600 Part III Diseases Due to Microbial Agents

Disseminated Candidiasis ICD-9: 112.5 ° ICD-10: B37 ◧ ○

■ Etiology. C. albicans, C. tropicalis, and other non- ■ Pathogenesis. Candida enters the blood stream
albicans species. having colonized venous access catheters or
■ Incidence. Fifth most common cause of nosocomial penetrated the intestinal mucosa. Candidemia
bloodstream infections in the United States. seeds the skin and internal organs, i.e.,
hepatosplenic candidiasis.
■ Risk Factors. Neutropenia. Venous access
catheters. Hospitalization.

Clinical Manifestation Course

Cutaneous Lesions. Small disseminated ery- Candidemia has high associated morbidity and
thematous cutaneous papules (Fig. 26-14). mortality.
Lesions may occur acutely or chronically.
Systemic Dissemination. Eye with retinal Treatment
changes. Liver, spleen, CNS
Fluconazole in nonneutropenic patients;
Differential Diagnosis triazoles echinocandins, caspofungin, micafun-
gin, anidulafungin, voriconazole and posacon-
Malassezia folliculitis, which occurs on the azole, as well as lipid formulations of ampho-
trunk of healthy individuals. tericin B.
Diagnosis
Lesional biopsy specimen: Candida yeast forms
are visualized in the dermis; Candida species
isolated on culture.

Figure 26-14. Invasive candidiasis with candi-

demia Multiple, erythematous papules on the hand of a
febrile patient with granulocytopenia associated with treat-
ment of acute myelogenous leukemia. The usual source of
the infection is the gastrointestinal tract. C. tropicalis was
isolated on blood culture; candidal forms were seen on le-
sional skin biopsy.
Section 26 Fungal Infections of the Skin, Hair, and Nails 601

Tinea Versicolor ICD-9: 111.0 ° ICD-10: B36.0 ●

■ Etiology. Associated with the superficial ■ Predisposing Factors. Sweating. Warm season
overgrowth of the mycelial form of Malassezia or climates; tropical climate. Hyperhidrosis;
furfur. Lipophilic yeast that normally resides in the aerobic exercise. Oily skin. Temperate zones:
keratin of skin (Fig. 26-15) and hair follicles of more common in summertime; 2% prevalence in
individuals at puberty and beyond. An opportunistic temperate climates; 20% in tropics. Application
organism, causing tinea or pityriasis versicolor (TV) of lipids such as cocoa butter predisposes young
and Malassezia folliculitis; it is implicated in the children.
pathogenesis of seborrheic dermatitis. Malassezia ■ Pathogenesis. Malassezia changes from
infections are not contagious; overgrowth of blastospore form to mycelial form under the
resident cutaneous flora (cutaneous microbiome) influence of predisposing factors. Dicarboxylic acid
occurs under certain favorable conditions. formed by enzymatic oxidation of fatty acids in
■ Clinical Findings. Chronic. Well-demarcated skin surface lipids inhibits tyrosinase in epidermal
scaling patches. Variable pigmentation: hypo- melanocytes and lead to hypomelanosis; the
and hyperpigmented; pink. Most commonly on enzyme is present in M. furfur.
the trunk.
■ Demography. Young adults. Less common when
sebum production is reduced or absent; tapers off
during fifth and sixth decades.

Clinical Manifestation Macules, sharply marginated (Figs. 26-16

to 26-19) round or oval in shape, varying in
Usually asymptomatic. Cosmetic concerns size. Fine scaling is best appreciated by gently
about dyspigmentation. Lesions present for abrading lesions. Treated or resolved lesions
months or years. lack scale. Some patients have findings of Mal-
assezia folliculitis and seborrheic dermatitis.

Figure 26-15. Malassezia furfur: KOH preparation Round yeast and elongated pseudohyphal forms, so-called
“spaghetti and meatballs.”
602 Part III Diseases Due to Microbial Agents

Figure 26-16. Pityriasis versicolor A 43-year-old white female with orange-tan lesions of
the lateral neck. Sharply marginated scaling macules.

Color. In nontanned skin, lesions are light brown Differential Diagnosis

(Fig. 26-18) or pink. On tanned skin, hypopig-
mented (Fig. 26-19). In brown- or black-skinned Hypopigmented Macules. Vitiligo, pityriasis alba,
persons, dark brown macules (Figs. 26-17 and postinflammatory hypopigmentation.
26-20). Brown of varying intensities and hues Scaling Lesions. Tinea corporis, seborrheic
(Fig. 26-18). In time, individual lesions may dermatitis, cutaneous T cell lymphoma.
enlarge and merge, forming extensive geo-
graphic areas.
Distribution. Upper trunk, upper arms, neck,
Laboratory Examinations
abdomen, axillae, groins, thighs, genitalia. Direct Microscopic Examination of Scales Pre-
Facial, neck, or scalp lesions occur in persons pared with KOH. Filamentous hyphae and glo-
applying creams or ointments or topical gluco- bose yeast forms, termed spaghetti and meatballs
corticoid preparations. are seen (Fig. 26-15).
Section 26 Fungal Infections of the Skin, Hair, and Nails 603

Figure 26-17. Pityriasis versicolor: neck

A 23-year-old obese black female with discolor-
ation of the neck for 1 year. Sharply marginated
brown scaling macules on the left side of the
neck. The velvety texture and hyperpigmenta-
tion of the skin of the neck is acanthosis nigri-
cans associated with obesity.

Figure 26-18. Pityriasis versicolor: chest

and arm A 36-year-old male with pigmented
patches on chest and arms for several years.
Multiple pink, well-demarcated scaling macules
becoming confluent on the neck, chest, flank,
and arm.
604 Part III Diseases Due to Microbial Agents

Figure 26-19. Pityriasis versicolor: back Multiple, small-to-medium-sized, well-

demarcated hypopigmented macules on the back of a tanned individual with white skin.

