. America that are in the same taxonomic
Gäumann (as reported in Jones, 2000) order as banana, the Zingiberales. Race 2 of
reported that plants were infected after he R. solanacearum, the cause of Moko disease,
inoculated female flowers and, based on the co-evolved on these banana relatives in the
symptoms of the disease and sequence in New World. Thus, unlike the blood disease
which they develop, it is clear that plant-to- bacterium, the Moko pathogen did not
plant movement occurs through the air. How evolve on banana.
the pathogen is disseminated and infects
banana, and whether and what insects are SYMPTOMS Externally, the oldest leaves in
involved should be researched. the canopy become chlorotic, wilt, buckle
and ultimately die (Ploetz et al., 1994b).
MANAGEMENT No resistance has been Younger leaves are then affected until the
reported among the edible clones, and dessert entire canopy is involved. Leaves remain
bananas appear to be most susceptible (Jones, attached to the pseudostem and eventually
2000). Whether the removal of male buds the pseudostem collapses. Suckers can also
would be as effective as it is against Moko be affected, and in addition to the above
disease has not been investigated. However, if symptoms their leaves may curve down-
female flowers are naturally infected, this wards as they die. If suckers are cut with
measure might not be expected to be effica- infested machetes, they become blackened
cious. Strict quarantine measures are needed and stunted in 2–4 weeks. When insect-
to ensure that this destructive disease does transmitted strains of the pathogen infect
not spread outside its current range. Under cushions on the peduncle, the male bud
no circumstance should traditional seed withers and darkens, and bacteria may ooze
pieces be moved from affected areas unless from the bud. The fruit may turn yellow and
they are known to be pathogen-free. their peel split.
Internally, affected fruit pulp is firm but
brown and later grey. On ‘Bluggoe’, the
Moko disease colour is more reddish brown and a
red–brown liquid may occur at the fruit cen-
Moko disease affects diverse dessert tre. The vascular system in the rhizome,
bananas, plantains and cooking bananas pseudostem and peduncle is also discoloured
(Ploetz et al., 1994b; Jones, 2000). ‘Bluggoe’ light to dark brown (Plate 22). Severed vascu-
ABB is especially susceptible, and the dis- lar strands exude a milky discharge of the
ease is named after a synonym of this culti- causal bacterium when placed in water.
var, ‘Moko’. The disease has probably been Internal and external symptoms of Moko
present in South America for over a century, and Panama disease are quite similar.
However, only Moko affects fruit, suckers • rigorous disinfestation of farm implements,
and plants younger than ~4 months. especially machetes that are used for bud
removal and mat maintenance; and
CAUSAL AGENT R. solanacearum is an aero- • destruction of affected and neighbouring
bic, Gram-negative, non-fluorescent, rod- plants with herbicides. These sites can be
shaped bacterium (Schaad et al., 2001). It is a replanted 6–12 months after all host
widespread and diverse pathogen that has residues have decayed.
been divided into five biovars based on
‘Bluggoe’ and other ABB cooking bananas
carbohydrate utilization, and five races that
with dehiscent bracts are most susceptible,
are determined by host range.
and are also sources of inoculum for com-
Race 1 of R. solanacearum causes a vascu-
mercial bananas (Ploetz et al., 1994b). In
lar wilt on some Musa taxa, but not on the
these situations, ‘Pelipita’ ABB, which has
edible cultivars or heliconia (Jones, 2000). In
persistent bracts, or clones with aborting
contrast, strains that cause Moko disease are
male buds could be used to replace the sus-
in biovar 1 and race 2; they are quite vari-
ceptible cultivars. Although alternative weed
able. They have restricted geographical dis-
hosts have been reported, their importance
tributions, occuring in a single country or
in the Moko disease cycle is debated.
region, and display varying levels of viru-
lence on different banana cultivars and heli-
conia. They also display distinct colony DISEASES THAT ARE CAUSED BY FUNGI
phenotypes on Kelman’s medium, and have
disparate abilities to persist in soil and be Fungi are the most important and prevalent
vectored by insects. Virulent isolates of the pathogens of banana. They affect all organs
bacterium produce extracellular polysaccha- of the host in the field and are the major
rides and are not motile. causes of pre-harvest yield reductions and
postharvest damage to and loss of fruit.
EPIDEMIOLOGY Root to root infection is
possible, and moving water can disseminate
the bacterium. However, spread usually Diseases of the Foliage
involves insects or man (Jones, 2000).
Trigona bees, wasps and other flying insects Black cross
have been reported to disseminate certain
strains of this pathogen (especially the SFR, This leaf spot disease is found in Australia,
and to a lesser extent B, strains) over 90 km. Indonesia, the Philippines and southwestern
Insect-driven epidemics can move rapidly Pacific, and is usually not a serious problem
due to the strength and range of the insects (Jones, 2000). Its symptoms are most conspic-
that are involved and the rate at which uous on the undersides of older leaves, and
plants become infectious. Within 15 days of consist of black, cross-shaped lesions that are
flower infection, SFR strains begin to ooze mature stroma of the causal fungus. Long
from bracts and peduncles to initiate another axes of the crosses run up to 6 cm along leaf
cycle of infection. Contaminated farm veins and short axes, up to 3 cm in length,
machinery, machetes that are used for prun- and occur at right angles (Plate 23). On the
ing, and infected fruit and rhizomes are all upper leaf surface, lesions are usually
effective vehicles of dissemination. restricted to black dots that silhouette the
lesion on the underside.
The ascomycete Phyllachora musicola
MANAGEMENT Regular inspection and
causes black cross leaf spot (Jones, 2000). It
eradication programmes are essential wher-
produces obpyriform to subglobose perithe-
ever Moko disease is established. These
cia that are immersed in host leaf tissue.
include:
Their ostioles emerge from the upper surface
• early recognition of the disease; of the leaf, and they form in stroma in groups
• removal of the male bud; of up to 40. Asci are cylindrical or somewhat
clavate, unitunicate, 150–190 × 16.5–20 ␮m, important disease of banana. It was first
and have a truncate apex with an apical ring reported on the Fijian island of Viti Levu in
(Fig. 4.3). Ascospores are one- or two-celled, 1963 (Rhodes, 1964), but was probably wide-
hyaline, smooth and 42–52 × 8–10 ␮m. The spread in the Southeast Asian/South Pacific
fungus has no known anamorph. region by that time (Jones, 2000). Its spread
worldwide has occurred fairly recently: it
first reached the western hemisphere
Black Sigatoka (Honduras) in 1972 and Africa (Zambia) in
1973. By 1991, the disease had spread
Black Sigatoka, which was known originally throughout the Americas and sub-Saharan
as black leaf streak, is currently the most Africa (Jones, 2000).
Fig. 4.3. (A–D) ascospores, (F) ascus tip with apical ring and (E) ascus of Phyllachora musicola (from CMI
description no. 1127). Bars = 10 ␮m.
Another disease, yellow Sigatoka, is and eumusae leaf spot (formerly called
treated separately in this chapter, but is men- Septoria leaf spot) is found in Malaysia,
tioned here due to its similar symptoms, the Mauritius, Nigeria, southern India, Sri
impact it and black Sigatoka have on banana, Lanka, Thailand and Vietnam (Jones, 2000).
and the relatedness of the respective causal They are covered individually in this
fungi. Yellow Sigatoka has a greater geo- chapter.
graphic distribution, but black Sigatoka is
more aggressive and has a wider host range CAUSAL AGENT Black Sigatoka is caused by
(Stover and Simmonds, 1987). On the the ascomycete, Mycosphaerella fijiensis
Cavendish clones that are used by the export (anamorph: Pseudocercospora fijiensis). A
trades, fungicidal control measures for black variant of the pathogen, M. fijiensis var.
Sigatoka are 3–6 times more expensive than difformis, is no longer recognized. M. fijiensis
those for yellow Sigatoka. In general, symp- is closely related to M. eumusae, the cause of
toms of black Sigatoka develop on the eumusae leaf spot, and M. musicola, the
Cavendish cultivars 8–10 days earlier than cause of yellow Sigatoka. DNA sequence
those of yellow Sigatoka. Black Sigatoka analyses suggest that these major leaf
affects plantain and banana cultivars that pathogens of banana may have evolved from
resist yellow Sigatoka, and causes greater a common ancestor (Carlier et al., 2000).
defoliation and yield losses. In most of the Conidia of M. fijiensis are produced in
lowland humid tropics, black Sigatoka has streaks early in their development, mainly
now displaced yellow Sigatoka as the pre- on the lower leaf surface (Jones, 2000).
dominant leaf spot on banana. Although Conidiophores are pale brown, single- to six-
yellow Sigatoka remains more important at celled, straight to geniculate, occasionally
elevations above 1000 m, there is evidence branched, subcylindric, 16.5–62.5 × 4–7 ␮m
that the black Sigatoka pathogen adapts to and in predominantly hypophyllous fascicles
higher elevations after it has been introduced (Crous and Mourichon, 2002) (Fig. 4.4).
into an area (Jones, 2000). In some areas in Conidiogenous cells are up to 25 ␮m long,
Latin America, the disease is now found as 2–4 ␮m wide at the apex, and have 1–3
high as 1500 metres above sea level (masl). minutely thickened scars. Conidia are sub-
hyaline, obclavate to cylindric-obclavate,
SYMPTOMS Symptoms begin as minute have an obclavate basal cell, usually six- to
reddish brown flecks on the lower leaf eight-celled, 10–120 × 2.5–5 ␮m, with hila
surface. As they progress, they become visi- that are slightly thickened and darkened
ble on the upper surface, elongate, darken along the rim. Although the presence of this
and often develop a wet appearance (Plate basal scar was shown recently to be phyloge-
24). Dark borders and yellow haloes netically unimportant in cercosporoid fungi
surround the spots as they exceed 1–2 cm in (the former anamorph genus for this
length, and as the spots mature their centres pathogen, Paracercospora, was based on this
become grey and sunken. In susceptible feature) (Crous and Mourichon, 2002), it is a
cultivars, spots coalesce until the entire leaf valuable diagnostic character that enables
surface is killed, and on plants that have this pathogen to be distinguished from M.
flowered no healthy leaf tissue may remain eumusae and M. musicola.
by the time fruit mature (Plate 25). In severe The teleomorph is virtually indistin-
cases, the bunch either does not develop guishable from that of M. eumusae and M.
fully or falls from the plant. The disease also musicola. The pseudothecia in which
causes fruit to ripen prematurely, which can ascospores are produced are mainly globose,
be a serious problem when fruit are shipped 47–85 ␮m in diameter and immersed in the
long distances. leaf tissue (Jones, 2000). They occur on both
Two other diseases cause symptoms that leaf surfaces although they are most com-
resemble those of black Sigatoka. mon on the upper side. Their ostioles pro-
Phaeoseptoria leaf spot is found in portions trude above the leaf surface and are dark
of Asia, Australia, Africa and the Americas, brown and conspicuous. Asci are bitunicate,
Fig. 4.4. Conidia and conidiophores of Pseudocospora fijiensis, anamorph of Mycosphaerella fijiensis (from
CMI description no. 413).
obclavate and lack paraphyses, and the EPIDEMIOLOGY Conidia and ascospores of
ascospores are colourless, 12.5–16.5 × the fungus are both infective. They are
2.5–3.8 ␮m, and two-celled with a con- formed under high moisture conditions and
stricted septum. are disseminated by wind (Rutter et al.,
M. fijiensis grows very slowly on artificial 1998). Ascospores are most important in
media. At optimal temperatures of between spreading the disease within plants and
24 and 28°C, single-conidium cultures reach plantations. Since they are killed after 6 h of
1 cm in diameter after 38 days on potato dex- UV radiation, Parnell et al. (1998) concluded
trose agar (PDA). that ascospores would probably not disperse
The fungus is heterothallic, and consider- more than a few hundred kilometres by
able pathogenic and genetic diversity has wind. In contrast, infected planting material
been reported among geographically dis- and leaves that are used as packing materials
persed isolates (Jones, 2000). Genetic analy- can move the pathogen great distances.
ses indicate that the centre of diversity for Leaves are infected indirectly via stomata
the pathogen is the Australasian–Southeast and, due to the greater abundance of stomata
Asian region (Carlier et al., 1996). There is there, the lower surface is the primary infec-
evidence that isolates from some areas attack tion site (Washington et al., 1998). The cardi-
banana cultivars that are resistant in other nal temperatures for ascospore germination
regions, and that the pathogen is capable of are 12, 27 and 36°C, and substomatal pene-
adapting to resistant cultivars in a given tration for conidia and ascospores occurs
location over time (Fullerton and Olsen, within 48–72 h on moist surfaces. Although
1995). Meiotic recombination in the pathogen free moisture is required for ascospore
probably plays a major role in generating germination, conidia can also germinate
diversity in this pathogen. under high humidity.
Further colonization of the leaf occurs via most by black Sigatoka. For example, plan-
epiphyllic hyphae of the pathogen that emerge tain yield losses of 33 and 76% were
from stomata and grow along the lower leaf recorded during, respectively, the first and
surface to other stomata. Under prolonged second cropping cycle in West Africa
wet conditions, an extensive network of (Mobambo et al., 1996). Under marginal con-
hyphae can cover and infect the leaf surface. ditions, production is often abandoned due
Transition periods (the length of time to low yields (Jones, 2000).
between the appearance of the first fleck Chemical control of first yellow, and then
symptom to the development of mature black, Sigatoka has evolved considerably
spots with grey centres) are affected by envi- over the last 60 years (Ploetz, 2000; Stover,
ronment, host genotype and pathogen iso- 1990a). Bordeaux mixture, first used in the
late, and ranged between 11 and 139 days. mid-1930s, was replaced by several succeed-
Important environmental factors include ing generations of protectant and, later, sys-
temperature (optimum: 25–28°C), moisture temic fungicides. Presently, a sterol
(optimum: free water on host surfaces) and biosynthesis inhibitor, tridemorph, several
shade (which reduces symptom develop- different sterol demethylation inhibitors,
ment by as much as 50%). Development rate most importantly propiconazole, and differ-
decreases dramatically as conditions become ent strobilurins are the most common sys-
drier, or are hotter or cooler than optimum. temics.
Likewise, development is much slower on In general, insensitivity develops in M.
resistant cultivars and where less aggressive fijiensis towards the systemic fungicides after
populations of the pathogen exist. prolonged use. Within 2–3 years of the
introduction of benomyl in Central America,
MANAGEMENT Management strategies vary resistance was observed, and by the late
according to the cultivars that are grown, the 1970s it was no longer effective in many
environment and the intended market for areas (Stover, 1990a). Recently, a 500-fold
the fruit (Fullerton and Stover, 1990). In increase in resistance to a strobilurin fungi-
export plantations that produce dessert cide, trifloxystrobin, was recorded after 4
bananas or plantains, frequent applications years of 6–11 applications year−1 in Costa
of fungicides are usually needed. Depending Rica (Chin et al., 2001). In contrast, tolerance
on the sensitivity of local populations of the to propiconazole has developed quite differ-
pathogen to the utilized fungicides, applica- ently. Reduced control with this fungicide
tion frequencies can range as high as 36 developed in Central America in the 1990s.
year−1 for dessert bananas and 19 year−1 for Romero and Sutton (1997) observed a rapid
plantains (Jones, 2000). Fungicide applica- shift towards insensitivity in three different
tions usually require airplanes or helicopters plantations in Costa Rica. However, unlike
and permanent landing strips and facilities the situation with benomyl, they observed
for mixing and loading the fungicides. When wide ranges in sensitivity in each plantation,
the high recurring expense of the spray and in no case was there evidence for the
materials themselves is considered, costs run predominance of a highly tolerant popula-
as high as 26% of the total cost of production tion. Although they speculated that individ-
for exported dessert bananas (Stover and uals with high levels of tolerance to
Simmonds, 1987). propiconazole were less fit than sensitive
Cultural practices are also used in com- strains, the cost of tolerance in M. fijiensis to
mercial situations. These include the removal this important fungicide has not been
of leaves with mature spots, and reducing researched.
humidity within plantations by increasing Due to resistance problems, the systemic
spacing between plants and providing effi- fungicides usually are applied in combination
cient drainage with permanent canals and or alternation with broad-spectrum, protec-
pumps. tant fungicides, such as the dithiocarbamates
Since most smallholders cannot afford and chlorothalonil. With the exception of
these control measures, they are affected chlorothalonil, these fungicides are usually
mixed with petroleum-based spray oils. The lesce and eventually turn brown (Plate 26).
oils themselves are fungistatic and retard the Blotchy necrotic areas develop where high
development of the pathogen in the leaf. concentrations of lesions are found, and they
When they are mixed in water emulsions are usually associated with chlorotic areas that
with fungicides, the resulting ‘cocktails’ pro- run parallel to the leaf veins. Alternatively, dif-
vide superior disease control. fuse, brown to blackish blotches develop on
Application schedules are determined the upper surface of older leaves without lin-
with disease forecast systems that incorpo- ear streaks. In both cases, large areas of the
rate data on disease severity within the plan- leaf surface can eventually die.
tation and environmental factors that affect
infection and disease development (Stover, CAUSAL AGENT Cladosporium musae pro-
1990). The models are based on the use of duces erect, dark brown conidiophores that
oils and systemic fungicides only, since have persistent branches at the apex, average
protectant fungicides have no curative effect 610 ␮m in length and have thick-walled
on symptom development. bases that are 6–8 ␮m wide (Fig. 4.5) (David,
Although some cultivars resist black 1988). Conidiogenous cells are terminal or
Sigatoka, resistance is poor among many intercalary. Conidia are ovate–cylindrical,
important types of banana, including export ellipsoidal or fusiform, and may have a con-
dessert AAA, AAB plantain, highland AAA stricted middle and one or more scars at
and AAB dessert (Table 4.3). Furthermore, each end. They form in branched chains, are
clones that resist black Sigatoka may be sus- 6–22 × 3–5 ␮m, mainly single-celled, thin-
ceptible to other problems such as Panama walled and almost hyaline.
disease, nematodes and weevil borer
(Cosmopolites sordidus). EPIDEMIOLOGY Conidia are carried by air
As fungicides lose their effectiveness currents and require free moisture to germi-
against black Sigatoka and subsistence pro- nate. Disease development is favoured by
duction continues to deteriorate, the demand high humidity.
for resistant genotypes will increase.
International breeding programmes, most MANAGEMENT Diverse AAA cultivars are
notably that of the Fundación Hondureña de susceptible, including those in the
Investigación Agrícola (FHIA) in La Lima, Cavendish subgroup, ‘Gros Michel’, the East
Honduras and the International Institute of African highland cultivars, ‘Pisang
Tropical Agriculture (IITA) in Onne, Nigeria, Berangan’ and ‘Pisang Nangka’. Based on
have made significant progress in incorpo- the susceptibility of other clones, in some
rating disease resistance in several breeding regions there may be pathogenic specializa-
targets (Jones, 2000). tion in the fungus. Although ‘Sucrier’ AA
was not susceptible in Côte d’Ivoire, ‘Kluai
Khai’ (a synonym of ‘Sucrier’) is the most
Cladosporium speckle susceptible cultivar in Thailand. Clones with
AAB genomes were also not susceptible in
Cladosporium speckle affects older leaves of Côte d’Ivoire, but ‘Dwarf Horn’ plantain
banana plants in humid environments AAB is susceptible in Panama.
(Stover, 1972). It is usually a minor problem, Although control measures usually are
but yields may be impacted in some areas. not needed, fungicides that are used against
The disease has been recorded in Africa, the Sigatoka leaf spots are effective.
Asia, Australasia, Oceania and tropical
America.
Cordana leaf spot (leaf blotch)
SYMPTOMS Symptoms reported from differ-
ent regions are similar (Jones, 2000). Pale This is a common, but usually innocuous
brown linear streaks, 0.3 × 1.5 mm, appear 3–4 disease of banana. It causes its greatest dam-
weeks after leaves unfurl. These enlarge, coa- age during rainy weather on the lower
Table 4.3. Reaction of important banana cultivars to Panama disease and yellow and black Sigatoka.
Reaction toa
Panama Yellow Black