Figure 26-20. Pityriasis versicolor: face A 18-year-old black female hypopigmented

scaling macule on chin. She had been applying cocoa butter to face since childhood.
Section 26 Fungal Infections of the Skin, Hair, and Nails 605

Wood’s Lamp. Blue-green fluorescence of for months after infection has been eradi-
scales; may be negative in individuals who cated.
have showered recently because the fluores-
cent chemical is water soluble. Vitiligo appears
as depigmented, white, and has no scale. Treatment
Dermatopathology. Budding yeast and hyphal
forms in the most superficial layers of the stra- Topitcal agents. Selenium sulfide (2.5%) lotion
tum corneum, seen best with periodic acid– or shampoo. Ketoconazole shampoo. Azole
Schiff (PAS) stain. Variable hyperkeratosis, creams (ketoconazole, econazole, micron-
psoriasiform hyperplasia, chronic inflamma- azole, clotrimazole). Terbinafine 1% solution.
tion with blood vessel dilatation. Systemic therapy Ketoconazole 400 mg stat, 1
hour before exercise. Fluconazole 400 mg stat.
Diagnosis Itraconazole 400 mg stat (drugs not approved for
use in TV in the United States).
Clinical findings confirmed by positive KOH Secondary prophylaxis. Topical agents weekly
preparation findings. or systemic agents monthly.
Malassezia Folliculitis. See “Infectious Follicu-
Course litis” Section 31.
Infection persists for years if predisposing Seborrheic Dermatitis. See “Seborrheic Derma-
conditions persist. Dyspigmentation persists titis” Section 2.

Trichosporon Infections ● ➔ ◐
■ Etiology. Trichosporon species of yeasts. Soil ■ Treatment. Topical or systemic azoles.
inhabitants. Microbiome of skin, respiratory and GI
tracts.

Clinical Manifestation t
Black piedra. Darkly pigmented, firmly

attached nodules (up to a few millimeters)
Piedra: Asymptomatic superficial fungal bio- on the hair shaft; weakens hair shaft with
film/colonization on hair shaft. Incidence high hair breakage. Scalp hair.
in tropical regions with high temperature and
humidity. Disseminated Trichosporonosis. Emerging oppor-
tunistic infection. Associated with neutropenia.
t
White piedra. White to beige nodules on hair Dissemination occurs to skin (erythematous or
shaft; soft; easily removed. Pubic, axillary, purpuric tender papules), lungs, kidneys, and
beard, and eyebrow/eyelash hair. spleen. Similar to disseminated candidiasis.

Tinea Nigra ICD-10: B36.1 ◧ ●

■ Superficial fungal colonization of the stratum ■ Clinical Manifestation. Brown to black macule(s)
corneum with well-defined borders (Fig. 26-21) that
■ Etiology. Hortaea werneckii, a dematiaceous or resemble silver nitrate stains. Distribution: Palm:
pigmented fungus. tinea nigra palmaris. Sole: tinea nigra plantaris
■ Epidemiology. More common in tropical climates. ■ Diagnosis. Direct microscopy, visualizing
Transmitted by direct inoculation onto the skin abundant branching septate hyphae.
from contact with decaying vegetation, wood, or ■ Management. Topical azole or alcohol gel
soil seems to be the mode of acquisition. sanitizer.
606 Part III Diseases Due to Microbial Agents

Figure 26-21. Tinea nigra Uniformly tan macule on the plantar foot, present for several years. KOH preparation
showed hyphae.

Dermatophytoses ICD-9: 110 ° ICD-10: B35.0-B36 ◐

■ Dermatophytes are a unique group of fungi ■ The term tinea is best used for dermatophytoses
capable of infecting nonviable keratinized and is modified according to the anatomic site of
cutaneous structures including stratum corneum, infection, e.g., tinea pedis.
nails, and hair. Arthrospores can survive in human ■ “Tinea” versicolor is referred to as pityriasis
scales for 12 months. Dermatophytosis denotes an versicolor except in the United States; it is not a
infection caused by dermatophytes. dermatophytosis but rather an infection caused by
■ Clinical Infection by Structure Involved. the yeast Malassezia.
Epidermal dermatophytosis. Dermatophytosis of ■ Tinea nigra is caused by a pigmented or
hair and hair follicles. Onychomycosis or tinea dematiaceous fungus, not a dermatophyte.
unguium: dermatophytosis of the nail apparatus.
■ Pathogenesis of dermatophytosis leading to
different clinical manifestations is schematically
depicted in Figs. 26-22 and 26-23.
Section 26 Fungal Infections of the Skin, Hair, and Nails 607

Figure 26-22. Epidermal dermatophyte infections

Dermatophytes (red dots and lines) within the stratum
corneum disrupt the horny layer and thus lead to scaling;
also elicit an inflammatory response (black dots symbol-
ize inflammatory cells), which may then manifest as ery-
thema, papulation, and vesiculation.

Figure 26-23. Hair follicle dermatophyte infec-

tions Hair shaft is involved (red dots) resulting in the de-
struction and breaking off of the hair. If the dermatophyte
infection extends farther down into the hair follicle, it will
elicit a deeper inflammatory response (black dots) and
this manifest as deeper inflammatory nodules, follicular
pustulation, and abscess formation.
TABLE 26-1 CLASSIFICATION OF TINEA PEDIS
Type Clinical Features Etiology