Genome Subgroup Cultivar disease Sigatoka Sigatoka
AA ‘Sucrier’ Rb S MS
‘Pisang Lilin’ R R R
AB ‘Ney Poovan’ S R
AAA ‘Ibota Bota’ Rb R R
Cavendish Rb S S
Gros Michel S S S
Lujugira-Mutika Rc R S
AAB ‘Silk’ HS SS MS
‘Mysore’ R R SS
Maia-Maoli/Popoulu S Sd MS
Plantain Rb Re MS
Pome ‘Pome’ MS SS S
ABB ‘Bluggoe’ S R MS
‘Pisang Awak’ MS R SS
‘Saba’ R R SS
‘Cardaba’ R R SS
‘Pelipita’ R R MS
AAAA ‘FHIA23’ Rb
‘I.C. 2’ S MS
AAAB ‘FHIA01’ R R R
AABB ‘FHIA03’ Rb R R
a Reactions are: HS (highly susceptible); S (susceptible); MS (moderately susceptible); SS (slightly
susceptible); and R (resistant). From: Stover and Simmonds (1987); Ploetz et al. (1994b); Pegg (2000).
b ‘Sucrier’, ‘Yangambi km 5’, plantains, ‘FHIA03’ and ‘FHIA 23’ succumb to race 4 but are otherwise
resistant. ‘Dwarf Parfitt’, a Cavendish cultivar, and somaclones of ‘Giant Cavendish’ from the Taiwan
Banana Research Institute (i.e. the GCTCV series) also resist race 4.
c Reports that clones in the Lujugira-Mutika subgroup are susceptible to Fusarium wilt (Ploetz et al.,
1994a) may be in error (Kangire and Rutherford, 2001).

d Resistance to yellow Sigatoka may exist in some accessions in the Maia-Maoli/Popoulu subgroup
(Jones, 2000).
e Resistance in plantains to yellow Sigatoka breaks down at high elevations.
leaves of plantains, and to a lesser extent on large portions of the leaf lamina can be
ABB cultivars. affected, especially when the disease occurs
in concert with the Sigatoka leaf spots.
SYMPTOMS Pale brown, oval patches,
ranging from one to several centimetres in CAUSAL AGENTS Two species cause Cordana
diameter, form towards the leaf margins and leafspot. Cordana musae was first described in
in association with wounds caused by other 1902 on Java (Jones, 2000). More recently,
diseases and leaf tears (Plate 27). Lesions are Ellis (1971) described a new species, C. john-
surrounded by bright yellow haloes and stonii, from Irian Jaya, peninsular Malaysia
have light grey, necrotic centres with con- and Tonga. It has also been recognized since
centric zonations that are most noticeable on in New South Wales and on Lord Howe and
the upper leaf surface. Lesions eventually Norfolk Islands (Priest, 1990). Its occurrence
may encompass entire leaf margins, and in cooler climates and absence in warmer
Fig. 4.5. (A) Base of conidiophore and (B) conidiophore and conidia of Cladosporium musae (from CMI
description no. 958).
production areas led Jones (2000) to specu- (Jones, 2000). Production occurs at night dur-
late that it tolerated cooler conditions than C. ing periods of dew or rainfall, and spore
musae. release takes place as vapour pressure
Conidiophores of each species are straight decreases; peak release of conidia occurs
or flexuous and septate (Ellis, 1971; Ellis and around 7 a.m. Under moist conditions, coni-
Holliday, 1972). Those of C. musae are pale to dia germinate and form appressoria within 8
mid-brown, smooth, up to 220 ␮m long and h of their deposition on the leaf surface.
4–6 ␮m in diameter with terminal and inter- After another several hours, infection pegs
calary swellings of 6–8 ␮m, and basal form on appressoria and penetrate the epi-
swellings of 8–11 ␮m (Fig. 4.6). Conidia are dermis directly. Healthy and necrotic banana
solitary, arising from small pegs on the ter- tissue are infected. However, since barriers
minal end of the conidiophores, obovoid to to infection are often created in healthy tis-
pyriform, two-celled, subhyaline to pale sue shortly after invasion, this is primarily a
brown, smooth, 11–18 ␮m long and 7–10 ␮m disease of wounded and weakened tissue.
at their widest point, and with a thickened
hilum. In contrast, conidiophores of C. john- MANAGEMENT In export plantations, where
stonii often are twisted at the base and up to the Sigatoka leaf spots are controlled with
300 ␮m long, and its conidia, although quite protectant or systemic fungicides, Cordana
similar to those of C. musae, are much larger, leaf spot is uncommon. Oil, used in combi-
ranging from 19 to 26 ␮m in length and 14 to nation with fungicides for control of the
16 ␮m in width (Fig. 4.7). Sigatoka leaf spots, was reported to increase
Cordana leaf spot when used alone. Also, oil
EPIDEMIOLOGY The pathogens sporulate is phytotoxic to plantain cultivars on which
abundantly on the undersides of lesions Cordana leaf spot is most severe. Specific
Fig. 4.6. Conidia and conidiophores of Cordana musae (from Ellis, 1971).
control measures for this disease usually are

not indicated.
Eumusae leaf spot
This disease is found in Malaysia, Mauritius,

Nigeria, India, Sri Lanka, Thailand and
Vietnam (Carlier et al., 2000). It was first rec-
ognized during surveys in the 1990s during
which the distribution of the Sigatoka leaf
spots in South and Southeast Asia was inves-
tigated. Surprisingly, none of the samples
yielded M. musicola, and M. fijiensis was iso-
lated from only a few. From most of the
samples, an undescribed species of Myco-
sphaerella was recovered that appeared to
have a Septoria anamorph. The original com-
mon name of the disease, Septoria leaf spot,
Fig. 4.7. Immature conidium and conidiophores of referred to this identification. Further exami-
Cordana johnstonii (from Ellis, 1976). nation of samples from other regions
expanded the disease’s range outside Asia, distinguished from those of M. musicola by
and recently has shown that the anamorph is their more cylindrical shape, subtruncate
a species of Pseudocercospora (Carlier et al., ends and shorter dimensions.
2000; Crous and Mourichon, 2002). Its dis-
parate geographic distribution and the close EPIDEMIOLOGY AND MANAGEMENT These topics
resemblence of its symptoms to those of the have not been researched, although there is
Phaeoseptoria and Sigatoka leaf spots sug- evidence that chemicals that are used against
gest that it may be present, but not recog- the Sigatoka leaf spots are effective (Jones,
nized, in countries not on the above list. At 2000).
this time, it appears to be the predominant
leaf spot in Thailand, and is common in
peninsular Malaysia, southern India and Sri Eyespot
Lanka (Jones, 2000).
This disease, which is also known as
SYMPTOMS The symptoms are very similar Drechslera leaf spot, occurs where Bermuda
to those of the Sigatoka leaf spots (Carlier et grass, the primary host of the pathogen, is
al., 2000; Jones, 2000). Faint brown streaks found beneath plants (Stover, 1972). It has
expand and become oval to elliptical (Plate been observed in Central America, Jamaica
28). They darken and develop a grey centre and Uganda, and is not economically impor-
and dark border as they mature. At this stage, tant.
the lesions are broader and larger than those Symptoms develop on suckers <2 m in
of the Sigatoka leaf spots. However, they do height. Lesions are oval or lenticular, as large
resemble those caused by Phaeoseptoria leaf as 16 × 8 mm, and develop a bleached grey-
spot, a disease for which Eumusae leaf spot ish centre as they mature (Fig. 4.8). The
initially was mistaken. On severely affected causal agent, Drechslera gigantea, sporulates
leaves, lesions coalesce, large portions of the on Bermuda grass, but not banana.
leaf die, and surrounding tissues yellow.
CAUSAL AGENT The causal fungus is M. Freckle

eumusae (anamorph: Pseudocercospora eumusae)
(Carlier et al., 2000; Crous and Mourichon, Freckle is common in Asia, Australia and the
2002). The species name refers to the section of Pacific (Jones, 2000). Reports in Africa and
Musa, Eumusae, in which the host taxa reside. the Caribbean may be in error. Freckle is one
The teleomorph of M. eumusae cannot be of the most serious problems affecting the
distinguished from that of M. fijiensis or M. Cavendish-based banana industry in Taiwan,
musicola (Crous and Mourichon, 2002). is becoming more important in export pro-
Pseudothecia are globose, 42–51 ␮m in duction in the Philippines, and damages
diameter, dark brown and have a short osti- ‘Pisang Berangan’ AAA in plantations in
ole. Eight two-celled ascospores, 12–16.5 × Malaysia. The disease usually is not impor-
3–4.5 ␮m, are produced in oblong asci. The tant in other situations.
fungus produces predominantly epiphyllous
sporodochia on dark brown substomatal SYMPTOMS The upper surface of older
stromata. Conidiophores are subhyaline to leaves is affected (Jones, 2000). Dark brown
pale olivaceous and pale brown at the base, to black spots, <1 mm across, give the leaf a
subcylindrical, single- to four-celled and greyish caste. They can coalesce in bands
10–25 × 3–5 ␮m with truncate ends. Its parallel to the leaf veins or run lengthwise
sporodochia develop similarly to those of M. down the leaf, due apparently to infective
musicola, but its conidiophores are much spores dripping down the leaf while it was
longer. Conidia of P. eumusae are subhyaline in the candela stage. Larger spots, up to
to pale olivaceous, subcylindrical, 18–65 × 4 mm across, may also form and aggregate in
2–3 ␮m, four- to nine-celled, and have sub- large tan areas. Pycnidia of the causal fungus
truncate ends without scars. Conidia can be that form in necrotic areas feel rough and are
Fig. 4.8. Symptoms of eyespot, caused by Drechslera gigantea (photo: R.C. Ploetz, UF).
a diagnostic feature for the disease (Plate 29). different races or species might cause freckle
Petioles, midribs, transition leaves, bracts in southern and Southeast Asia, one of which
and fruit can also be affected. Symptoms spread to Taiwan and the northern Pacific,
begin developing on 2- to 4-week old fruit, and the other that spread to Australasia and
but are most conspicuous at harvest the South Pacific. Whether the similar but
(Punithalingham and Holliday, 1975). distinct fungi that van der Aa (1973) and
Punithalingham and Holliday (1975)
CAUSAL AGENT Guignardia musae (ana- described represent the taxa that Jones (2000)
morph: Phyllosticta musarum) causes freckle. deduced is not known.
Pycnidia are most common on the host, and
are 60–170 ␮m in diameter, globose, brown EPIDEMIOLOGY Although the role that
to black, and occur individually or in groups ascospores play in spreading the disease is
(van der Aa, 1973). Conidiogenous cells are not known, conidia are important (Jones,
cylindrical or conical and 4–11 × 2.5–5 ␮m. 2000). They are dispersed in water and
Conidia, 15–18 × 9–10 ␮m, are aseptate, usually travel only a short distance. On
obovoid, ellipsoidal or short cylindrical with moist host surfaces at 24°C, they germinate
a rounded apex and truncate base. They are in 2–3 h, and after 12 h form irregular,
indented, may have a single 8–16 ␮m long hyaline appressoria in grooves between host
apical appendage, and are encased in a epidermal cells. After 24–72 h, scattered cells
gelatinous 1–3 mm thick envelope. Perithecia discolour. After 96 h, >60% of the appresso-
are 70–220 ␮m in diameter, globose and ria are associated with necrotic cells, and
papillate. Asci are 35–85 × 20–25 ␮m, eight- necrosis is more rapid and extensive where
spored, clavate to cylindrical, and usually several appressoria develop in an area.
have a short stalk. Ascospores, 17–22 × Fine penetration hyphae that develop
8–10 ␮m, are aseptate, and ovoid to oblong under appressoria swell to a diameter of
ovoidal. Spermatia, 6–10 × 0.5–2 ␮m, are 3–5 ␮m upon entering the cell. Inter- and
aseptate, cylindrical, or dumb-bell-shaped. intracellular hyphae subsequently invade
Punithalingham and Holliday (1975) surrounding epidermal cells, but rarely pen-
described as G. musae an ascomycete that dif- etrate beneath the fifth layer. In Taiwan, the
fered somewhat from van der Aa’s (1973) incubation period varies from 20 days in
description. Chuang (1981) felt that it was a warm, wet weather to 60 days when it is dry
saprophyte on diseased tissue. and cool.
Based on host range and symptomatology Pycnidia develop in lesions of all sizes.
(see below), Jones (2000) speculated that two Secondary infections intensify symptoms that
then often extend laterally on leaves in Lesions develop as brown specks on the
streaks. Conidia are dispersed from leaves to underside of the leaf. As they enlarge, tan
fruit. Continuous infection in the presence of and brown blotches develop on the upper
rain or dew results large areas eventually surface. Surrounding areas become chlorotic
dying. and then necrotic. Acrodontium simplex
Freckle affects M. acuminata ssp. banksii causes leaf speckle. Its brown, erect conidio-
and M. schizocarpa in Papua New Guinea, but phores are septate, single or sparsely
M. balbisiana is not known to be affected any- branched and 41–90 ␮m long. Conidia are
where (Jones, 2000). In southern Asia, a wide oval, 2.9–3.8 × 1.9 ␮m and cover the conidio-
range of cultivars is affected, including: phore terminus. Symptoms identical to those
‘Pisang Berangan’ and those of the Cavendish described above were associated with the
subgroup (both AAA); ‘Silk’, ‘Horn’ and tropical speckle agent, Periconiella musae, in
‘French’ plantain and Mysore (all AAB); and Queensland and Vietnam.
‘Pisang Awak’, ‘Bluggoe’, ‘Pelipita’, ‘Saba’
and ‘Kluai Teparot’ (all ABB). In contrast, in
Hawaii and Taiwan, Cavendish cultivars are Malayan leaf spot
susceptible but ‘Bluggoe’ is resistant, whereas
in Australasia and the South Pacific, the This is usually a minor disease in Fiji, Tonga,
Cavendish clones are resistant and ‘Bluggoe’ Western Samoa and the highlands of penin-
is susceptible (Jones, 2000; D.R. Jones, per- sular Malaysia and Papua New Guinea
sonal communication, 2002). The differential (Stover; 1972; Jones, 2000). Severe develop-
response of the latter cultivars in these ment occurs in areas of Fiji with >1 m of
regions suggests that different taxa may cause annual rainfall when temperatures are below
freckle in these areas. Studies to clarify this 24°C, and on some local cultivars in Papau
situation are warranted since the existence of New Guinea.
different freckle pathogens would have
Symptoms vary in the different locations.
important quarantine implications for coun-
In Fiji, lesions on the upper leaf surface are
tries in which Cavendish-based trades exist
diamond-shaped, light grey, 2–4 × 3–5.5 mm,
but are not affected seriously by this disease
and have 0.5 mm wide black borders.
(e.g. Australia).
Profuse growth of the causal fungus,
Haplobasidion musae, occurs on the leaf
MANAGEMENT Where freckle is important
undersurface. In Malaysia, lesions have dark
on exported fruit (especially Taiwan), removal
purple borders, are pale grey on the upper
of diseased leaves and protection of bunches
and pale brown on the lower surface, and are
with bags is carried out (Jones, 2000). Several
fungicides that are effective against black either ellipsoid (2–4 × 3–12 mm) or round
Sigatoka are also used against freckle, includ- (2–5 mm in diameter). Lesions are similar in
ing mancozeb and two sterol demethylation Papua New Guinea, and large patches of
inhibitors, propiconazole and flusilazole. confluent necrosis can develop. Symptoms
develop as early as the second or third leaf
on local ‘Mala’ AA.
Leaf speckle Single to six conidiophores of H. musae
are produced at the ends of hyphae that arise
This disease is found in Southeast Asia, and through the epidermis on the leaf ’s lower
is usually a minor problem on diverse culti- surface (Fig. 4.9). They are straight or flexu-
vars (Jones, 2000). However, it has been serious, pale brown, one- to four-celled and
ous in Cavendish AAA export plantations in 50–110 × 4–6 ␮m. They terminate in a sub-
Taiwan since 1981 after disease forecast sys- globose apex that bears spherical, 4–8 ␮m
tems were begun for black Sigatoka control. diameter, sporogenous cells. Conidia are
Severe leaf speckle developed when fungi- spherical, brown, verrucose, 4–6 ␮m in
cides were not used after bunch initiation. diameter, and borne singly or in chains of
Dithiocarbamates in oil are effective. two to five.
Fig. 4.9. Conidia and conidiophores of Haplobasidium musae, cause of Malayan leaf spot (from CMI
Although control measures usually are Disease development is greatest under