Interdigital (acute and Most common type; frequently overlooked T. rubrum most common cause of
chronic) two patterns: dry and moist with chronic tinea pedis; T. mentagrophytes
maceration causes more inflammatory lesions
Dry Scaling of webspace, may be erosive T. rubrum
Moist (macerated) Hyperkeratosis of webspace with T. mentagrophytes
maceration of stratum corneum
Moccasin (chronic Keratoderma Most often caused by T. rubrum,
hyperkeratotic or especially in atopic individuals; also
dry) Epidermophyton floccosum
Inflammatory or Blisters in nonoccluded skin Least common type; usually caused by
bullous (vesicular) T. mentagrophytes var. mentagrophytes
(granular). Resembles an allergic
contact dermatitis
Ulcerative An extension of interdigital type into T. rubrum, E. floccosum,
dermis due to maceration and T. mentagrophytes, C. albicans
secondary (bacterial) infection
Dermatophytid Presents as a vesicular eruption of the T. mentagrophytes, T. rubrum
fingers and/or palmar aspects of the hands
secondary to inflammatory tinea pedis. A
combined clinical presentation also occurs.
Candida and bacteria (S. aureus, GAS,
P. aeruginosa) may cause superinfection
608 Part III Diseases Due to Microbial Agents

Epidemiology and Etiology Predisposing Factors. Atopic diathesis: Cell-me-

diated immune deficiency for T. rubrum. Topical
Etiology. Three genera of dermatophytes (“skin immunosuppression by application of glucocor-
plants”): Trichophyton, Microsporum, Epidermoph- ticoids: tinea incognito. Systemic immunocom-
yton. More than 40 species are currently rec- promised: Patients have a higher incidence and
ognized; approximately 10 spp. are common more intractable dermatophytoses; follicular
causes of human infection. abscesses and granulomas may occur (Majoc-
t
Trichophyton rubrum is the most common chi granuloma).
cause of epidermal dermatophytosis and
onychomycosis in industrialized nations. Classification
Currently, 70% of the U.S. population expe-
rience at least one episode of T. rubrum infec- In vivo, dermatophytes grow only on or within
tion (usually tinea pedis). Soldiers wearing keratinized structures and, as such, involve the
occlusive boots in tropical climates devel- following:
oped “jungle rot”—extensive tinea pedis t
&QJEFSNBM
EFSNBUPQIZUPTJT
5JOFB
GBDJBMJT

with secondary bacterial infection. In U.S. tinea corporis, tinea cruris, tinea manus,
adults, T. rubrum is the most common cause tinea pedis.
of dermatophytic folliculitis. t
%FSNBUPQIZUPTFT
PG
OBJM
BQQBSBUVT
5JOFB

t
5JOFB
DBQJUJT
&UJPMPHZ
JO
DIJMESFO
WBSJFT
HFP- unguium (toenails, fingernails). Onychomy-
graphically. Trichophyton tonsurans: Most com- cosis (more inclusive term, including nail
mon cause in North America and Europe. infections caused by dermatophytes, yeasts,
Previously, M. audouinii, T. violaceum: Europe, and molds).
Asia, and Africa. t
%FSNBUPQIZUPTFT
PG
IBJS
BOE
IBJS
GPMMJDMF

Age of Onset. Children have scalp infections Dermatophytic folliculitis, Majocchi granu-
(Trichophyton, Microsporum). Young and older loma, tinea capitis, tinea barbae.
adults have intertriginous infections. The inci-
dence of onychomycosis is correlated directly Pathogenesis
with age; in the United States, up to 50% of in-
dividuals aged 75 years have onychomycosis. Dermatophytes synthesize keratinases that
Demography. Adult blacks may have a lower digest keratin and sustain existence of fungi in
incidence of dermatophytosis. Tinea capitis is keratinized structures. Cell-mediated immunity
more common in black children. and antimicrobial activity of polymorphonu-
Geography. Some species have a worldwide clear leukocytes restrict dermatophyte patho-
distribution; others are restricted to particular genicity. Host factors that facilitate dermatophyte
continents or regions. However, T. concentricum, infections: atopy, topical and systemic glucocorti-
the cause of tinea imbricata, is endemic to the coids, ichthyosis, collagen vascular disease. Local
South Pacific and parts of South America. T. factors favoring dermatophyte infection: sweating,
rubrum was endemic to Southeast Asia, West- occlusion, occupational exposure, geographic
ern Africa, and Australia but now occurs com- location, high humidity (tropical or semitropi-
monly in North America and Europe. cal climates). The clinical presentation of der-
Transmission. Dermatophyte infections can be matophytoses depends on several factors: site
acquired from three sources: of infection, immunologic response of the host,
and species of fungus. Dermatophytes (e.g.,
t
.PTU
DPNNPOMZ
GSPN
BOPUIFS
QFSTPO
<VTV- T. rubrum) that initiate little inflammatory
ally by fomites, less so by direct skin-to-skin response are better able to establish chronic
contact (tinea gladiatorum)] infection. Organisms such as Microsporum canis
t
'SPN
BOJNBMT
TVDI
BT
QVQQJFT
PS
LJUUFOT cause an acute infection associated with a brisk
t
-FBTU
DPNNPOMZ
GSPN
TPJM inflammatory response and spontaneous resolu-
Classification of Dermatophytes. Based on their tion. In some individuals, infection can involve
ecology, dermatophytes classified: the dermis, as in kerion and Majocchi granuloma.
t
Anthropophilic: Person-to-person transmis-
sion by fomites and by direct contact. Laboratory Examinations
t
Zoophilic: Animal-to-human by direct con-
tact or by fomites. Direct Microscopy
t
Geophilic: Environmental. See Fig. 26-24.
Section 26 Fungal Infections of the Skin, Hair, and Nails 609