not needed, maneb was effective. Spray oil humid, warm conditions, and on old, senesc-
enhanced disease development. ing leaves. Diverse cultivars are affected, and
control measures that are used for the
Sigatoka leaf spots are effective.
Mycosphaerella speckle
This disease has a worldwide distribution, Phaeoseptoria leaf spot

but is a significant problem only in sub-
tropical Australia (Stover, 1972) and South This disease damages ‘Mysore’ and
Africa (Viljoen et al., 2002). Symptoms occur ‘Nendran’ (both AAB) in Kerala State, India
below the fourth leaf, and consist of smoky (Jones, 2000). It is also found in Cameroon,
patches on the upper leaf surface and tan Colombia, Ghana, Guyana, Honduras, Kenya,
irregular blotches on the lower surface (Plate Queensland, Sabah, Trinidad, Uganda and
30). Under wet conditions, these appear Zanzibar. This disparate distribution suggests
water soaked and exude droplets of mois- that the disease may be found elsewhere.
ture. The blotches darken, becoming purple The symptoms resemble those of the
to black, speckled and visible on both leaf Sigatoka leaf spots. Lesions are elliptical to
surfaces. Associated tissues yellow, and even- oval, 1–2 cm wide, and pale yellow with
tually the speckled areas coalesce and bleach dark borders and chlorotic haloes
to grey on the lower, and tan on the upper (Punithalingham, 1983). As spots merge,
surface. they form large necrotic areas. Young leaves
Pseudothecia of the causal fungus, are not affected.
Mycosphaerella musae, appear at this stage. Phaeoseptoria musae produces light to dark
They are 45–99 × 34–81 ␮m, scattered, glo- brown, subglobose, 85–145 ␮m in diameter,
bose, black and immersed in host tissue. Asci ostiolate pycnidia that are immersed and later
are eight-spored, obclavate and 24–44 × erumpent in host tissue (Punithalingham,
8–12 ␮m, and ascospores are hyaline, obtuse 1983) (Fig. 4.10). Conidia are 22–30 ×
to cylindrical, two-celled and 9–16 × 2–3 ␮m. 2.5–3 ␮m, three- to five-celled, hyaline to
Conidia are not produced on the host, but pale brown, straight or slightly curved,
form on agar after 4–5 days. They are cylindrical to slightly clavate, with a
Cercospora-like, average 127 × 2.9 ␮m, are rounded or truncate base and gradually nar-
usually verrucose and have a basal scar. rowed apex.
Fig. 4.10. (A) Vertical section of an immersed pycnidial conidioma, and (B) and (C) conidia of
Phaeoseptoria musae (from CMI description no. 772).
Nothing is known about the disease’s epi- Teliospores are subglobose, ovoid or oblong,
demiology or management. brown, 23–35 × 17–25 m, and have a
rounded or slightly acute apex. Pedicels are
persistent, hyaline and ~60 m in length.
Rust The form genus Uredo includes all species
in which only the uredinal stage is known
This is generally a minor disease in the east- (Alexopoulos et al., 1996). Uredo musae differs
ern hemisphere (Mulder and Holliday, 1971). from Uromyces musae in having more
It affects a wide range of AA, AAA, AAAA, crowded uredia, urediospores with thinner
AAB and ABB cultivars (Jones, 2000). walls (~1.5 m) and more pronounced echin-
ulations (Cummings, 1941).
SYMPTOMS Small brown to black streaks
develop primarily on the underside of older EPIDEMIOLOGY AND MANAGEMENT Urediospores
leaves. As they enlarge and coalesce, the of Uromyces musae are wind-disseminated and
associated tissues become chlorotic and then germinate on wet leaf surfaces (Jones, 2000).
necrotic. Rusty brown masses of uredosori of No hosts other than Musa spp. are known.
the pathogens cover the lesion surfaces. Control is usually not required, although
severe outbreaks have occurred in Cavendish
AAA plantations in Western Samoa.
CAUSAL AGENTS Authenticated specimens
of Uromyces musae are only known from
Africa, and all collections in the Pacific
islands have been referred to Uredo musae. Tropical speckle
(Firman, 1976).
Uredia of Uromyces musae are round and This disease is found throughout the humid
pulvinate (Mulder and Holliday, 1971). tropics. Although it affects younger leaves
Urediospores are globose to subglobose or than the Sigatoka leaf spots (as young as the
ellipsoid, finely echinulate, light brown, third leaf), it causes no economic damage or
20–28 × 17–24 m, and have a 2.5 m thick growth reduction.
wall (Fig. 4.11). Telia are scattered or aggre-
gated, oblong or ellipsoid, 0.5–1.0 mm in SYMPTOMS Two types of symptoms have
length to up to 3 mm when confluent. been described (Jones, 2000). One appears as
Fig. 4.11. (A) Urediospores and (B) teliospores of Uromyces musae (from CMI description no. 295).
circular blotches, ≤4 cm in diameter, which CAUSAL AGENT There is some controversy

are chlorotic on the upper and tan on the over the taxonomy of the pathogen (Jones,
lower leaf surface. Dense aggregations of 2000). Ellis (1971, 1976) indicated that two
dark brown or black pinpoint specks are evi- fungi were involved. Periconiella musae was
dent on the upper surface, and erect groups associated with the second symptom
of conidiophores of the causal fungus are described above, and Veronaea musae with
visible when the lower surface is examined the first. Although the fungi were quite simi-
obliquely. Blotches can merge to form large lar, the conidiophores of P. musae were
tan areas, but the affected tissues generally reported to be branched and those of V.
are not killed. musae were unbranched. However, de Hoog
The second symptom consists of dark (1977) indicated that specimens of V. musae
grey to black patches on the lower leaf that, often produced branched conidiophores, and
when viewed with a hand lens, are densely that the two fungi should be considered a
packed tiny black specks. Individual single species, Ramichloridium musae (Fig.
blotches are less distinct on the upper sur- 4.12). In the absence of recent studies that
face, and are smaller than those for the first clearly distinguish P. musae and V. musae, it
symptom but can merge to involve large sec- will be assumed that R. musae is the correct
tions of the leaf. As for the first symptom, epithet for this pathogen.
thick lawns of conidiophores are evident on Conidia of R. musae are 5.5–8.5 × 2–2.6 ␮m,
the lower surface. Symptoms can also hyaline to subhyaline, thin-walled, ellipsoidal
develop on leaf midribs, peduncles and tips and have inconspicuous basal scars (de Hoog,
of fingers, the latter of which can make 1977). Conidiogenous cells are vertical, pale
‘Umalag’ (AAA, Cavendish subgroup) fruit brown, cylindrical and terminal on conidio-
unmarketable in the Philippines. phores that are up to 500 ␮m high, 1.8–2.5 ␮m
wide, four- to ten-celled, golden brown and
SYMPTOMS Pale green flecks, <1 mm long,

become chlorotic streaks, 3–4 × 1 mm
(Mulder and Holliday, 1974). They broaden,
lengthen, turn brown to rusty, and become
surrounded by chlorotic haloes (Plate 30). As
they mature, they enlarge to 12–15 (up to 50)
× 2–5 mm, darken and then become grey
with a dark brown or black border.
Coalescence of spots can kill large areas. In
general, these symptoms resemble those of
black Sigatoka and Eumusae leaf spot.
CAUSAL AGENT Yellow Sigatoka is caused

by Mycosphaerella musicola (anamorph:
Pseudocercospora musae). Conidia are pale
olivaceous brown, cylindric to obclavate-
cylindric, straight, curved or undulate, 10–80
(up to 100) × 2–6 ␮m, and four- or more
celled (Fig. 4.13) (Mulder and Holliday, 1974).
They have a rounded or obtuse apex and,
unlike those of M. fijiensis, do not have a
basal scar. The two species can also be distin-
guished with PCR (Johanson and Jeger, 1993).
Conidia form singly and terminally on conid-
Fig. 4.12. Conidia and condiophores of iophores that are densely packed in dark
Ramichloridium musae (from Ellis, 1971). brown to black stroma, 15–35 ␮m in diameter,
that erupt through stomata. Conidiophores
are pale olivaceous brown, single-celled,
thick-walled. They arise from epiphyllic
borne terminally on stromatal hyphae,
mycelium on the lower surface of leaves.
straight or slightly curved, rarely branched,
narrow towards the apex, rounded, mostly
EPIDEMIOLOGY AND MANAGEMENT The pathogen
ampulliform and 5–25 × 2–6 ␮m.
is not very aggressive, and penetrates and
Pseudothecia are formed primarily on the
kills only cells that are adjacent to stomata on
upper leaf surface in mature spots. They are
the lower leaf surface. The disease affects
36.8–72 ␮m in diameter, dark brown or
diverse AA, AAA, AAB and ABB cultivars, as
black, and erumpent with a short ostiole.
well as M. schizocarpa and M. acuminata ssp.
Asci are 14.4–18 × 3–4 ␮m, and bear eight
banksii. Control measures are rarely needed.
two-celled ascospores.
Yellow Sigatoka EPIDEMIOLOGY Both conidia and ascospores

are infective. Ascospores and conidia are
Yellow Sigatoka, which is also known as formed under high moisture conditions, and
Sigatoka, was the most important leaf spot are disseminated by wind and, in the case of
disease of banana before the spread of black conidia, also by rain and irrigation water.
Sigatoka (Jones, 2000). It also originated in Due to their small size, ascospores are more
the Southeast Asian/South Pacific region, important than conidia in spreading the dis-
but global epidemics of yellow Sigatoka ease long distances.
began decades before those of black Major infection occurs above 21°C, and
Sigatoka. By the 1950s, the disease had the candela and the first fully opened leaf are
spread to most producing regions. Very few primary infection sites (Stover, 1972). Several
production areas (e.g. Canary Islands, Egypt distinct patterns of symptoms can develop
and Israel) are free of the disease. depending on the infective spore and when
Fig. 4.13. Conidia and conidiophores of Pseudocercospora musae, anamorph of Mycosphaerella musicola
(from CMI description no. 414).
infection occurs. Ascospore infection is ance of symptoms can range from 11 to >100
evident as tip spotting where spots are con- days, and between streak development and
fined to the apical third of the leaf, usually their maturation into brown spots from 2 to
near the margins. When the opening, newly >100 days.
developed leaf is infected by conidia, line
spotting occurs where lines of spots are MANAGEMENT Wide ranges of susceptibil-
found in more basal locations on the leaf. ity occur among different cultivars, and
When streaks are evident on the left margin resistance increases as the relative proportion
of the third and fourth leaf, infection by of the B genome increases (Table 4.3).
ascospores and conidia probably occurred However, there are exceptional situations
during the candela stage. Finally, infection of where AA and AAA clones are resistant.
the first leaf results in a more random spot- Although the AAB plantains are resistant at
ting over the entire leaf. low elevations, they are susceptible at high
Ascospore and conidium germination is elevation in Puerto Rico, Colombia, West
sensitive to temperature. Optimum ranges Africa and elsewhere.
are 25–26°C for ascospores and 25–29°C for The history of chemical control of this dis-
conidia, and germination rates decline dra- ease is found in the section on black
matically once temperatures approach 20°C. Sigatoka. The same chemistries and strate-
Optimum rates for the growth of ascospore gies that are used against black Sigatoka are
germ tubes, 25°C, is ~2°C lower than for M. also highly effective against yellow Sigatoka.
fijiensis, and this is thought to explain at least
partially the prevalence of yellow Sigatoka at Diseases of Fruit
higher elevations.
Disease development is enhanced when Anthracnose
infection densities and light intensities are
high. On susceptible cultivars, the time Anthracnose is one of the most common and
between spore germination and the appear- important diseases of banana fruit (Jones,
2000). It is primarily a postharvest disease Sutton (1992) indicated that there is some
that affects the peel and crown surface area doubt over whether Glomerella musarum, as
(crown rot), but can also develop when green described by Petch in 1917, is the actual
fruit are injured. teleomorph of C. musae. A more recent report
in which the teleomorph was produced in
SYMPTOMS Small brown spots begin to the laboratory used the epithet Glomerella
appear on all parts of the peel as fruit ripen. musae, although no formal description of it
These expand and coalesce to form large was made (Rodriguez and Owen, 1992).
depressed, black to brown areas of decay Until such time, Glomerella sp. should be
that often are covered with orange to used when referencing the teleomorph
salmon-coloured masses of conidia of the (personal communication, Amy Rossman).
causal fungus (Plate 31). The pulp is affected C. musae can be distinguished from
only after fruit become overripe. C. gloeosporioides by its longer and wider
Lesions that develop on wounded green conidia and faster growth rate on artificial
fruit are black and in the shape of the media at 24°C. C. gloeosporioides/G. cingulata
wound. These lesions may be surrounded by can be recovered from decaying bananas, but
chlorotic haloes, and can invade the pulp C. musae has adapted to, and is the most pre-
under warm conditions. dominant cause of anthracnose on, banana.
Conidia of C. musae are hyaline, single-
CAUSAL AGENT The causal fungus, Colleto- celled, elliptical to oval and 11–17 ⳯ 3–6 ␮m
trichum musae, resembles in many ways the (Fig. 4.14).
more common cause of anthracnose on other
fruit, C. gloeosporioides. The identity and EPIDEMIOLOGY C. musae is a common com-
correct name of its teleomorph is confused. ponent of the microflora within the banana
Fig. 4.14. (A) Acervulus, (B) conidiophores, (C) conidia and (D) appressoria formed by hyphae (left) and
germinated conidia (right) of Colletotrichum musae (from CMI description no. 222).
canopy. Work in Guadeloupe indicated that spreads uniformly, causing a brownish black
floral parts and bracts are most important discoloration of the peel and a softening of
sources of inoculum, and that a threefold the pulp. The affected area of the peel
reduction in the severity of this disease was becomes wrinkled and encrusted with pycni-
realized when these sources were removed at dia of the pathogen. The pulp is reduced to a
flowering (de Lapeyre de Bellaire et al., 2000). soft, rotten mass and a dark grey mould
Conidia are formed under wet conditions and grows on the peel surface under high
are dispersed in rain, primarily within the humidity. The rate of disease development
same plant or bunch. Rain is also required for increases during ripening and can spread to
infection. In Guadeloupe, disease severity was adjacent fingers. Infected clusters tend to
significantly correlated with cumulative rain- ripen prematurely, and fully mature fruit are
fall during the first 35 days after flowering, most susceptible. Microscopic examination
and the disease was controlled completely if of spores may be necessary to distinguish
fruit were protected from rain with covers. this disease from tip rot caused by
C. musae forms melanized appressoria on Botryosphaeria dothidea (anamorph: Fusicoccum
the fruit peel shortly after conidia germinate. aesculi).
These infections usually remain latent until
ripening begins. CAUSAL AGENT The disease’s common name
comes from the former name of the
MANAGEMENT Anthracnose can be a serious pathogen’s anamorph, Botryodiplodia theo-
problem when shipped fruit ripen prema- bromae. Botryosphaeria rhodina (anamorph:
turely in the ship’s hold. Minute quantities Diplodia theobromae) is described in Chapter 1.
of ethylene, that are produced by both the
pathogen and the host, initiate the climac- EPIDEMIOLOGY B. rhodina is a common
teric ripening process. The importance of inhabitant of decaying banana trash (Ploetz
ethylene control and shipping green fruit et al., 1994b). Conidia are disseminated by
from plantations in which the Sigatoka leaf
spots have been well controlled was men-
tioned in the introduction to this chapter.
Removal of flower debris and other tis-
sues that harbour the pathogen is beneficial,
as is the protection of fruit from injury. In
export production, fruit are routinely
washed and dipped in fungicide before they
are packed and cooled for shipment. Where
such measures are not available (e.g. most
domestic and smallholder production),
anthracnose can cause significant losses.
Botryodiplodia finger rot
This postharvest decay is common when