coverslip. The preparation is gently heated

with a match or lighter until bubbles begin
to expand, clarifying the preparation. Excess
KOH solution is blotted out with bibulous
or lens paper. Condenser should be “racked
down.” Epidermal dermatophytosis: positive
unless patient has been effectively treated.
90% of cases positive. Variations in KOH with
fungal stains: Swartz–Lamkin stain and chlora-
zol black E stain.
Microscopy Dermatophytes are recognized
as septated, tubelike structures (hyphae or
mycelia; Fig. 26-24).
Wood’s lamp examination: Hairs infected
with Microsporum spp. fluoresce greenish. Coral
red fluorescence of intertriginous site confirms
diagnosis of erythrasma.
Figure 26-24. Dermatophytes: KOH preparation Fungal Cultures. Specimens collected from
Multiple, septated, tubelike structures (hyphae or myce- scaling skin lesions, hair, and nails. Scale and
lia) and spore formation in scales from an individual with hair from the scalp are best harvested with
tinea pedis. tooth or cervical brush; the involved scalp is
brushed vigorously; keratinaceous debris and
hairs then placed into fungal culture plate.
Culture on Sabouraud’s glucose medium. Re-
peat cultures recommended monthly.
Sampling
Dermatopathology DLSO. PAS or methena-
t
Skin: Collect scale with a no. 15 scalpel
mine silver stains are more sensitive than KOH
blade, edge of a glass microscope slide,
preparation or fungal culture in identification
brush (tooth or cervical brush). Scales are
of fungal elements in DLSO.
placed on center of microscope slide, swept
into a small pile, and covered with a cover-
slip. Recent application of cream/ointment Treatment
or powder often makes identification of fun-
gal element difficult/impossible. Topical agents for epidermal dermatophyto-
t
Nails: Keratinaceous debris is collected with ses: Imidazoles (clotrimazole, miconazole,
a no. 15 scalpel blade or small curette. Distal ketoconazole, econazole, oxiconazole, sulcon-
lateral subungual onychomycosis (DLSO): azole, sertaconazole); allylamines (naftifine,
debride from the undersurface of nail of terbinafine); naphthionates (tolnaftate); substi-
most proximally involved site or nail bed; tuted pyridine (ciclopirox olamine).
avoid nail plate. Superficial white onycho-
mycosis: superficial nail plate. Proximal Systemic Antifungal Agents
subungual onychomycosis (PSO): undersur-
t
5FSCJOBåOF
NH
UBCMFU
"MMZMBNJOF
.PTU

face of proximal nail plate; obtain sample
effective oral antidermatophyte antifungal;
by using a small punch biopsy tool, boring
low efficacy against other fungi. Approved
through involved nail plate to undersurface;
for onychomycosis in the United States.
obtain keratin from undersurface of the
t
*USBDPOB[PMF
NH
DBQTVMFT
PSBM
TPMVUJPO

involved nail plate.
(10 mg/mL): Intravenous. Triazole. Needs
t
Hair: Remove hairs by epilation of broken
acid gastric pH for dissolution of capsule.
hairs with a needle holder or forceps. Place
Raises levels of digoxin and cyclosporine.
on microscope slide and cover with glass
Approved for onychomycosis in the United
coverslip. Skin scales from involved hairy
States.
site can be obtained with a brush (tooth or
t
'MVDPOB[PMF


NH
UBCMFUT
PSBM

cervical).
suspension (10 or 40 mg/mL); 400 mg IV.
Preparation of sample potassium hydroxide t
,FUPDPOB[PMF
NH
UBCMFUT
/FFET
BDJE

5–20% solution is applied at the edge of cov- gastric pH for dissolution of tablet. Take
erslip. Capillary action draws solution under with food or cola beverage; antacids and H2
610 Part III Diseases Due to Microbial Agents

blockers reduce absorption. The most hepa- Dermatophytoses of Epidermis

totoxic of azole drugs; hepatotoxicity occurs Epidermal dermatophytoses are the most com-
in an estimated one of every 10,000–15,000 mon dermatophytic infection. May be associ-
exposed persons. Not approved for treat- ated with dermatophytic infection of hair/hair
ment of dermatophyte infections in the follicles and/or the nail apparatus. Synonym:
United States. Ringworm.

Tinea Pedis ICD-9: 110.4 ° ICD-10: B35.3 ◐

■ Dermatophytic infection of the feet. ■ Course. Provides breaks in the integrity of the
■ Clinical Findings. Erythema, scaling, maceration, epidermis through which bacteria such as S.
and/or bulla formation. Infections at other sites aureus or group A streptococcus (GAS) can invade,
such as tinea cruris usually associate initial tinea causing skin or soft-tissue infection.
pedis. ■ Synonyms. Athlete’s foot. Jungle rot.

Epidemiology Pain with secondary bacterial infection (Fig.

25-30).
Age of Onset. Late childhood or young adult Interdigital Type. Two patterns: dry scaling
life. Most common, 20–50 years. (Fig. 26-26); maceration, scaling, fissuring of
Predisposing Factors. Hot, humid climate; oc- toe webs (Fig. 26-27). Hyperhidrosis common.
clusive footwear; hyperhidrosis. Most common site: between fourth and fifth
toes. Infection may spread to adjacent areas of
feet.
Clinical Manifestation
Moccasin Type. Well-demarcated scaling with
Duration: months to years to lifetime. Often, erythema with minute papules on margin, fine
prior history of tinea pedis, and tinea unguium white scaling, and hyperkeratosis (Figs. 26-28
of toenails. Usually asymptomatic. Pruritus. and 26-29) (confined to heels, soles, lateral

Figure 26-25. Tinea pedis and onychomycosis in father and son The foot of a 5-year-old male with tinea pedis
(ringworm lesion) and toenail dystrophy shown with his father’s foot with similar, but more advanced, findings. The son
most likely became infected with dermatophyte from fomite in his home. Both father and son had atopic diathesis with
history of atopic dermatitis.
Section 26 Fungal Infections of the Skin, Hair, and Nails 611

Figure 26-26. Tinea pedis: interdigital dry type The interdigital space between the toes shows ery-
thema and scaling; the toenail is thickened, indicative of associated distal subungual onychomycosis.