shipped bananas are in transit for more than
14 days (Stover, 1972). The disease has been
reported from Central and South America,
the Caribbean, India, Taiwan and the
Philippines (Ploetz et al., 1994b).
SYMPTOMS Symptoms usually begin at the Fig. 4.15. Symptoms of Botryodiplodia finger rot at
flower-end of the finger or at a wound site the flower end of a ‘Bluggoe’ fruit (photo: R.C.
(Fig. 4.15) (Ploetz et al., 1994b). The decay Ploetz, UF).
wind and water, and infection occurs and Lukezic, 1966a). Conidia are dissemi-
through tissues at the flower-end of fingers nated by wind, and can remain viable for at
and wounds. The fungus grows very slowly least 5 weeks when exposed to fluctuating
at <20°C, and optimum growth and rotting humidity and temperature. C. hayi can also
occurs between 25 and 30°C. survive in dried foliar tissues for 15 weeks as
mycelium. Spore release peaks during after-
MANAGEMENT This disease can be con- noon hours that usually coincide with the
trolled by minimizing fruit injury, treating highest daily wind velocities. Spore densities
with systemic fungicides, rapidly reducing and spotting incidence are the highest dur-
fruit temperatures following harvest and ing periods with high rainfall.
excluding over-mature fruit from shipment.
Reducing the caliper (grade) and age of fruit
that are shipped will probably suppress dis- Cigar-end rot
ease development when transit times exceed
14 days. Measures utilized against crown rot Cigar-end rot is an economically important
are also helpful. disease in Central and West Africa (Ploetz et
al., 1994b). It also occurs in the Canary
Islands, Egypt, India, Iran, South Africa,
Brown spot South America and the West Indies.
Brown spot was first described in 1965, but SYMPTOMS One or all fingers on a hand
was probably present in commercial planta- may be affected (Fig. 4.16). The first symp-
tions much earlier (Kaiser and Lukezec, toms are a localized darkening and wrin-
1965). Brown spot was common during kling of the peel at the tip (Ploetz et al.,
warm, rainy weather in the western hemi- 1994b). A black band and a narrow chlorotic
sphere, where its presence varied greatly but region between infected and healthy tissues
was most severe in Mexico, Honduras and border the darkened area. In Trachysphaera
Guatemala. Although losses of entire tip-rot, the surface of the lesion becomes cov-
bunches and up to 20% of the hands occurred ered with white spores that turn pink or
at packing stations in these countries, brown brown as they mature, giving the finger tip
spot is no longer important. Strategies used
against pitting disease are effective.
Brown spot occurs on peduncles, fruit
crowns and fingers. Spotting is generally
more prevalent on inner whorl fingers, and
only occurs >50 days after fruit emergence.
The spots are irregular, light to dark brown
with irregular margins, average 5–6 mm in
diameter, and are surrounded by a water-
soaked halo. They are not as sunken as those
caused by pitting disease and do not increase
in size or number during ripening. Brown
spots are centred on stomata and no aerial
mycelium or fructifications are produced
within the spot.
Brown spot is caused by Cercospora hayi.
Conidia are hyaline, 3–4 × 90–150 ␮m, with
truncate bases and acute tips and more than
five-celled. Dead banana and weed foliage
are the principal sources of inoculum, and
conidia form on dead leaf trash within 16 h Fig. 4.16. Cigar-end rot on fingers of ‘Dwarf
at 23–26°C and saturated humidities (Kaiser Cavendish’ AAA (photo: R.C. Ploetz, UF).
the greyish, ashen appearance usually asso- hyaline to brownish, verticillately branched
ciated with cigar-end rot. The pulp under- and 4–6 × 150–400 ␮m; phialides are 14–37 ×
goes a dry rot and becomes mummified. A 1.5–5 ␮m.
wet rot can occur when secondary organisms
are also present. In Verticillium tip-rot, the EPIDEMIOLOGY The frequency of cigar-end
pulp is characteristically dry and fibrous rot increases during periods of high humid-
with grey, powdery spore masses occurring ity and rainfall. Conidia of V. theobromae are
on the lesion. wind disseminated and infect dying flower
parts (Meredith, 1965). V. theobromae is a
CAUSAL AGENTS Trachysphaera fructigena common colonizer of banana flowers and
and Verticillium theobromae cause cigar-end leaf trash. The source of T. fructigena inocu-
rot in Central and West Africa (Ploetz et al., lum is unknown. In West Africa, cigar-end
1994b). T. fructigena has not been reported in rot incidence is highest along plantation bor-
the western hemisphere, but V. theobromae ders and on plants grown at higher eleva-
has been reported in both hemispheres. tions (Tezenas du Montcel and Laville, 1977).
Conidiophores of T. fructigena are erect, Optimum growth of T. fructigena occurs at
usually have a terminal vesicle, and conidia 24°C, whereas cigar-end rot caused by the
arise singly or in whorls from its apex fungus is favoured by moderate (20°C) fol-
(Holliday, 1970). Conidia are 13–48 ␮m in lowed by higher (<27°C) temperatures.
diameter, echinulate, spherical, hyaline and Optimal growth of V. theobromae occurs at
borne on 10–30 ␮m long pedicels. Oogonia 25°C.
are somewhat pyriform and 24 × 40 ␮m. In fruit infected only with V. theobromae,
Oogonial walls are thick and have irregular, premature ripening and postharvest rotting
sac-like outgrowths (Fig. 4.17). The do not occur. In contrast, fruit infected with
antheridia are amphigynous and completely T. fructigena continues to rot after harvest.
surround the oogonial stalk. New T. fructigena infections can occur either
Solitary or small groups of conidiophores in dehanding and delatexing tanks or in con-
of V. theobromae are produced on infected taminated ripening rooms. These new infec-
tissues. Conidia are hyaline, ellipsoidal to tions typically occur at freshly cut crown
subcylindrical, 3–8 × 1.5–3 ␮m, and are borne surfaces and peel injury sites caused by
terminally on tapering phialides and aggre- improper handling.
gate into rounded, mucilaginous, translus-
cent heads (Fig. 4.18) (Hawksworth and MANAGEMENT Cigar-end rot control begins
Holliday, 1970). Conidiophores are erect, in the field with the frequent removal of dead
Fig. 4.17. (A) Oospores and (B) oogonia and antheridia of Trachysphaera fructigena (from CMI description
no. 229).
addition, some of the causal fungi have been

reported to produce mycotoxins (Jiménez et
al., 1997) or cause changes in the quantity
and quality of soluble sugars in fruit
(Odebode and Sanusi, 1996). Damage is most
severe when fruit are in transit for more than
14 days. Losses can be substantial, especially
in Europe where fruit is displayed on hooks.
SYMPTOMS Crown rot is first observed on

fruit that are in transit for more than 7 days.
It begins as a softening and blackening of
tissues at the cut crown surface (Plate 31).
Greyish white, pink or white mould that
may be present on the cut surface at this
early stage is known as crown mould.
Fig. 4.18. (A) Verticillate conidiophore and (B)
Crown rot spreads rapidly during ripening,
conidia of Verticillium theobromae (from CMI
and can spread into the pedicel, and ulti-
mately the pulp when severe or if
flowers followed by bagging bunches with Ceratocystis paradoxa is present.
perforated polyethylene sleeves (Ploetz et al., A water-soaked, dark band of creased and
1994b). Bracts and dead flower parts accumu- bruised tissue becomes evident on pedicels
late in the fruit bags and should be removed a that are flexed excessively during handling
few weeks after bagging. Field sanitation, as and transit. The crease turns black, enlarges
practised for fruit spot control, is helpful in and withers as pedicel rot progresses. When
reducing V. theobromae inoculum pressure and Colletotrichum musae is present, pink spore
subsequent cigar-end rot. Packing station san- masses may appear on the blackened tissue
itation is essential to reduce postharvest infec- under moist conditions. Pedicel rot can also
tion and rot caused by T. fructigena. Infected result from infection at mechanical injury
fruit should be culled prior to dehanding to sites, peduncle rot and severe pitting disease.
avoid contamination of dehanding and dela-
texing tank water with T. fructigena spores. CAUSAL AGENTS A complex of fungi causes
Fungicide sprays may be necessary during crown rot (Greene and Goos, 1963; Kaiser
some peak cigar-end rot seasons (Tezenas du and Lukezic, 1966b; Griffee, 1976; Knight et
Montcel, 1981). al., 1977; Johanson and Blazquez, 1992). The
pathogens vary based on location, time of
year and other factors. C. musae (Fig. 4.14) is
Crown and pedicel rot most important, but the following species
have also been indicted: Acremonium sp., C.
Crown and pedicel rot can be major problems paradoxa, Diplodia theobromae, Fusarium monil-
on exported fruit, and are present in all iforme, F. pallidoroseum, F. subglutinans (Fig.
banana-growing regions (Jones, 2000). These 4.19), Nigrospora sphaerica and V. theobromae
diseases were not important when the export (Fig. 4.18). Snowden (1990) indicated that N.
trades relied on fruit of ‘Gros Michel’ AAA sphaerica and N. oryzae (Fig. 4.20) were con-
since these fruit were shipped as intact sidered by some to be synonymous.
bunches. With the trades’ conversion to the Recently, O’Donnell et al. (1998) redescribed
Cavendish AAA cultivars in the 1960s came isolates of F. subglutinans from banana as a
the need to remove and pack individually new species, F. concentricum, based on DNA
hands of its more fragile fruit, thereby opening sequence analyses.
the crown area to invasion by various fungi. The mycotoxigenic species include F. con-
Crown and pedicel rot cause significant centricum, F. moniliforme and F. subglutinans
aesthetic damage and drop of fingers. In (reports of the latter species may be of F.
Fig. 4.19. Counterclockwise from upper left: microconidia, macroconidia and conidiophores of Fusarium
subglutinans (from CMI description no. 23).
Fig. 4.20. (A) Transverse section of perithecia, (B) ascus and (C) ascospores of Khuskia oryzae, and (D)
conidia and conidiophores of its anamorph, Nigrospora oryzae (from CMI description no. 311).
concentricum) (Chakrabarti and Ghosal, 1986; fruit. Prompt (<48 h after harvest) and rapid
Jiménez et al., 1997; Logrieco et al., 1998). fruit temperature reduction also aids crown
Unfortunately, toxigenicity of these species rot control.
has been tested in maize cultures, rather than Diverse measures for managing this dis-
banana. Whether these species produce ease were reviewed recently (Krauss and
mycotoxins in banana and colonize fruit to Johanson, 2000). Postharvest treatment with
the extent that they represent bone fide human fungicides usually is essential for exported
health risks has not been investigated. bananas (Shillingford and Sinclair, 1978).
Fungicides can be applied with dips, sprays
EPIDEMIOLOGY The causal fungi are or recirculating drenches. Those approved
common colonizers of banana leaves, for use depend on the country of destination.
flowers, bracts and transitional leaves Fruit destined for the USA and Europe can
(Stover, 1972). They sporulate on decaying be treated with thiabendazole or imazalil.
debris and are disseminated by wind and Other measures that reduce disease develop-
water-splash to all parts of the fruit. Infection ment include hot water (50°C) dips for 20
occurs primarily at the cut surfaces of min, retrimming the crown surface once it is
crowns during either dehanding with con- in the packing house, and using controlled
taminated knives or contact with infested atmospheres, various fruit coatings or
wash water. Spores from fruit surfaces and natural products (Reyes et al., 1998; Krauss
decaying flower parts that remain attached and Johanson, 2000). In general, control with
to the fingers tend to accumulate in wash the later products is either inconsistent or
water. Spores present in the wash water can does not achieve the levels realized with
be drawn several millimetres into the fungicides.
vascular system at the wound site where
they germinate and cause a rot (Greene and
Goos, 1963). Other spores may germinate at Deightoniella fruit speckle and black tip
the cut surface and invade the adjacent cells.
Susceptibility to crown rot is increased by Deightoniella torulosa causes Deightoniella
desiccation of crowns, poor crown-trimming speckle, which is also known as swamp spot,
techniques and poor dehanding practices and black tip, which is also known as tip-end
that result in crushed subsurface crown rot (Stover, 1972). The same fungus also
tissues. The use of dull knives during trim- causes Deightoniella leaf spot. All three
ming causes ragged edges and favours entry diseases are relatively minor problems wher-
of crown rot organisms into adjacent, sound ever banana is grown.
tissue. Speckles occur on fruit at all stages of
Crown rot incidence and severity vary maturity and consist of reddish brown to
depending on the organisms that gain entry black spots, up to 2 mm in diameter, with a
and climatic conditions, and certain groups dark green halo. The disease is important
of fungi and bacteria appear to act synergis- only during the wet season, and control mea-
tically in boxed bananas. Hot, dry conditions sures for pitting disease are also effective
prior to harvest tend to favour crown rot against it. Cultural practices that reduce
development. moisture in the plantation are also helpful.
Black tip symptoms consist of a slowly
MANAGEMENT Crown rot control begins in advancing black lesion at the flower-end of
the field with good sanitation, as practised one or more fingers. A single side of the
for pitting disease control (Stover, 1972). finger is usually affected, and the diseased
Good hygiene in packing stations and clean area is bordered by a pale yellow or narrow,
water in dehanding and delatexing tanks are grey margin. Old lesions tend to rupture and
essential. Trimmed crowns should have a pale brown mould can develop under moist
bevelled edges since sharp edges are sensi- conditions. V. theobromae can infect fruit
tive to handling injury and can result in through black tip lesions and transform black
increased disease in otherwise good quality tip into cigar-end rot. Black tip can be con-
trolled by removing leaf trash and improving lesion, 1.0–3.5 × 0.5–1.5 cm. Large spots
drainage to reduce humidity in the field. occasionally expose the pulp. Diamond spots
D. torulosa is a common component of the begin to appear as the fruit approaches
airborne microflora within plantations. harvest grade, and latent infection is
Conidiophores arise singly or in small common. Lesion size and disease incidence
groups from hyphae or swollen cells (Fig. can increase during transit and ripening.
4.21) (Subrumanian, 1968). They are septate, A complex of fungi causes diamond spot.
brown, 6–10 ␮m wide, are swollen to A strain of C. hayi, which differs from that
13–16 ␮m in diameter at the apex, and can involved with brown spot, is accompanied
have up to six successive proliferations of the by F. pallidoroseum, F. solani and, less com-
same dimension. Conidia are blastospores monly, other Fusarium species. The species in
and are produced singly. They are straight or the complex are prevalent on decaying and
slightly curved, obpyriform to obclavate, dead leaf trash where they sporulate under
subhyaline to smoky olive, usually four- to moist conditions. They are part of the air-
six-celled, and 35–70 × 13–25 ␮m. borne microflora commonly found in banana
plantations.
Latent infections are common, and lesion
Diamond spot development frequently occurs during tran-
sit and ripening. The same procedures used
Diamond spot was first described in 1968 against pitting disease control diamond spot.
and was common in parts of the Americas
and the Philippines (Berg, 1968). It is no
longer an important disease. Pitting
Diamond spot first appears on the peel of
Pitting disease, which is also known as
green fruit as slightly raised, yellow spots,
Johnston spot, is found in Asia, Africa,
3–5 mm in diameter (Fig. 4.22). Since
Australia, the Canary Islands, the Caribbean,
infected cells do not grow at the same rate as
and Central and South America (Stover,
adjacent healthy cells, a longitudinal crack
1972; Snowdon, 1990). Losses of up to 50% of
develops through the spot that is sur-
the fruit in packing stations occurred in some
rounded by a yellow halo. The tissue
Central American areas in the 1960s. Pitting
exposed by the crack and the yellow halo
was once considered the most important
becomes necrotic, collapses, turns black and
fruit spot disease in Central America, but is
appears as a sunken, diamond-shaped
now less important. Cavendish cultivars are
more susceptible than ‘Gros Michel’ AAA
and plantains.
SYMPTOMS Small, reddish sunken spots

develop on maturing fruit (Stover, 1972;
Snowdon, 1990). As fruit begin to ripen, they
enlarge to 4–6 mm in diameter, become
brown and are surrounded by a reddish
brown border. The fruit pulp is not damaged
even when lesion centres crack. Smaller spots
that develop on the pedicle and crown can
cause finger drop. Lesions can also develop
on leaves of young water suckers and transi-
tion bracts. They are shallow, sunken and
larger than those on fruit and, unlike those
on fruit, support sporulation of the pathogen.
Fig. 4.21. Conidia and conidiophore of CAUSAL AGENT Pitting disease is caused
Deightoniella torulosa (from Ellis, 1971). by Pyricularia grisea (its teleomorph,
Fig. 4.22. Severe symptoms of diamond spot in the Philippines (photo: R.H. Stover).
Magnaporthe grisea, is uncommon) (Stover, common and can result in unacceptable lev-
1972). It is isolated readily from pitting els of pitting disease during transit and
disease lesions or as conidia from recently ripening. However, since severe pitting
collapsed, dry banana foliage when placed in occurs only after prolonged periods of high
a moist chamber.
Conidia are attached singly at the broader
end in scarpioid cymes, ovate to pyriform
with a small basal apiculus, three-celled,
essentially hyaline and 17–19 × 6.5–8.5 ␮m
(Fig. 4.23). Although P. grisea closely resem-
bles P. oryzae (a rice pathogen), these fungi
are host specific (Meredith, 1963). P. grisea
sporulates poorly on most agar media, but
sporulates abundantly on autoclaved
Commelina erecta leaves.
EPIDEMIOLOGY Pitting disease is most

prevalent during periods of high rainfall.
The principal source of inoculum is dead
leaves and bracts. Conidia are disseminated
by wind currents and are present throughout
the year in Central American banana planta-
tions. They germinate and form appressoria
on green fruit within 4–8 h under high
humidity. The optimum temperature for
appressorial formation and infection is
24–26°C.
In the laboratory, lesion development can
occur on green fruit within 2–3 weeks of
inoculation. In contrast, fruit in the field
seldom develop lesions until 3 weeks before
harvest. The fungus may remain dormant in
infected tissues until the fruit nears maturity Fig. 4.23. Conidia and conidiophores of Pyricularia
or until after harvest. Latent infections are grisea (from Ellis, 1971).
rainfall and where control measures are infects the cut pedicel surface and proceeds
inadequate, it has become a minor problem to colonize and liquefy the pulp. Externally,
in export plantations where intensive control the peel becomes bluish tan during ripening.
of foliar diseases is practised. Packing fruit only in hands and treatment
with standard postharvest fungicides con-
MANAGEMENT All symptomatic fruit are trols the disease.
culled at packing stations. Frequent removal
of inoculum reservoirs in the field is essential
(Halmos, 1970). All collapsed and dying Diseases of the Rhizome and Pseudostem
banana foliage, transition leaves and bracts
should be removed at regular intervals dur- Cylindrocladium root rot
ing the rainy weather. Fruit can be protected
with fungicide sprays prior to bagging with This disease can cause significant root
perforated polyethylene film or with perfo- damage in its own right, but is most serious
rated polyethylene film dusted with fungi- when it interacts with Radophlous similis, the
cide. Fungicides used for fruit spot control burrowing nematode (Jones, 2000). It has
depend on tolerances established in import been reported on several different cultivars
countries; maneb, mancozeb, benomyl and in Cameroon, Costa Rica, Côte d’Ivoire,
thiophanate methyl are common (Guyon, Guadeloupe and Martinique.
1970). Cortical tissues of banana roots are killed
and blackened by at least two species,
Sooty blotch and sooty mould Cylindrocladium gracile and Calonectria
spathiphylli (anamorph: Cylindrocladium
These diseases produce similar diffuse, spathiphylli). Cy. gracile has no known telo-
smoky grey to black areas on the finger and morph. Macroconidiophores consist of a
crown surface. They are superficial, do not stipe, penicilliate fertile branches, a stipe
affect the pulp and often are not dis- extension and a terminal vesicle (Fig. 4.24)
tinguished (e.g. Stover, 1972). Sooty mould (Crous, 2002). Stipes are septate, hyaline,
requires excreta (honeydew) of mealybugs smooth and 50–150 × 5–6 ␮m. The stipe
and aphids to develop, whereas sooty blotch extensions are septate, straight to flexuous,
does not. 140–350 ␮m long, 2.5–3 ␮m at the apical
Sooty blotch occurs in Australia, Costa septum above which is a clavate 2–6 ␮m
Rica and probably other locations (Jones et wide vesicle. The conidiogenous apparatus is
al., 1993; T. Sutton, NCSU, personal commu- 35–75 long, 15–60 wide with 10–25 × 3–5 ␮m
nication, 2001; R. Ploetz, personal observa- single- or two-celled primary branches and
tions). It is caused by Chaetothyrina musarum 10–18 × 3–5 ␮m single-celled secondary
and does not warrant specific management. branches. Conidia are cylindrical, rounded at
Stover (1972, 1975) reported that the most the ends, 38–65 × 3.5–6 ␮m and straight.
common cause of sooty mould in the Ca. spathiphylli produces orange to red
Americas and the Philippines was perithecia that are subglobose to ovoid,
Cladosporium cladosporioides. It occurs most 380–655 ␮m high and 340–650 ␮m in
frequently during cool, rainy weather, is con- diameter (Fig. 4.25) (Crous, 2002). Asci are
trolled with insecticides or by covering two- to eight-spored, clavate and 120–230 ×
bunches with insecticide-impregnated poly- 7–25 ␮m, and ascospores are aggregated in
ethylene bags, and is described in Chapter 6. the upper third of the ascus, are hyaline,
guttulate, fusoid with rounded ends, one- to
three-septate and 22–65 × 3–7 ␮m. Macro-
Squirter disease
conidiophores are composed of a stipe, peni-
This disease occurs when single fingers are cilliate fertile branches, a stipe extension and
packed (Stover, 1972; Snowdon, 1990). It is a terminal vesicle. Stipes are septate, hyaline,
caused by Khushia oryzae (anamorph: smooth and 120–150 × 6–8 ␮m. The stipe
Nigrospora oryzae) (Fig. 4.20). The pathogen extensions are septate, straight to flexuous,
Fig. 4.24. (A) Macroconidiophores and vesicles and (B) conidia of Cylindrocladium gracile (from CMI
170–326 ␮m long, 3–4 ␮m at the apical sep- Caribbean and Costa Rica as Cy. pteridis (Fig.
tum and terminate in a globose or ellipsoid 4.26). Although Riséde and Simoneau (2001)
to obpyriform 8–15 ␮m wide vesicle. The later concluded that these isolates were more
conidiogenous apparatus is 60–150 ␮m long, appropriately assigned to Cy. gracile, Crous
40–90 wide with 18–40 × 4–6 ␮m single- or (2002) indicated that this conclusion should
two-celled primary branches and 18–30 × be re-examined since the isolates were larger,
4–6 ␮m single-celled secondary branches. 69–86 × 5.6–6.2 ␮m, than was typical for Cy.
Conidia are cylindrical, rounded at the ends, gracile (conidia of Cy. pteridis are 50–130 ␮m
45–120 × 5–7 ␮m and straight. × 4–6 ␮m). Cy. musae was reported from
Riséde and Simoneau (2001) examined Costa Rica as a new species (Semer et al.,
the morphology and genetic variation of iso- 1987), but recent results indicate that it is
lates from banana in Cameroon, the synonymous with Cy. spathiphylli (Riséde
Caribbean and Costa Rica. RFLP analyses of and Simoneau, 2001).
the intergenic spacer region (IGS) confirmed The epidemiology and management of
the presence of Cy. gracile and Ca. this disease have not been reported.
spathiphylli, and the Calonectria teleomorph
was formed in crosses of Ca. spathiphylli iso-
lates, but not Cy. gracile. Marasmiellus rot
Two additional species have been
reported on Musa. Riséde (1994) tentatively This widespread disease occurs in neglected
identified isolates from Cameroon, the plantings, and in sandy, gravelly or poorly
Fig. 4.25. (A) Conidiophore, vesicles and conidia, and (C) chlamydospores of Cylindrocladium spathiphylli,
and (B) asci and (D) ascospores of its teleomorph, Calonectria spathiphylli. Bar = 10 ␮m (from CMI
drained soils (Stover, 1972). The pathogen rhizomorphs that may develop between leaf
Marasmiellus inoderma colonizes dead and sheaths have a mushroom odour, and
dying banana trash and is a pathogen on basidiocarps of the pathogen form on the
weakened plants. Outer leaf sheaths dry and pseudostem and soil surface under moist
plants become stunted. Water-soaked, brown conditions. The fruiting structures are brown-
oval patches of necrosis develop on the inner ish to salmon coloured on the top, turning
leaf sheaths and may extend to the pseudo- pale later, are 5–15 mm in diameter and have
stem’s centre, but not the rhizome. Roots are widely spaced gills on the bottomside.
covered in white mycelium, develop a black- Basidiospores of the fungus are wind dis-
ened tip and ultimately shrivel and have a seminated. Where the disease is a problem,
brown cortex. Whitish mycelium and improved plantation sanitation and manage-
Fig. 4.26. (A) Chlamydospores, (B) macroconidiophore, vesicles and conidia, (C) microconidiophore,
vesicles and conidia of Cylindrocladium pteridis, and (D) asci, (E) ascospores and (F) perithecium of its
teleomorph, Calonectria pteridis. All bars except that for the perithecium (20 ␮m) equal 10 ␮m (from CMI
ment are indicated. In particular, dead banana is now found in all banana-producing
tissue and other trash should be removed. regions except islands in the South Pacific,
the Mediterranean, Melanesia and Somalia.
Panama disease (Fusarium wilt) SYMPTOMS The first internal symptom, a

reddish brown discoloration of the xylem,
Panama disease, which is also known as develops in feeder roots, the initial sites of
Fusarium wilt, originated in Southeast Asia, infection. It progresses to the rhizome and is
but was first reported in Australia in 1876 most prominent where the stele joins the cor-
(Ploetz and Pegg, 1997). It was responsible tex. As the pseudostem is colonized, faint
for destructive epidemics in export planta- brown streaks or flecks become evident on
tions of ‘Gros Michel’ AAA before the 1960s and within older leaf sheaths. Eventually,
that caused the trades to convert to the large portions of the xylem turn brick red to
Cavendish cultivars. It is widely spread, and brown (Plate 32).
The first external symptoms of Panama small and do not develop fully. Internal
disease are a yellowing of the oldest leaves symptoms in the pseudostem are similar to
or a longitudinal splitting of the lower por- those of Panama disease and include con-
tion of the outer leaf sheaths on the pseu- spicuous brown to purple vascular strands
dostem of plants that are usually more than 4 (Fig. 4.27). In a previous study, Fusarium
months old. This is followed by wilting and oxysporum was recovered from 59% of the
buckling of leaves at the petiole base. In symptomatic highland AAA samples that
some cases, these leaves remain green. As were examined, but only 14% of these (three
the disease progresses, younger and younger of 22) were vegetatively compatible with the
leaves collapse, until the entire canopy con- causal agent of Panama disease, F. oxysporum
sists of dead or dying leaves. f. sp. cubense (Ploetz et al., 1994a). Kangire
Symptoms of Moko disease, caused by and Rutherford (2001) reported that they
race 2 of the bacterium R. solanacearum, can were unable to recover F. oxysporum from
be confused with those caused by Panama affected plants. Thus, the true cause of this
disease. However, Moko causes wilt and problem is not clear. Since affected plants are
chlorosis on plants that are younger than 4 usually found in areas where household or
months old, and also discolours internal por- animal wastes have been discarded, current
tions of fruit. hypotheses focus on an edaphic aetiology.
Two disorders of unknown aetiology can
be confused with Panama disease. The term CAUSAL AGENT F. oxysporum f. sp. cubense is
‘false Panama disorder’ was used by Deacon a soilborne hyphomycete (Domsch et al.,
et al. (1985) to identify a condition of 1980). It is one of more than 100 formae
Cavendish cultivars in South Africa that speciales (special forms) of F. oxysporum that
resembled Panama disease. The disorder
also occurs on Cavendish clones in the
Canary Islands, and elsewhere on other
dessert and plantain cultivars (AAA, AAB
and ABB genomes), including Colombia,
Grenada, Panama and Suriname (summa-
rized by de Beer et al., 2001). External symp-
toms are similar to those of Panama disease,
but internally affected plants exhibit only
discontinuous wine-coloured vascular strands
without the browner, more extensive and
continuous vascular discoloration caused by
Panama disease. The disorder is thought to
be caused by a combination of stress factors
such as drought, cold temperatures, soil
compaction and nutrient imbalance (de Beer
et al., 2001).
In the highlands of western Uganda,
another disorder, matooke wilt, occurs at ele-
vations above 1300 m. Originally reported on
the highland AAA cultivars (Lujugira-
Mutika subgroup), it is now also recognized
on introduced cultivars (not specified)
(Kangire and Rutherford, 2001). Leaves on
affected plants generally are healthy, but
may be smaller and exhibit marginal necro-
sis. Affected pseudostems are thin, often dry Fig. 4.27. Internal symptoms of matooke wilt in
in appearance, and may buckle, especially Uganda. Note their resemblance to symptoms of
after the fruit bunch has emerged. Fruit are Panama disease (photo: R.C. Ploetz, UF).
cause vascular wilts of flowering plants. It or plantain production areas in Western