Figure 26-27. Tinea pedis: interdigital macerated type A 48-year-old male with athlete’s foot and
hyperhidrosis for years. The skin of the webspace between the fourth and fifth toes is hyperkeratotic and
macerated (hydration of the stratum corneum). The KOH+ preparation shows septated hyphae, confirming
the diagnosis of dermatophytosis. Wood’s lamp demonstrated coral-red fluorescence confirming concomitant
erythrasma. P. aeruginosa was isolated on bacterial culture.
612 Part III Diseases Due to Microbial Agents

Figure 26-28. Tinea pedis: moccasin type A 65-year-old female with scaling feet for years. Sharply marginated
erythema of the foot with a mild keratoderma associated with distal/lateral subungual onychomycosis, typical of T. rubrum
infection.

borders of feet). Distribution: Sole, involving Differential Diagnosis

area covered by a ballet slipper. One or both feet
may be involved with any pattern; bilateral in- Interdigital Type. Erythrasma, pitted keratolysis
volvement more common. Moccasin Type. Psoriasis, eczematous dermati-
Inflammatory/Bullous Type. Vesicles or bullae tis (dyshidrotic, atopic, allergic contact), pitted
filled with clear fluid (Fig. 26-30). Pus usually keratolysis.
indicates secondary infection with S. aureus Inflammatory/bullous type. Bullous impe-
infection or GAS. After rupturing, erosions tigo, allergic contact dermatitis, dyshidrotic
with ragged ringlike border. May be associ- eczema, bullous disease.
ated with “id” reaction (autosensitization
or dermatophytid). Distribution: Sole, instep,
Laboratory Examinations
webspaces.
Ulcerative Type. Extension of interdigital tinea Direct Microscopy (Fig. 26-24). In bullous type,
pedis onto plantar and lateral foot (Fig. 26-30). examine scraping from the inner aspect of
May be secondarily by S. aureus. bulla roof for detection of hyphae.

Figure 26-29. Tinea pedis: moccasin type A 63-year-old male with scaling feet for years. Sharply marginated ery-
thema of the medial foot with a mild keratoderma. Tinea corporis was also present on the forearms and dorsum of hands.
Section 26 Fungal Infections of the Skin, Hair, and Nails 613

Figure 26-30. Tinea pedis: bullous and ulcerative types A 34-year-old female with painful
blisters in the webspaces and on the plantar foot. Tinea pedis was secondarily infected with S. aureus.
A dermatophytid reaction was present on the hands with small vesicle on the fingers.

Wood’s Lamp. Negative fluorescence usually Course

rules out erythrasma in interdigital infection.
Erythrasma and interdigital tinea pedis may Tends to be chronic. May provide portal of
coexist. entry for soft-tissue infections, especially in
Culture. Dermatophytes can be isolated in patient’s venous stasis. Without secondary
11% of normal-appearing interspaces and 31% prophylaxis, recurrence is the rule.
of macerated toe webs. Candida spp. may be
copathogens in webspaces. In individuals with
Treatment
macerated interdigital space, S. aureus, P. aeru-
ginosa, and diphtheroids are commonly isolat- See p. 609.
ed. S. aureus causes secondary infection.

Diagnosis
Demonstration of hyphae on direct micros-
copy, isolation of dermatophyte on culture.
614 Part III Diseases Due to Microbial Agents

Tinea Manuum ICD-9: 110.2 ° ICD-10: B35.2 ◐

■ Chronic dermatophytosis of the hand(s). ■ Usually associated with tinea pedis.
■ Often unilateral, most commonly on the dominant
hand.

Clinical Manifestation palms and lateral fingers, similar to lesions of

bullous tinea pedis. Secondary changes: Lichen
Frequently symptomatic. Pruritus. Dyshidrotic simplex chronicus, prurigo nodules, secondary
type: Episodic symptoms of pruritus. S. aureus infection. Distribution: Diffuse hyperker-
Well-demarcated scaling patches, hyper- atosis of the palms with pronounced involve-
keratosis, fissures on palmar hand (Fig. 26-31). ment of palmar creases or patchy scaling on
Borders well demarcated; central clearing. May the dorsa and sides of fingers; 50% of patients
extend onto dorsum of hand with follicular pap- have unilateral involvement. Usually associated
ules, nodules, and pustules with dermatophytic with tinea pedis (Fig. 26-32) and tinea cruris. If
folliculitis. Dyshidrotic type: Papules, vesicles, chronic, often associated with tinea unguium of
bullae (uncommon on the margin of lesion) on fingernails and toenails (Fig. 26-32).

Figure 26-31. Tinea manuum Erythema and scaling of the right hand, which was associated with bilateral tinea
pedis; the “one-hand, two-feet” distribution is typical of epidermal dermatophytosis of the hands and feet. In time, distal/
lateral subungual onychomycosis occurs on the fingernails.
Section 26 Fungal Infections of the Skin, Hair, and Nails 615

Figure 26-32. Tinea manuum, tinea pedis, and onychomycosis A 57-year-old male immunosuppressed renal
transplant recipient with extensive epidermal dermatophytosis of hands, feet, and nail. The feet are initially infected;
infection spreads to hands, arms, and nails.

Differential Diagnosis Treatment

Atopic dermatitis, lichen simplex chronicus, Must eradicate tinea unguium of fingernails as
allergic contact dermatitis, irritant contact der- well as toenails; also tinea pedis and tinea cru-
matitis, psoriasis vulgaris. ris, otherwise, tinea manuum will recur.
Oral agents eradicate dermatophytoses of
hands, feet, and nails: Terbinafine: 250 mg daily
Course for 14 days. Itraconazole: 200 mg daily for 7
Chronic, does not resolve spontaneously. After days. Fluconazole: 150–200 mg daily for 2–4
treatment, recurs unless onychomycosis of weeks. Note: Eradication of fingernail onycho-
fingernails, feet, and toenails is eradicated. Fis- mycosis requires longer use.
sures and erosions provide portal of entry for
bacterial infections.
616 Part III Diseases Due to Microbial Agents

Tinea Cruris ICD-9: 110.3 ° ICD-10: B35.6 ◐

■ Subacute or chronic dermatophytosis of the upper to the lower leg. “Always” associated with tinea
thigh and adjacent inguinal and pubic regions. A pedis, the source of the infection.
better name is tinea inguinalis (groin); cruris refers

Clinical Manifestation 26-34 and 26-35). Scrotum and penis are rarely
involved.
Months to years duration. Often, history of
long-standing tinea pedis and prior history of
tinea cruris. Differential Diagnosis
Large, scaling, well-demarcated dull red/tan/
brown plaques (Fig. 26-33). Central clearing. Erythrasma, Candida intertrigo, intertriginous
Papules, pustules may be present at margins: psoriasis, tinea, or pityriasis versicolor.
dermatophytic folliculitis. Treated lesions: lack
scale; postinflammatory hyperpigmentation
in darker-skinned persons. In atopics, chronic
Treatment
scratching may produce secondary changes of Prevention. After eradication minimize reinfec-
lichen simplex chronicus. Distribution. Groins tion with shower shoes and antifungal powders;
and thighs; may extend to buttocks (Figs. Antifungal Agents. See p. 609

Figure 26-33. Tinea cruris (inguinalis): acute A

80-year-old female with pruritic inguinal rash for several
weeks. She was being treated with prednisone for polymy-
algia rheumatica. Typical inflamed rings and arcs are seen
on the proximal thigh and adjacent inguinal area.
Section 26 Fungal Infections of the Skin, Hair, and Nails 617

Figure 26-34. Tinea cruris (inguinalis): subacute A 20-year-old male with pruritic inguinal rash for several
months. He was a college wrestler. Concomitant dermatophyte infection was also present on the feet, trunk, and face. He
was treated with oral terbinafine.

Figure 26-35. Tinea cruris (inguinalis): chronic A 65-year-old male with pruritic inguinal rash for many months.
The skin of the proximal thigh is lichenified from chronic rubbing and scratching. He had applied topical corticosteroid to
the site. He also had tinea pedis and onychomycosis.
618 Part III Diseases Due to Microbial Agents

Tinea Corporis ICD-9: 110.5 ° ICD-10: B35.4 ◧ ◐

■ Dermatophyte infections of the trunk, legs, arms, T. tonsurans caused tinea corporis in parents of
and/or neck, excluding the feet, hands, and groin. black children with tinea capitis.
■ Etiology. Most commonly caused by T. rubrum.
M. canis lesions are often inflammatory or bullous.

Clinical Manifestation Differential Diagnosis

Scaling, sharply marginated plaques. Periph- Allergic contact dermatitis, atopic dermatitis,
eral enlargement and central clearing (Figs. 26- annular erythemas, psoriasis, seborrheic der-
36 through 26-39) produce annular configura- matitis, pityriasis rosea, pityriasis alba, tinea
tion with concentric rings or arcuate lesions; versicolor, erythema migrans, subacute lupus
fusion of lesions produces gyrate patterns. Sin- erythematosus, cutaneous T cell lymphoma.
gle and occasionally scattered multiple lesions.
Psoriasiform plaques. Lesions of zoophilic
infection (contracted from animals) are more
Diagnosis
inflammatory, with marked vesicles, pustules, See “Direct Microscopy (Fig. 26-24),” and culture.
crusting at margins. Papules, nodules, pus-
tules: dermatophytic folliculitis, i.e., Majocchi
granuloma.
Treatment
See p. 609

Figure 26-36. Tinea corporis: tinea incognito An 80-year-old male with a rash on buttocks for 1 year. Erythema-
tous patches on the buttocks, some with sharp margination, others with clearing, and excoriations. He had been treating
the pruritus with topical corticosteroid. Tinea cruris, tinea pedis, and onychomycosis were also present.
Section 26 Fungal Infections of the Skin, Hair, and Nails 619

Figure 26-37. Tinea corporis A 80-year-old female

with red, scaling lesions on the lower leg. Lesions were
present under a foot brace that occluded the skin. Cor-
ticosteroid has been applied to the site. Tinea corporis
was associated with tinea pedis and onychomycosis (see
inset).

Figure 26-38. Tinea corporis: tinea incognito A 60-year-old renal transplant recipient has been treating thigh rash
with topical corticosteroid for several months. Blotchy erythema with areas of atrophy and scale on the right medial upper
thigh bordering the inguinal area. Tinea pedis and onychomycosis were also present. KOH preparation showed septated
hyphae. Topical steroid facilitates dermatophyte growth, suppressing the immune response, creating an undiagnosed
infection, tinea incognito.
620 Part III Diseases Due to Microbial Agents

Figure 26-39. Tinea corporis: inflammatory A 13-year-

old female with inflammatory lesion on the arm for 1 week. A
younger sibling had tinea capitis. Acutely inflamed edematous
exudative annular plaque on the upper arm.

Tinea Facialis ◧ ◐
■ Dermatophytosis of the glabrous facial skin. Well- ■ Etiology. T. tonsurans associated with tinea
circumscribed erythematous patch. More commonly capitis in black children and their parents. T.
misdiagnosed than any other dermatophytosis. mentagrophytes, T. rubrum most commonly; also
■ Synonym: Tinea faciei M. audouinii, M. canis.

Clinical Manifestation morphous light eruption, phototoxic drug

eruption, lymphocytic infiltrate.
Well-circumscribed macule to plaque of vari-
able size; elevated border and central regres- Diagnosis
sion (Figs. 26-40 and 26-41). Scaling is often
minimal. Pink to red; in black patients, hyper- See “Direct Microscopy,” and culture.
pigmentation. Any area of face but usually not
symmetric. Treatment
See p. 609
Differential Diagnosis
Seborrheic dermatitis, contact dermatitis, ery-
thema migrans, lupus erythematosus, poly-
Section 26 Fungal Infections of the Skin, Hair, and Nails 621

Figure 26-40. Tinea facialis A 5-year-old girl with inflammatory lesion on the periorbital skin. Papules are dermato-
phytic folliculitis of vellus hairs. The site has previously been treated with hydrocortisone cream.