contains pathogenic and saprophytic strains Africa and Latin America, it could cause sig-
that cannot be distinguished morphologi- nificant damage.
cally. Colonies are white to purple on PDA, Vegetative or somatic compatibility has
grow 4–7 mm day⫺1 at 24°C, and have slight been used extensively to characterize this
to copious aerial mycelium. Sporodochia are pathogen, and >20 VCGs have been reported
tan to orange, and sclerotia are blue and sub- to date (Jones, 2000). Phylogenetic work indi-
merged. cates that the pathogen originated in
Micro- and macroconidia are produced on Southeast Asia, and probably co-evolved
branched and unbranched monophialides. with its banana host in this region (Ploetz
Microconidia are 5–16 × 2.4–3.5 ␮m, one- or and Pegg, 1997).
two-celled, oval- to kidney-shaped, and are
borne in false heads. Macroconidia are 27–55 EPIDEMIOLOGY Rhizomes (‘suckers’) are
× 3.3–5.5 ␮m, four- to eight-celled and used traditionally as vegetative seedpieces for
sickle-shaped with foot-shaped basal cells. banana. Because they are usually free of
Chlamydospores are 7–11 ␮m in diameter, symptoms when they are infected by F.
usually globose and are formed singly or in oxysporum f. sp. cubense, they often are respon-
pairs in hyphae (terminal and intercalary) or sible for its dissemination. F. oxysporum f. sp.
conidia. Atypically for the species, chlamy- cubense can also spread in soil and running
dospores are not produced by isolates in water, and on farm implements and machin-
vegetative compatibility group (VCG) 01214. ery. Work in the early export plantations indi-
Four races of F. oxysporum f. sp. cubense cated that susceptible clones could not be
have been described, only three of which replanted successfully in infested sites for up
affect banana (race 3 is a pathogen of to 30 years due to the long-term survival of F.
Heliconia spp.). Race 1 caused the epidemics oxysporum f. sp. cubense in soil and as a para-
on ‘Gros Michel’ and also affects ‘Maqueño’ site of non-host weed species (Waite and
AAB, ‘Silk’ AAB, ‘Pome’ AAB, ‘Pisang Dunlap, 1953; Stover, 1962).
Awak’ ABB and the hybrid ‘I.C.2’ AAAA. Root tips are the initial sites of infection,
Race 2 affects cooking bananas, such as and wounded rhizome surfaces are appar-
‘Bluggoe’ ABB, and some bred tetraploids. ently minor infection courts. In most cases,
Race 4 is most destructive since it affects root tip infections are stopped shortly after
race 1 and race 2 suscepts as well as the the pathogen reaches the xylem due to the
Cavendish cultivars, plantains and other formation of gels and tyloses, and vascular
bananas that are resistant to races 1 and 2. collapse. However, some of these infections
Until recently, it had been reported only in are not recognized early enough in suscepti-
subtropical regions where cold winter tem- ble cultivars, and the colonization of the
peratures are thought to be predisposing fac- xylem and associated parenchymal tissues
tors (Moore et al., 1993). However, continues unabated. Macroconidia and
considerable damage has occurred in chlamydospores that form on dead or dying
Cavendish monocultures in tropical plants are significant survival structures of
Southeast Asia within the last decade. A dis- the pathogen.
tinct population of the pathogen, VCG
01213–01216, is responsible for the latter out- MANAGEMENT Few effective options exist
breaks. It affects the same clones as race 4 in for managing this lethal disease. In work in
the subtropics, but does not require predis- South Africa, methyl bromide significantly
posing factors. VCG 01213–01216/tropical reduced disease incidence, but was effective
race 4 is found currently in Australia for less than 5 years since the fumigated
(Northern Territory), Indonesia (Halmahera, areas were recolonized by the pathogen
Irian Jaya, Java, Sulawesi and Sumatra), (Herbert and Marx, 1990). Pseudostem/rhi-
peninsular Malaysia and Papua New Guinea. zome injections of carbendazim and potas-
Were it to spread to the Cavendish-depen- sium phosphonate have provided erratic or
dent export trades in the western hemisphere unrepeatable control (Lakshmanan et al.,
1987; Herbert and Marx, 1990; Davis et al., pathogens, and should be used to establish
1994). Heat treatment of soil was used new plantings whenever possible. It should
recently to control the spread of the be noted, however, that plants grown from
pathogen in the Philippines, but this method plantlets are more susceptible to Panama dis-
will probably suffer the fate described for ease than those that are grown from rhi-
methyl bromide-treated soil. zomes (Smith et al., 1998). In addition, since
Soils that suppress the development of meristem culturing usually does not elimi-
Panama disease are found in several differ- nate the important viral pathogens, such
ent locations (Stover, 1962, 1990b; Chuang, planting material should be virus indexed or
1988; Peng et al., 1999; Domínguez et al., otherwise known to be free of these
2001). Diverse attributes have been associ- pathogens. Although the expense of plantlets
ated with this trait. Stolzy and co-workers may make their use in subsistence agricul-
(reviewed by Toussoun, 1975) associated dis- ture impractical, plantlets could be used to
ease suppression with chemical and physical initiate nurseries for producing pathogen-
factors and found its closest association with free, conventional seedpieces.
soils in which a clay fraction of the montmo- Genetic resistance offers the greatest
rillonoid type was found. In the Canary promise for managing this disease in
Islands, suppression was associated with infested soils. To date, pre-existing cultivars
electrical conductivity, Na content and the have been identified that perform well in dif-
structural stability of soil aggregates ferent regions and against different popula-
(Domínguez et al., 2001). In studies in tions of the pathogen (Table 4.3). Resistant
Australia, the addition of CaCO3, Ca(OH)2, hybrids have also been produced in the
CaSO4 or Fe-EDDHA to soil reduced germi- breeding programmes. Although these gen-
nation of chlamydospores of the pathogen as erally lack the flavour or postharvest attrib-
well as disease severity under controlled utes that are found in the susceptible
conditions (Peng et al., 1999). Whether these cultivars, progress is being made.
treatments would be effective in the field
was not examined. Unfortunately, the con-
version of large-scale tracts of conducive Pseudostem heart rot
field soil to a suppressive condition has not
been reported. This disease was important on injured ‘Gros
Studies on the biological and cultural con- Michel’ AAA, but has become unimportant
trol of this disease have begun only recently. after the trades coverted to the Cavendish
Arbuscular mycorrhizal fungi have been clones (Stover, 1972). It is uncommon on
shown to reduce disease severity in short- other clones, and is usually associated with
term greenhouse studies, but results from wounding.
long-term field studies have not been The centre whorl of leaves darkens and
reported. Soil amendments, endophytic fungi becomes necrotic. Initially the decay is firm,
and rhizosphere bacteria currently are being but later softens and develops a foul odour
examined in Australia and South Africa. due to secondary colonization by bacteria.
Achieving success with these or other The associated leaves become yellow or
approaches is a daunting task due to the high brown upon emergence and may or may not
susceptibility of the cultivars for which pro- open. In extreme instances, the entire canopy
tection is sought (usually Cavendish clones) and pseudostem collapse. Damage is not sys-
and the perennial nature of the crop in most temic, and only one or a few pseudostems in
areas. The success of these strategies should a mat are affected. Plants can recover and
be greater in areas where banana is treated as throw a new set of leaves.
an annual or single-cycle crop (e.g. Taiwan). The cause of this disease may be con-
Susceptible clones can be grown if fused, since two different fungi have been
pathogen-free propagation material is used reported. Stover (1972) indicted Fusarium
in non-infested soil. Tissue-cultured plantlets moniliforme (Fig. 4.28) and listed a Gibberella
are free of bacterial, fungal and nematode fujikuroi teleomorph. In contrast, Reinking
Fig. 4.28. Counterclockwise from upper left: microconidia, macroconidia and conidiophores of Fusarium
moniliforme (from CMI description no. 22).
(1937) mentioned both F. moniliforme and F. coffeae, P. goodeyi and Helicotylenchus multicinc-
subglutinans (Fig. 4.19), and suggested that tus, although Rotylenchus reniformis and sev-
further studies were warranted to clarify eral species of Meloidogyne are are also
whether both or only one of the species common. In general, these pests damage roots
caused heart rot. Over six decades after this and the structural integrity of the banana mat,
paper was published, the situation is still not and provide entry points for root-rotting
clear. Whether the heart rot F. subglutinans is fungi. They have also been associated with an
synonymous with the newly described F. increased susceptibility to the banana weevil,
concentricum (see section on crown rot in this Cosmopolites sordidus (Speijer et al., 1993).
chapter) is also not known.
Heart rot is not a major concern unless
plantations either are poorly maintained or Burrowing nematode root rot (blackhead
have been damaged by flooding, wind or toppling disease)
other agents.
In general, the burrowing nematode, R.
similis, is the most important nematode pest
DISEASES THAT ARE CAUSED BY of banana (Gowen and Quénéhervé, 1990;
NEMATODES Sarah et al., 1996). It has a pantropical distrib-
ution and is found in all banana-producing
Worldwide, 151 species of nematodes in 43 areas except the Canary Islands, Cape Verde
genera have been reported on Musa spp. Islands, Cyprus, Crete, Israel, Mauritius,
(Gowen and Quénéhervé, 1990). The most Taiwan and the highlands of East Africa. It
important are Radopholus similis, Pratylenchus has a serious impact on export production of
the Cavendish clones, and is also common of several fungal pathogens, including
on cooking bananas and plantains in Puerto Cylindrocarpon musae (Fig. 4.29),
Rico and in lowland central and eastern Cylindrocladium spp. (see section on
Africa. The nematode has a relatively wide Cylindrocladium root rot in this chapter),
host range that includes weed and crop Acremonium stromaticum and Rhizoctonia
species. Its wide distribution undoubtedly is solani (Jones, 2000).
due to the movement of infected hosts. For The most conspicuous symptom is the
example, Marin et al. (1998) indicated that at blackhead toppling syndrome in which
least three separate introductions of the pseudostems lodge and expose the black-
species occurred as different banana clones ened remains of roots and the blackened, but
were disseminated in the New World. intact, rhizome. It results from the reduced
mechanical strength of the root system and
can occur on plants of any age. It is most
Symptoms
common, however, on plants with a bunch
R. similis causes dark brown to black necrotic and during excessive rain and wind.
patches on root and rhizome surfaces. The Uprooted plants often fall with attached
entire cortex of roots can be killed, but the suckers. Blackhead toppling differs from rhi-
stele is not affected; in cross-section, a sharp zome breakage caused by C. sordidus, in
demarcation between the cortex and stele is which the lower portion of the rhizome
evident. Damage is enhanced in the presence remains in the soil.
Fig. 4.29. (A) Macroconidia, (B) microconidia, (C) conidiogenous cells and (D) thick-walled resting
structures of Cylindrocarpon musae (from CMI description no. 927).
Causal agent are either no longer registered or are too

expensive.
R. similis is a migratory, endoparasitic nema-
In established banana plantations, success-
tode that completes its life cycle in 20–25
ful control is limited to the use of organophos-
days, and whose cardinal temperatures are
phate and carbamate nematicides. They are
17, 30 and 33°C (Sarah et al., 1996). Its rela-
applied as granules at the base of plants or as
tively high optimum temperature for
emulsifiable concentrates via drip irrigation.
growth generally restricts it to the lowland
As for the broad-spectrum soil fumigants, the
tropics.
number of nematicides that retain registration
Pathogenic and genetic variation occur
is being reduced continually.
among populations from different regions
Many important banana cultivars are sus-
and from other hosts. On banana, some
ceptible to R. similis. Stoffelen et al. (2000)
populations from Africa are more patho-
tested the resistance of 14 clones to this
genic than others in the Caribbean,
nematode that varied in their resistance to to
Queensland and Sri Lanka, and another
Panama disease. Only three clones that resist
pathotype from Puerto Rico is more patho-
Panama disease, two accessions of ‘Pisang
genic on plantain than other bananas (Sarah
Jari Buaya’ AA and one of ‘Yangambi Km5’
et al., 1996). Although differences in various
AAA, were resistant to R. similis. None of the
genetic characters exist, the species gener-
cultivars in this study were resistant to the
ally is uniform.
lesion nematode, Pratylenchus coffeae.
Epidemiology
Lesion nematode damage
All life stages are vermiform and mobile.
Females are infective, but males have an P. coffeae and P. goodeyi are serious pests of
atrophied stylet and are not. Eggs are laid in bananas (Bridge et al., 1997). They cause lodg-
the cortex, and the entire life cycle can be ing and lesions on roots and rhizomes of
completed within the root. banana that are identical to those caused by R.
similis. They usually appear in roots in concert
with several different fungi, including
Management
Fusarium oxysporum, F. redolens, F. sambucinum,
Meristem cultured plantlets should be used Nigrospora musae and Rhizoctonia solani.
in new production areas where banana has P. coffeae has a pantropical geographic
not been grown previously (Gowen and distribution and a wide host range that
Quénéhervé, 1990; Sarah et al., 1996). includes important crop species (Bridge et
Traditional suckers can be treated with a al., 1997). Its worldwide occurrence is traced
nematicide or in hot water (52–55°C for 15–20 to the dissemination of infected planting
min) after all symptomatic tissues have been materials. It is the most important nematode
removed. However, since the latter measures species on banana in many areas in Central
are not totally effective, there is some risk and South America, as well as Southeast
when they are used in non-infested soil. Asia. In Africa, its more localized distribu-
Where sites are infested with the nema- tion suggests that it was introduced there
tode, fallowing for 12 months or rotation only recently.
with a non-host is preferred, but often not In contrast, P. goodeyi is only known on
desirable. In addition to taking land out of banana and occurs in the Canary Islands and
production this practice can be a challenge the cooler banana-growing regions of Africa.
since it is difficult to eliminate all suckers of In Africa, it is usually only found in small-
the previous crop. Flooding is also effective, holder production, which would explain
but requires level areas with access to large why it has not been distributed as widely as
quantities of water. Effective fumigants that P. coffeae and R. similis.
had been used to disinfect fields in the past These species can be misidentified as R.
generally are no longer used since they similis (Bridge et al., 1997). They are migra-
tory endoparasites, and both juvenile and Banana mild mosaic