Figure 26-41. Tinea facialis A 83-year-old immuno-

suppressed male with a history of prednisone treatment for
polymyalgia rheumatica and chronic lymphatic leukemia.
Note a facial lesions and a new nodule. Well-demarcated
erythema and scaling in the beard area. SCC in situ is pres-
ent on the left eyebrow. The tumor on the left neck is B-
cell lymphoma; this lesion regressed when prednisone was
tapered.
622 Part III Diseases Due to Microbial Agents

Tinea Incognito ◧ ◐
■ Epidermal dermatophytosis, often associated with ■ Occurs after the topical application of a
dermatophytic folliculitis. glucocorticoid preparation to a site colonized or
infected by dermatophyte.

Clinical Manifestation within involved sites is dermatophytic folliculitis.

Epidermal atrophy caused by chronic glucocorti-
Variably inflamed patches. Occurs when an coid application may be present.
inflammatory dermatophytosis is mistaken
for psoriasis or an eczematous dermatitis (Figs.
26-35–26-38 and 26-40). Involved sites often
Treatment
have exaggerated features of epidermal der- Systemic antifungal therapy may be indi-
matophytoses, being a deep red or violaceous. cated due to deep involvement of the hair
Scaling often not apparent. Papules or pustule apparatus. See p. 609.

Dermatophytoses of Hair
■ Dermatophytes are capable of invading hair ■ Dermatophytic folliculitis
follicles and hair shafts, causing: ■ Majocchi granuloma
■ Tinea capitis ■ Two types of hair involvement are seen (see
■ Tinea barbae Fig. 26-42).

Figure 26-42. Dermatophytic folliculitis. Ectothrix

type: mycelia and arthroconidia are seen on the surface
of the hair follicle (extrapilary). Endothrix type: hyphae and
arthroconidia occur within the hair shaft (intrapilary).
Section 26 Fungal Infections of the Skin, Hair, and Nails 623

Tinea Capitis ICD-9: 110.5 ° ICD-10: B35.0 ◧ ◐

■ Dermatophytic trichomycosis of the scalp, ■ Severe, painful inflammation with painful,
predominantly in preadolescent children. boggy nodules that drain pus (kerion) and
■ Clinical presentations vary widely: result in scarring alopecia
■ Noninflammatory scaling ■ Synonyms: Ringworm of the scalp, tinea tonsurans
■ Scaling and broken-off hairs

Epidemiology and Etiology t
Kerion. Variant of endothrix with boggy

inflammatory plaques.
Toddlers and school-age children (6–10 years t
Favus. Variant of endothrix with arthroconidia
of age) most commonly affected. Much more and airspaces within hair shaft. Very uncom-
common in blacks than in whites in the mon in Western Europe and North America.
United States. Etiology varies from country In some parts of the world (Middle East,
to country and from region to region. Species South Africa), however, it is still endemic.
change in time due to immigration. Infections
can become epidemic in schools and institu-
tions, especially with overcrowding. United Clinical Manifestation
States: Random fungal cultures in urban study
Noninflammatory Infection. Scaling. Diffuse or
detected a 4% infection rate and a 12.7% colo-
circumscribed alopecia. Occipital or posterior
nization rate among black children.
auricular adenopathy.
t
United States and Western Europe. 90% of “Gray patch” tinea capitis (Fig. 26-43). Par-
cases of tinea capitis caused by T. tonsurans. tial alopecia, often circular in shape, showing
Less commonly, M. canis. numerous broken-off hairs, dull gray from
t
Eastern and Southern Europe, North Africa. T. their coating of arthrospores. Fine scaling
violaceum with fairly sharp margin. Hair shaft becomes
brittle, breaking off at or slightly above scalp.
Transmission. Person-to-person, animal-to-per-
Small patches coalesce, forming larger patches.
son, via fomites. Spores are present on asymp-
Inflammatory response minimal, but massive
tomatic carriers, animals, or inanimate objects.
scaling. Several or many patches, randomly
Pathogenesis. Scalp hair traps fungi from the
arranged, may be present. Microsporum species
environment or fomites. Asymptomatic colo-
may show green fluorescence with Wood’s
nization is common. Trauma assists inocula-
lamp. Differential diagnosis: Seborrheic derma-
tion. Dermatophytes initially invade stratum
titis, psoriasis, atopic dermatitis, lichen sim-
corneum of scalp, which may be followed by
plex chronicus, and alopecia areata.
hair shaft infection. Spread to other hair fol-
“Black Dot” Tinea Capitis. Broken-off hairs near
licles then occurs.
the scalp give appearance of “dots” (Fig. 26-44)
(swollen hair shafts) in dark-haired patients.
Dots occur as affected hair breaks at surface of
Classification
scalp. Tends to be diffuse and poorly circum-
t
&DUPUISJY
JOGFDUJPO
0DDVST
PVUTJEF
IBJS
scribed. Low-grade folliculitis may be pres-
shaft. Hyphae fragment into arthroconidia, ent. Resembles seborrheic dermatitis. Usually
leading to cuticle destruction. Caused by caused by T. tonsurans, T. violaceum. Differen-
Microsporum spp. (M. audouinii and M. canis) tial diagnosis: Seborrheic dermatitis, psoriasis,
(Fig. 26-42). atopic dermatitis, lichen simplex chronicus,
t
&OEPUISJY
JOGFDUJPO
0DDVST
XJUIJO
IBJS
chronic cutaneous lupus erythematosus, alo-
shaft without cuticle destruction (Fig. 26-42). pecia areata.
Arthroconidia found within hair shaft. Kerion. Inflammatory mass in which remain-
Caused by Trichophyton spp. (T. tonsurans in ing hairs are loose. Characterized by boggy,
North America; T. violaceum in Europe, Asia, purulent, inflamed nodules, and plaques (Fig.
parts of Africa). 26-45). Usually painful; drains pus from mul-
t
iBlack dot” tinea capitis. Variant of endothrix tiple openings, like honeycomb. Hairs do not
resembling seborrheic dermatitis. break off but fall out and can be pulled without
624 Part III Diseases Due to Microbial Agents

Figure 26-43. Tinea capitis: “gray patch” type A large, round, hyperkeratotic plaque of alopecia due to breaking
off of hair shafts close to the surface, giving the appearance of a mowed wheat field on the scalp of a child. Remaining
hair shafts and scales exhibit a green fluorescence when examined with Wood’s lamp. M. canis was isolated on culture.

Figure 26-44. Tinea capitis: “black dot” variant A subtle, asymptomatic patch of alopecia due to breaking off of
hairs on the frontal scalp in a 4-year-old black child. The lesion was detected because her infant sister presented with
tinea corporis. T. tonsurans was isolated on culture.
Section 26 Fungal Infections of the Skin, Hair, and Nails 625

Figure 26-45. Kerion A 5-year-old black boy with an inflammatory mass on the scalp unresponsive to oral antibiot-
ics. The bobby swelling with multiple pustules and postauricular lymphadenopathy. T. tonsurans was isolated on fungal
culture. He was successfully treated with oral terbinafine for 4 weeks. (From Proudfoot LE, Morris-Jones R. Kerion celsi.
N Engl J Med 2012;366:1142. Used with permission.)

pain. Follicles may discharge pus; sinus for- Direct Microscopy. Skin scales contain hyphae
mation; mycetoma-like grains. Thick crusting and arthrospores. Ectothrix: arthrospores can
with matting of adjacent hairs. A single plaque be seen surrounding the hair shaft in cuticle.
is usual, but multiple lesions may occur with Endothrix: spores within hair shaft. Favus: loose
involvement of entire scalp. Frequently, asso- chains of arthrospores and airspaces in hair
ciated lymphadenopathy is present. Usually shaft (Fig. 26-42).
caused by zoophilic (T. verrucosum, T. mentagro- Fungal Culture. Growth of dermatophytes usu-
phytes var. mentagrophytes) or geophilic species. ally seen in 10–14 days.
Heals with scarring alopecia. Bacterial Culture. Rule out bacterial infection,
Favus. Latin for honeycomb. Early cases show usually S. aureus or GAS.
perifollicular erythema and matting of hair. Lat-
er, thick yellow adherent crusts (scutula) com-
posed of skin debris and hyphae that are pierced
Course and Treatment
by remaining hair shafts (Fig. 26-46). Fetid odor. Chronic untreated kerion and favus, especially
Shows little tendency to clear spontaneously. if secondarily infected with S. aureus, result in
Often results in scarring alopecia. Differential scarring alopecia. Regrowth of hair is the rule
diagnosis: Impetigo, ecthyma, crusted scabies. if treated with systemic antifungal agents (see
p. 609).
Laboratory Examinations
Wood’s Lamp. T. tonsurans does not fluoresce.
626 Part III Diseases Due to Microbial Agents

Figure 26-46. Tinea capitis: favus Extensive hair loss with atrophy, scarring, and so-called scutula, i.e., yellowish
adherent crusts present on the scalp; remaining hairs pierce the scutula. T. schoenleinii was isolated on culture.

Tinea Barbae ICD-9: 110.0 ° ICD-10: B35.0 ■ ◐

■ Dermatophytic folliculitis involving the Resembles tinea capitis, with invasion of the hair
androgen-sensitive beard and moustache areas. shaft.

Etiology Beard and moustache areas, rarely, eyelashes,

eyebrows.
T. verrucosum, T. mentagrophytes var. mentag- Regional lymphadenopathy, especially if of
rophytes, most commonly. May be acquired long duration and if superinfected.
through animal exposure. T. rubrum an uncom-
mon cause.
Differential Diagnosis
S. aureus folliculitis, furuncle, carbuncle, acne
Clinical Manifestation vulgaris, rosacea, pseudofolliculitis.
Pustular folliculitis (Fig. 26-47), i.e., hair fol- Laboratory Examinations. See p. 608.
licles surrounded by red inflammatory papules,
pustules, nodules, or plaques. Involved hairs Treatment
are loose and easily removed. With less fol- Topical agents ineffective. Systemic antifungal
licular involvement, there are scaling, circular, therapy required (see p. 609).
reddish patches (tinea facialis) in which hair is Dermatophytic Folliculitis. See “Infectious Fol-
broken off at the surface. Papules may coalesce liculitis” in Section 31.
to inflammatory plaques topped by pustules.
Kerion: boggy purulent nodules and
plaques as with tinea capitis (Fig. 26-48).
Section 26 Fungal Infections of the Skin, Hair, and Nails 627

Figure 26-47. Tinea barbae A 63-year-old male with

pustules in beard area for several months. A large pustule
in an inflammatory nodule is seen on the moustache area.
Extensive subtle tinea facialis was also present. Tinea pe-
dis, onychomycosis, and tinea cruris were present as well.
KOH preparation was positive; T. rubrum was detected on
dermatophyte culture. Bacterial culture was negative for
pathogens. Facial lesions resolved with oral terbinafine.

Figure 26-48. Tinea bar-

bae with kerion and tinea
facialis Confluent, painful
papules, nodules, and pustules
on the upper lip (kerion). Epi-
dermal dermatophytosis (tinea
facialis) with sharply margin-
ated erythema and scaling is
present on the cheeks, eyelids,
eyebrows, and forehead. T.
mentagrophytes was isolated
on culture. In this case, the
organism caused two distinct
clinical patterns (epidermal in-
volvement, tinea facialis versus
follicular inflammation, tinea
barbae), depending on whether
glabrous skin or hairy skin was
infected (see also Fig. 26-23).