adult stages are capable of invading roots.
Like R. similis, they can complete their Filamentous, virus-like particles have been
entire life cycle in roots. Control measures noted frequently in germplasm collections
are similar to those listed for R. similis, and field specimens (Rivera et al., 1992;
although rotation and fallowing are less Anonymous, 1993; Lockhart, 1994; Belalcázar
effective for P. coffeae due to its wide host et al., 1998; Caruana and Galzi, 1998). Recent
range. research indicates that a single virus, Banana
mild mosaic virus (BanMMV), is present in
most cases (Gambley and Thomas, 2001). All
Spiral nematode Musa genotypes appear to be susceptible.
The economic impact of mild mosaic is not
The spiral nematode, Helicotylenchus multi- known, but observations in Latin America
cinctus, occurs in most regions where banana indicate that banana and plantain yields may
is grown, but is most important in the sub- be affected (B.E.L. Lockhart, Minnesota,
tropics and at high elevations in the tropics 1998, personal communication).
(McSorley and Parrado, 1986). In subtropical
areas where R. similis is uncommon, H. multi-
Symptoms
cinctus often is the most important nematode
on this crop. It causes significant damage in Symptoms of infection are inconsistent and
Argentina, Cuba, Cyprus, Florida, Israel, in many cases may not develop. ‘Ducasse’
Lebanon and South Africa. (ABB, syn. ‘Pisang Awak’) has been observed
H. multicinctus causes lesions on root sur- with chlorotic mosaic and streak symptoms
faces and destruction of small feeder roots. in the field, but these symptoms usually dis-
The damage is superficial, and penetrates the appear as plants mature. Transitory chlorotic
root cortex only slightly and not the rhizome. leaf streaks were noted on some leaves of
However, root damage can be severe, result- ‘Daluyao’ (AAB, Plantain subgroup) under
ing in yield loss and lodging. glasshouse conditions, and ‘Pisang Seribu’
H. multicinctus is an endoparasite that can (AAB) displays silvery streaks on the leaf
complete its life cycle in the root cortex. Over lamina. Plants of ‘Gros Michel’ (AAA) from
40 plant species are reported to be hosts. Latin America have displayed large chlorotic
Nematode-free sites and planting material blotches on the leaves, stunting and delayed
are the best ways to combat this problem. bunch development (Jones, 2000).
Otherwise, the measures listed for R. similis Mixed infections of BanMMV and Banana
can be used. Due to its less invasive colo- streak virus (BSV) are common. In such cases,
nization, seedpieces can be disinfested by symptoms are reminiscent of those caused
removing all root tissue from rhizomes by BSV alone (Jones, 2000). In mixed infec-
(McSorley and Parrado, 1983). Treatment tions with Cucumber mosaic virus (CMV),
with hot water is also effective, and it need BanMMV seems to cause additional leaf
not be as severe as that used for R. similis necrosis (Caruana and Galzi, 1998).
(50–55°C for 7.5 minutes).
Causal agent
DISEASES OF BANANA THAT ARE BanMMV virions are flexuous filaments
CAUSED BY VIRUSES ~580 nm long and 14 nm wide (Jones, 2000).
The genome is single-stranded (ss) RNA of
Bunchy top is by far the most serious virus- ~7.4 kb, contains five open reading frames,
induced disease of banana worldwide (Dale, 3′- and 5′-untranslated regions and a poly
1987). However, other virus-induced dis- (A) tail. BanMMV is related to, but distinct
eases are also damaging and/or widespread. from, the Carlavirus, Foveavirus and
The most significant of these diseases are Potexvirus genera (Gambley and Thomas,
covered below alphabetically. 2001).
Polyclonal antisera that have been pre- as infectious chlorosis, heart rot, virus sheath
pared against isolates from ‘M’bouroukou’ rot, cucumber mosaic and banana mosaic
(AAB, Plantain subgroup), ‘Pisang Seribu’ (Magee, 1930; Wardlaw, 1961; Stover, 1972).
AAB (B.E.L. Lockhart, Minnesota, 2001, per-
sonal communication) and ‘Ducasse’ (C.F
Symptoms
Gambley and J.E. Thomas, unpublished)
work well in immunosorbent electron Symptoms are affected by environment and
microscopy (ISEM), but the ‘Pisang Seribu’ the strain of CMV. Although infected leaves
antiserum is best for enzyme-linked may be symptomless, they typically have
immunosorbent assay (ELISA). All isolates chlorotic stripes, stippling or line patterns, or
that have been tested with polyclonal anti- a more general mosaic (Plate 33) (Yot-Dauthy
bodies are serologically related. Monoclonal and Bové, 1966; Ploetz et al., 1994b). Fruit
antibodies (mAbs) have been prepared to an may be distorted and display chlorotic
isolate from ‘Cardaba’ ABB, and these have streaks or a mosaic. At temperatures below
been used in tissue blot and western blot 24°C, symptoms are often more severe and
assays (Caruana et al., 1995). A sensitive may include heart rot (Ploetz et al., 1994b).
triple antibody sandwich ELISA has been Severe strains of the virus can cause leaf dis-
developed which uses polyclonal coating tortion and necrosis. In the past, symptoms
antibodies and the mAbs (M.L. Iskra- were often confused with those caused by
Caruana, Montpellier, 1999, personal com- BSV (e.g. Wardlaw, 1961; Stover, 1972).
munication). BanMMV can also be detected
by reverse transcription (RT)–PCR in total
Causal agent
nucleic acid extracts from infected plants and
by immunocapture RT–PCR using crude sap Banana mosaic disease is caused by CMV
extracts (Gambley et al., 1999). (Yot-Dauthy and Bové, 1966), a member of
the genus Cucumovirus (Family Bromoviridae).
The virus has a tripartite ssRNA genome
Epidemiology
encapsidated in isometric virions 28–30 nm
Vegetative propagation through conven- in diameter (Francki et al., 1979; Palukaitis et
tional planting material and tissue culture is al., 1992). A satellite RNA is encapsidated
the only known means of transmission of with some isolates from Israel, and is respon-
BanMMV, although field transmission in sible for symptom attenuation (Gafny et al.,
mixed infections with the aphid-transmitted 1996).
CMV was suspected in Guadeloupe CMV isolates have been divided into sub-
(Caruana and Galzi, 1998). BanMMV has not groups I and II based on serology and
been transmitted mechanically to banana or nucleic acid hybridizations (Devergne and
herbaceous indicators, or with the banana Cardin, 1973; Piazolla et al., 1979; Owen et al.,
aphid, Pentalonia nigronervosa (Caruana et al, 1990; Palukaitis et al., 1992). Subgroup I pre-
1995). dominates in the tropics and subtropics
(Hasse et al., 1989; Ploetz et al., 1994b) and
includes most, but not all, isolates from
Management
banana (Hu et al., 1995; Singh et al., 1995;
The use of indexed, virus-free vegetative Gafny et al., 1996).
planting material is recommended. A number of methods are available for the
diagnosis of CMV in banana, including serol-
ogy, nucleic acid hybridization and PCR
Banana mosaic (Diekmann and Putter, 1996). Inconsistent
symptom expression and the similarity of
Banana mosaic was first described in New symptoms induced by other viruses, such as
South Wales, Australia, in 1930 (Magee, 1930, BSV and Banana bract mosaic virus (BBrMV),
1940b) and now occurs in most banana- limit the value of symptoms for diagnosis.
growing areas worldwide. It is also known Serological detection is reliable, and a
number of ELISA kits are available commer- ease in banana because these non-colonizing
cially. A range of polyclonal and monoclonal species can transmit the virus after feeding
antibodies detects a wide range of virus only for a few seconds. A combination of
strains, or differentiates subgroups I and II roguing and insecticides has been reported
(Hasse et al., 1989; Diekmann and Putter, to give good control in commercial planta-
1996). Sensitive nucleic acid-based methods, tions (Adam, 1962), but is probably not cost-
especially PCR, are being used increasingly effective (Jeger et al., 1995). Roguing alone
in banana (Hu et al., 1995; Singh et al., 1995; has given adequate control (Stover, 1972).
Sharman et al., 2000a). Pentalonia nigronervosa is not usually con-
sidered a significant vector of CMV.
However, large populations have been
Epidemiology
observed on shoot tips of Commelina diffusa
CMV infects at least 800 plant species. in West Africa, and may play a role in infec-
Resistance is not known to occur in Musa, tion of banana and subsequent within-crop
although Stover (1972) noted that M. spread (Jones, 2000).
balbisiana was free of symptoms in the field. As CMV is transmitted in vegetative
CMV is transmitted in a non-persistent propagules, including tissue-cultured
manner by at least 75 aphid species plantlets, it is important that planting mater-
(Palukaitis et al., 1992), and often is seed ial comes from virus-free sources. It has been
transmitted in other hosts. CMV may also be suggested that a severe strain of CMV in
seed transmitted in banana (Gold, 1972), so Morocco was imported in planting material
seedlings need to be tested if they come from (Bouhida and Lockhart, 1990). Mother plants
a plant whose virus status is unknown. should be free of symptoms and indexed to
Although CMV can be sap transmitted ensure freedom from CMV. The virus has
experimentally, this probably is not impor- been eliminated from banana by heat treat-
tant in the field. ment of rhizomes followed by apical meris-
Weeds or nearby crop plants are the pri- tem culture (Berg and Bustamante, 1974),
mary sources of inoculum, and spread from and through cryopreservation (Helliot et al.,
banana to banana appears to be less common 2002). However, it is generally more cost-
(Stover, 1972). Commelina is a common weed and time-effective to obtain virus-free
host in banana plantations, as are vegetable mother plants from another source. Tissue-
crops, such as cucurbits, tomatoes and pep- cultured plantlets should also be protected
pers, which often are intercropped with from infection in nurseries during the
bananas. acclimatization phase.
Management
Banana streak
Alternative hosts should be removed from
within and around banana plantings. Banana streak (mosïque à tirets) was first
Growing bananas next to non-hosts (e.g. described as distinct from ‘typical’ mosaic
rice) instead of susceptible vegetable crops caused by CMV in Côte d’Ivoire (Lassoudière,
reduced mosaic in Taiwan (Tsai et al., 1986). 1974, 1979). Illustrations of what appears to
Roguing infected banana plants in planta- be banana streak had been presented as
tions is advisable, as it eliminates these CMV-induced mosaic in earlier publications
plants as potential sources of infection. These (Wardlaw, 1961; Yot-Dauthy and Bové, 1966;
plants are also likely to have a poor yield Stover, 1972).
and to bear symptomatic fruit. Banana streak has a worldwide distribu-
Most aphid vectors do not colonize tion (Jones, 2000), although disease incidence
bananas, but high transient populations of varies greatly between districts and in differ-
inefficient species can still result in the trans- ent cultivars. ‘Mysore’ AAB, a popular
mission of CMV to banana. Insecticides are dessert banana from India, appears to be
unlikely to be effective in controlling the dis- universally infected with BSV (Ploetz et al.,
1994b). The economic impact of BSV ity (Lassoudière, 1974, 1979; Dahal et al.,
depends not only on its direct effect on fruit 2000; Daniells et al., 2001a). Yield depression
yield and quality, but also on the quarantine increases through successive cropping
restrictions imposed on many improved, but cycles, and is more apparent under subopti-
infected hybrids. mal growth conditions. Reported losses have
ranged from 6 to 45% (Lassoudière, 1979;
Daniells et al., 2001a).
Symptoms
Symptom expression is very variable, and
Causal agent
influenced by virus strain, host cultivar and
physiology, and the environment (Gauhl and The causal virus, BSV, was first identified in
Pasberg-Gauhl, 1994; Ploetz et al., 1994b; Morocco (Lockhart, 1986). BSV (genus
Dahal et al., 1998b; Daniells et al., 2001a). The Badnavirus) has bacilliform virions ~30 nm ×
most common symptoms are continuous or 130–150 nm. It has a double-stranded (ds)
discontinuous chlorotic streaks running par- DNA genome of ~7.4 kbp and replicates via
allel to the leaf veins, and range from promi- reverse transcription (Lockhart and
nent to very sparsely distributed (Plate 34). Olszewski, 1993). Isolates of BSV are highly
The streaks darken over time, and may heterogeneous, and induce a range of symp-
become brown or black (Plate 35). In some toms. They also differ serologically and
cases, spindle-shaped lesions or chlorotic genomically (Lockhart and Olszewski, 1993;
blotches occur (Jones, 2000). A range of other Geering et al., 2000). Banana can also be
symptoms are sometimes associated with the infected experimentally with a related bad-
disease, including splitting of the pseu- navirus, Sugarcane bacilliform virus (SCBV)
dostem, heart rot, leaf and pseudostem (Bouhida et al., 1993). Since some isolates of
necrosis, petiole and pseudostem streaks, SCBV and BSV have closely related
aberrant bunch emergence and altered leaf genomes, the distinction between these two
phyllotaxy (Lassoudière, 1979; Gauhl and species is blurred (Braithwaite et al., 1997;
Pasberg-Gauhl, 1994; Jones, 2000; Daniells et Geering and Thomas, 2002).
al., 2001a). Young, infected, suckers usually Sequences of BSV are integrated into the
display few, if any, symptoms (Lassoudière, genomes of Musa and Ensete (LaFleur et al.,
1979; Daniells et al., 2001a). 1996). These sequences are very variable, and
Symptom expression is sporadic over probably include many ‘dead’ and partial
time, and not all leaves on an infected plant inserts of a number of virus strains (LaFleur
may display symptoms. Similarly, not all et al., 1996; A.D.W. Geering, Brisbane, 2001,
infected plants in a stand will have symp- personal communication). At least one inte-
toms at the same time. The factors responsi- grated BSV sequence appears to give rise to a
ble for inconsistent symptom expression are circularized, transcriptionally active episo-
unclear. Lower temperatures, or possibly mal form of the virus after excision from the
temperature fluctuations, have been corre- Musa genome and two homologous recombi-
lated with symptom expression (Lockhart, nations (Harper et al., 1999b; Ndowora et al.,
1995; Dahal et al., 1998b, 2000). However, the 1999; Hull et al., 2000). This ‘active’ integrant
developmental stage of the plant may also be of strain BSV-OL is linked to the B genome of
important, as the proportion of plants with Musa (Geering et al., 2001). Hybridization
symptoms was shown to increase pro- and propagation by tissue culture are likely
gressively during each cropping cycle triggers for episomal expression of inte-
(Lassoudière, 1979; Daniells et al., 2001a). grants (Ndowora et al., 1999; Dallot et al.,
Daniells et al. (2001a) also noted greater 2001), and BSV-OL is a common contaminant
expression during rapid plant growth at in new hybrids that are produced by banana-
bunch initiation during warm periods. breeding programmes. Other strains of BSV
Streak can deform fruit and bunches, might also be integrated and give rise to epi-
lengthen the cropping cycle and reduce somal infections (A.D.W. Geering, Brisbane,
bunch size, and fruit number, size and qual- 2001, personal communication).
Epidemiology isolates and the presence of integrated BSV

sequences (Lockhart and Olszewski, 1993;
BSV is transmitted in a semi-persistent man-
Geering et al., 2000). False positives due to
ner by the mealybugs Planococcus citri,
integrated viral sequences can be avoided
Saccharicoccus sacchari and possibly other
with immunocapture PCR (Harper et al.,
species (Dahal et al., 1998a; Jones, 2000;
1999a). Both BSV strain-specific (Geering et
Kubiriba et al., 2001b). Field spread of BSV is
al., 2000) and degenerate (Lockhart and
slow and appears to be of limited signifi-
Olszewski, 1993; Ahlawat et al., 1996; N.E.
cance in most locations (Lockhart, 1995;
Olszewski and B.E.L. Lockhart, Minnesota,
Daniells et al., 2001a; Kubiriba et al., 2001a).
2000, personal communication) PCR primers
However, this may not be the case in some
are available.
commercial plantations of Cavendish culti-
vars in Ecuador, where BSV is a serious
problem (Jones, 2000).
Bract mosaic
The major means of spread is in vegeta-
tive planting material. The virus is neither
Symptoms of bract mosaic were first noted
mechanically transmissible nor soilborne.
on Mindanao in 1979 (Magnaye and Espino,
Although there is some evidence that BSV is
1990). The disease is widespread in the
seed transmitted (Daniells et al., 1995; Jones,
Philippines, and has also been recorded from
2000), this was before integration of BSV in
India and Sri Lanka (Rodoni et al., 1997;
the host genome was recognized. The nat-
Thomas et al., 1997). Although Banana bract
ural and experimental host range of BSV is
mosaic virus (BBrMV) has also been recorded
restricted to Musa and Ensete species, and a
in Thailand and Vietnam, symptoms there
wide range of Musa cultivars and genotypes
were more characteristic of CMV-induced
are susceptible (Jones, 2000).
mosaic. In Western Samoa, a plant doubly
infected by BBrMV and BSV showed symp-
toms of streak only (Rodoni et al., 1999).
Management
Limited data are available on the eco-
The use of virus-free planting material is cru- nomic impact of bract mosaic. In one study
cial since the virus is spread primarily by conducted in Mindanao, yield losses of up to
vegetative propagation. However, the selec- 40% were noted in ‘Cardaba’ ABB and
tion of suitable planting material is ham- ‘Lakatan’ AAA (Kenyon et al., 1996; Thomas
pered by the difficulties in visually and Magnaye, 1996).
diagnosing BSV infection and identifying
such a heterogeneous virus with diagnostic
Symptoms
assays. Visual inspections should be con-
ducted on all leaves and on a number of Mosaic patterns on bracts are diagnostic and
occasions during the cropping cycle. distinct from symptoms caused by all other
Fluctuations in virus titre and the serologi- known viruses of banana. Mosaic patterns,
cal heterogeneity of BSV combine to make stripes and spindle-shaped streaks may also
ELISA assays unreliable (Dahal et al., 1998a,b; be visible on the pseudostem when outer leaf
Daniells et al., 2001a). With the currently avail- sheaths are removed and on the petioles and
able antisera, some BSV isolates are also midribs. The colour of symptoms depends on
poorly detected by ELISA (Ndowora, 1998). host pigmentation, and can vary from
Immunosorbent electron microscopy using chlorotic or yellow, through red, brown and
partially purified virus preparations (Bouhida even black. Leaf symptoms, consisting of spin-
et al., 1993) and broad-spectrum antiserum dle-shaped lesions and streaks running paral-
(Ndowora, 1998) seems to detect all isolates lel to the veins, are not always evident, but can
and is generally more sensitive than ELISA occur on young plants that have been infected
(Lockhart, 1995; Thottappilly et al., 1998). recently. Suckering is also suppressed, and
Nucleic acid-based assays are compro- suckers that do emerge are distorted and
mised by the genomic heterogeneity of BSV deeply pigmented (Anonymous, 1995).
In the Philippines, chlorotic streaks may 1999) and/or monoclonal (J.E. Thomas,
be present on peduncles, and a high disease Brisbane, 1996, unpublished) antibodies. It
incidence is associated with increased levels can also be detected by PCR in total nucleic
of malformed fruit in commercial planta- acid extracts from infected plants, using
tions. In India, petioles and peduncles of either virus-specific or degenerate potyvirus
‘Nendran’ AAB become brittle and fruit is group primers (Bateson and Dale, 1995;
only rarely carried to maturity. If fruit does Thomas et al., 1997), and by immunocapture
mature, it is undersized. Mosaics can be seen PCR using crude sap extracts (Sharman et al.,
on the fruit of other cultivars (Jones, 2000). 2000b). Virion concentration in infected
Initial symptoms in aphid-inoculated plants is relatively low, and the virions
plants include broad, chlorotic patches along usually are not detected readily by direct
the major leaf veins, surrounded by a rusty electron microscopy of sap.
red border and green or reddish streaks or
spindle-shaped lesions on the petioles. Leaf
Epidemiology
symptoms, consisting of spindle-shaped
lesions and streaks running parallel to the BBrMV is transmitted by at least three
veins, are not always evident, but can occur species of aphids: Aphis gossypii,
on young plants that have been infected Rhopalosiphum maidis and Pentalonia nigroner-
recently. vosa (Magnaye and Espino, 1990; Muñez,
1992; Diekmann and Putter, 1996). P.
nigronervosa transmitted BBrMV after an
Causal agent
acquisition access period of 1 min, indicating
BBrMV has flexuous virions, 750 × 11 nm that transmission is of the non-persistent
(Muñez, 1992; Bateson and Dale, 1995; type (Muñez, 1992). Efficiency of transmis-
Thomas et al., 1997). Virions contain a major sion with the latter species was <10%
coat protein of ~39 kDa, a buoyant density in (Caruana and Galzi, 1998).
caesium chloride of 1.29–1.31 g cm−3 and an Attempts to transmit BBrMV by sap inoc-
A260/280 of 1.17 (Thomas et al., 1997). ulation to herbaceous indicator plants so far
Nucleotide sequence analysis indicates that have been unsuccessful (Magnaye and
BBrMV is a distinct potyvirus (Bateson and Espino, 1990; Muñez, 1992; Diekmann and
Dale, 1995; Rodoni et al., 1997, 1999; Thomas Putter, 1996; S. Cohen, Montpellier, 1996,
et al., 1997). All isolates of BBrMV tested are personal communication). However, occa-
closely related serologically (Thomas et al., sional sap transmission from banana to
1997; Rodoni et al., 1999). Identity at the banana has been reported (L.V. Magnaye and
nucleotide level within the coat protein gene L. Herradura, Davao, 1998, personal com-
was >87% for isolates from the Philippines, munication). The virus can be transmitted
India, Western Samoa and Vietnam (Thomas through vegetative planting material in-
et al., 1997; Rodoni et al., 1999). cluding suckers, bits, rhizomes and micro-
Although bract mosaic-affected banana propagated plantlets.
plants from India and the Philippines The natural and experimental host range of
frequently also contain BanMMV (M.L. BBrMV appears to be restricted to Musa. The
Iskra-Caruana and J.E. Thomas, 1998, virus has been detected in a wide range of nat-
Montpellier and Brisbane, personal com- urally infected banana cultivars and geno-
munication), BBrMV alone appears to be the types, and no resistance to the virus is known.
causal of bract mosaic. BBrMV virions have
been aphid transmitted to healthy banana
Management
test plants that subsequently developed
bract mosaic (Caruana and Galzi, 1998). The use of indexed, virus-free planting mate-
Both serological and nucleic acid-based rial is the best means of control. Roguing and
assays are now available for BBrMV. The sanitation programmes have been intro-
virus can be detected by ELISA using poly- duced into commercial production areas in
clonal (Thomas et al., 1997; Rodoni et al., the Philippines (Magnaye, 1994).
Bunchy top minor veins on the lower portion of the lam-

ina. The streaks form ‘hooks’ as they enter
It is probable that bunchy top originated in the midrib and are best seen from the under-
the centre of origin of the genus Musa in the side of the leaf in transmitted light. The ‘dot-
south and southeast Asian–Australasian dash’ symptoms can sometimes also be seen
region. Banana bunchy top was first reported on the petiole (Plate 37). Successive leaves
in Fiji in 1889, but was almost certainly pre- become shorter and narrower and often have
sent as early as 1879 (Darnell-Smith, 1924; chlorotic, upturned margins. The leaves
Magee, 1953). Interest in the disease arose become brittle and erect, giving the plant a
due to its effects on the Cavendish-based bunched appearance.
export industry that began there in 1877. Its Once infected, plants rarely produce a
peak production of 788,000 bunches in 1892 bunch and do not fruit in subsequent years.
declined to 147,000 bunches by 1895, mainly When infected late in the growing cycle, they
because of bunchy top. Other early records may fruit, but the bunch stalk and fruit are
include Egypt in 1901 (Fahmy, 1924, in small and distorted. On plants infected very
Magee, 1927) and Australia and Sri Lanka in late, only a few dark green streaks may
1913 (Magee, 1953). appear on the tips of the flower bracts
Due to rapid expansion of the banana (Thomas et al., 1994).
industry in Australia and use of infected Mild disease symptoms are expressed in
planting material, bunchy top extended some banana cultivars and Musa species. The
along a 300 km range from central New dark green leaf and petiole streaks, so diag-
South Wales to southern Queensland nostic in most cultivars in the Cavendish
between 1913 and 1927 (Magee, 1927). subgroup, can be rare or absent in other cul-
Production in the industry peaked in 1922, tivars (Magee, 1953). Severely affected plants
but 3 years later had collapsed, with produc- of ‘Veimama’ (AAA, Cavendish subgroup)
tion in the most affected areas reduced by have been observed to recover to later pro-
90–95% (Magee, 1927). Recently, severe out- duce few if any symptoms (Magee, 1948). In
breaks have occurred in Pakistan (Khalid addition, symptomless strains and mild
and Soomro, 1993) and Hawaii (Ferreira et strains that produce only limited vein clear-
al., 1989). ing and dark green flecks have been reported
The countries in which bunchy top has from Taiwan (Su et al., 1993).
been authenticated are listed in Table 4.4.
Reports from East Malaysia (Sabah), West
Causal agent
Malaysia and Papua New Guinea (Magee,
1953; Wardlaw, 1961) need verification. In only 3 years, Magee (1927) determined
Significantly, Hawaii is the only location in that the causal agent was a virus transmitted
the western hemisphere where the disease is by Pentalonia nigronervosa and in infected
present. planting material. He also proposed manage-
ment strategies that still form the basis of
Australia’s control programmes today.
Symptoms
Banana bunchy top virus (BBTV) is pre-
Symptoms of bunchy top are distinctive sumed to be the causal agent of bunchy top,
(Magee, 1927). Plants can become infected at even though the disease has not been pro-
any stage of growth. The first leaf to emerge duced via inoculation with purified virions
from infected suckers can develop severe or cloned genomic components. BBTV
symptoms. The leaves are rosetted and small virions are associated intimately with the
with very chlorotic margins that tend to turn disease (Harding et al., 1991; Thomas and
necrotic (Plate 36). Dark green streaks are Dietzgen, 1991) and are always detected in
usually evident in the leaves. In contrast, symptomatic plants (Dietzgen and Thomas,
symptoms usually appear in the second leaf 1991; Thomas, 1991; Thomas and Dietzgen,
to emerge after aphid inoculation. They con- 1991; Karan et al., 1994). Virions are ico-
sist of a few dark green streaks or dots on the sahedra, ~18–20 nm in diameter, have a coat
Table 4.4. Countries in which banana bunchy top disease has been recorded.a
Region/country Year first recorded BBTV detected
Pacific
Australia 1927 +
Fiji 1927 +
Guam 1982
Hawaii (USA) 1991 +
Kiribati (formerly Gilbert Islands) 1980
New Caledonia 2001 +
Samoa (American) 1967
Samoa (Western) 1967 +
Tonga 1967 +
Tuvalu (formerly Ellice Islands) 1926
Wallis Island 1933
Asia
China 1996 +
India 1953 +
Indonesia 1978 +
Japan (Bonin Islands) 1926
Japan (Okinawa) 1993 +
Malaysia (Sarawak) 1995 +
Pakistan 1993 +
Philippines 1961 +
Sri Lanka 1921 +
Taiwan 1961 +
Vietnam 1969 +
Africa
Burundi 1988 +
Central African Republic 1996
Congo 1961 +
Democratic Republic of Congo (formerly Zaire) 1982
Egypt 1927 +
Gabon 1982 +
Malawi 1997 +
Rwanda 1988
a References for specific records are found in Thomas and Iskra-Caruana (2000).
protein of Mr ~20,000 Da, a sedimentation nucleotide sequences of components 1, 3 and

coefficient of ~46S and a buoyant density of 6 (Karan et al., 1994, 1997; Wanitchakorn et
1.29–1.30 g cm⫺3 in caesium sulphate (Wu al., 2000). The ‘South Pacific’ group com-
and Su, 1990c; Dietzgen and Thomas, 1991; prises isolates from Australia, Fiji, Western
Harding et al., 1991; Thomas and Dietzgen, Samoa, Tonga, Burundi, Egypt and India,
1991). Purified preparations have an A260/280 whilst the ‘Asian’ group comprises isolates
of 1.33 (Thomas and Dietzgen, 1991). The from the Philippines, Taiwan and Vietnam.
virus possesses a multicomponent genome, Polyclonal and monoclonal antibodies are
consisting of at least six circular ssDNA com- now used routinely in ELISAs to detect
ponents each ~1000–1100 nucleotides long BBTV in field and tissue culture plants, as
(Burns et al., 1995; Xie and Hu, 1995; Karan et well as in single viruliferous aphids (Wu and
al., 1997). Su, 1990b; Dietzgen and Thomas, 1991;
Although biologically similar, isolates Thomas and Dietzgen, 1991; Thomas et al.,
have been divided into two groups based on 1995; Geering and Thomas, 1996). All isolates
tested from Africa, Australia, Asia and the multiplication in or transmission of BBTV to
Pacific region are related serologically the parthogenetic offspring of the aphid
(Thomas, 1991). BBTV is also detected in vector (Magee, 1940a; Hafner et al., 1995; Hu
plant tissue and viruliferous aphids with et al., 1996). Reported transmission efficien-
DNA and RNA probes, labelled either non- cies for individual aphids range from 46 to
radioactively or with 32P (Hafner et al., 1995; 67% (Magee, 1927; Wu and Su, 1990a; Hu et
Xie and Hu, 1995), and by PCR (Xie and Hu, al., 1996), and the virus is acquired more
1995). Substances in banana sap that inhibit efficiently by nymphs than adults (Magee,
PCR can be circumvented by immunocap- 1940a).
ture PCR (Sharman et al., 2000). P. nigronervosa is found worldwide on
banana, M. textilis, and other species in the
Musaceae and related families (Wardlaw,
Epidemiology
1961; R.N. Allen, Brisbane, 1996, personal
BBTV is transmitted by P. nigronervosa and in communication). Some host preference is
vegetative planting material (conventional displayed and it is transferred with difficulty
and micropropagated), but not by mechanical between some host species.
inoculation (Magee, 1927; Drew et al., 1989; Spread of the virus over long distances is
Ramos and Zamora, 1990; Wu and Su, 1991). by infected planting material, and it is by
Magee (1927) showed that banana bunchy top this means that new plantings in isolated
was systemic and concluded that the virus areas usually become infected. Dissemination
was restricted to the phloem tissue (Magee, over short distances from these foci is by the
1939). Following aphid inoculation, symp- banana aphid. Allen (1978b, 1987) showed
toms generally do not appear until two or that in Australia the average distance of sec-
more leaves are produced (Magee, 1927). This ondary spread of the disease by aphids was
period can vary between 19 days in summer only 15.5–17.2 m. Nearly two-thirds of the
and 125 days in winter (Allen, 1978a). The new infections were within 20 m of the
virus can only be recovered by aphids from nearest infected plant, and 99% were within
the first or subsequent symptomatic leaves 86 m. Allen and Barnier (1977) showed that if
(Magee, 1940a). Suckers produced in infected a new plantation was adjacent to a diseased
mats generally develop symptoms before plantation, there was an 88% probability that
reaching maturity (Magee, 1927). the disease would move into the new plan-
Using RNA probes and PCR, Hafner et al. tation within 12 months. This was reduced to
(1995) demonstrated that BBTV replicates for 27% if the plantations were separated by
a short period at the site of aphid inocula- 50–1000 m, and to <5% if they were 1000 m
tion, then moves down the pseudostem to apart. The average interval between infection
the basal meristem, and ultimately to the rhi- of a plant and spread of the disease from it
zome, roots and newly formed leaves. Trace by aphids to other plants (the disease latent
levels of virus were detected eventually by period) equalled the time needed for 3.7
PCR in leaves formed prior to inoculation, leaves to emerge. The maximum rate of leaf
but replication was not demonstrated, con- emergence occurred during the summer
sistent with the inability to transmit the virus (Allen, 1987).
by aphids from such leaves (Magee, 1940a). BBTV infects a wide range of cultivars in
BBTV is transmitted by P. nigronervosa in a the Eumusa and Australimusa series of edible
circulative, non-propagative manner (Magee, banana, Ensete ventricosum, and the following
1927). The transmission parameters reported taxa: M. balbisiana (Magee, 1948; Espino et al.,
from Hawaii (Hu et al., 1996) and Australia 1993), M. acuminata ssp. banksii and M. textilis
(Magee, 1927) are, respectively: minimum (Magee, 1927), M. velutina (Thomas and
acquisition access period of 4 and 17 h; Dietzgen, 1991), M. coccinea, M. jackeyi, M.
minimum inoculation access period of ornata and M. acuminata ssp. zebrina (A.D.W.
15 min and of 30 min to 2 h; and retention of Geering and J.E. Thomas, Brisbane, 1998,
infectivity after removal from virus source of personal communication). Although hosts
13 and 20 days. No evidence was found for outside the Musaceae have been reported,
these results have not been corroborated (for

a summary, see Jones, 2000).
Management
Although there are no confirmed reports of
immunity to bunchy top, differences in sus-
ceptibility between cultivars have been
noted (Magee, 1948; Jose, 1981; Muharam,
1984; Espino et al., 1993). All AA and AAA
cultivars evaluated by Espino et al. (1993)
were highly susceptible. However, mild or
no symptoms developed on some cultivars
containing the B genome including,
‘Bungaoisan’ AAB (plantain subgroup) and
‘Abuhon’ (ABB). Although cultivars in the
Cavendish subgroup generally are highly
susceptible, not all cultivars with an AAA
genome are so susceptible. For example, the
concentration of BBTV virions and the pro-
portion of plants infected by aphid inocula-
tion is higher in the Cavendish clone
‘Williams’ than in ‘Gros Michel’. Symptoms
are also slower to develop and less severe on
‘Gros Michel’ (A.D.W. Geering and
J.E. Thomas, Brisbane, 1997, personal com- Fig. 4.30. Signpost at the entry to a banana
munication). plantation in Queensland, Australia. Strict
Magee (1927) proposed a range of mea- quarantine measures that were enacted to combat
sures for the control of bunchy top. They banana bunchy top in Australia in the late 1920s
involved two major components, exclusion were responsible for rejuvenating the banana
of the disease from non- or slightly affected industry in this country (photo: R.C. Ploetz, UF).
areas, and eradication of infected plants. In
Australia, the following control measures contiguous plants in a mat and preventing
were legislated (Magee, 1936) and remain in regrowth (Beaver, 1982). In total, these
force to this day: measures enabled the complete rehabilita-
tion of the Australian banana industry.
● registration of all banana plantations;
Attempts to control bunchy top by control-
● establishment of quarantine zones (Fig.
ling the aphid vector have met with limited
4.30);
success.
● restrictions on the movement and use of
planting material;
● regular inspections of all banana planta-
Acknowledgements
tions for bunchy top;
● ongoing education and extension pro-
The authors thank David Jones for reviewing
grammes for growers; and
the chapter, and Anne Desjardins for infor-
● prompt destruction of all infected plants.
mation on mycotoxological species of
The last of these measures is critical and Fusarium. R. Harry Stover is thanked for use
involves first killing aphids on the plant with of his contributions to our understanding of
kerosene or insecticide, and then killing all banana diseases during the last 50 years.

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4 Diseases of Banana and Plantain

Randy C. Ploetz1, John E. Thomas2 and Walter R. Slabaugh3

Introduction diploid, triploid or tetraploid hybrids among

Signiﬁcance as Agricultural Commodity

Banana is now grown in almost all areas

Alligator skin Light abrasions on fruit peel caused by leaves or bracts

Table 4.2. Continued.

Verticillium tip rot Verticillium theobromae

Rhizome rot Vascular Wilts

This is the most important of the rhizome Blood disease

Panama Yellow Black

1994a) may be in error (Kangire and Rutherford, 2001).

control measures for this disease usually are

Eumusae leaf spot

This disease is found in Malaysia, Mauritius,

CAUSAL AGENT The causal fungus is M. Freckle

Although control measures usually are Disease development is greatest under

This disease has a worldwide distribution, Phaeoseptoria leaf spot

circular blotches, ≤4 cm in diameter, which CAUSAL AGENT There is some controversy

SYMPTOMS Pale green ﬂecks, <1 mm long,

CAUSAL AGENT Yellow Sigatoka is caused

Yellow Sigatoka EPIDEMIOLOGY Both conidia and ascospores

Botryodiplodia ﬁnger rot

This postharvest decay is common when

addition, some of the causal fungi have been

SYMPTOMS Crown rot is ﬁrst observed on

SYMPTOMS Small, reddish sunken spots

EPIDEMIOLOGY Pitting disease is most

Panama disease (Fusarium wilt) SYMPTOMS The ﬁrst internal symptom, a

cause vascular wilts of ﬂowering plants. It or plantain production areas in Western

Causal agent are either no longer registered or are too

tory endoparasites, and both juvenile and Banana mild mosaic

Epidemiology isolates and the presence of integrated BSV

Bunchy top minor veins on the lower portion of the lam-

Region/country Year ﬁrst recorded BBTV detected

protein of Mr ~20,000 Da, a sedimentation nucleotide sequences of components 1, 3 and

these results have not been corroborated (for

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