ICD-9: 110 ○ ICD-10: B35.0-B36
Dermatophytes are a unique group of fungi capable of infecting nonviable keratinized cutaneous structures including stratum corneum, nails, and hair. Arthrospores can survive in human scales for 12 months. Dermatophytosis denotes an infection caused by dermatophytes.
Clinical Infection by Structure Involved. Epidermal dermatophytosis. Dermatophytosis of hair and hair follicles. Onychomycosis or tinea unguium: dermatophytosis of the nail apparatus.
Pathogenesis of dermatophytosis leading to different clinical manifestations is schematically depicted in Figs. 26-22 and 26-23.
The term tinea is best used for dermatophytoses and is modified according to the anatomic site of infection, e.g., tinea pedis.
“Tinea” versicolor is referred to as pityriasis versicolor except in the United States; it is not a dermatophytosis but rather an infection caused by the yeast Malassezia.
Tinea nigra is caused by a pigmented or dematiaceous fungus, not a dermatophyte.
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 symbolize inflammatory cells), which may then manifest as erythema, papulation, and vesiculation.
Hair follicle dermatophyte infections Hair shaft is involved (red dots) resulting in the destruction 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 26-1Classification of Tinea Pedis |Favorite Table|Download (.pdf) Table 26-1 Classification of Tinea Pedis
|Type ||Clinical Features ||Etiology |
|Interdigital (acute and chronic) ||Most common type; frequently overlooked two patterns: dry and moist with maceration ||T. rubrum most common cause of chronic tinea pedis; T. mentagrophytes causes more inflammatory lesions |
|Dry ||Scaling of webspace, may be erosive ||T. rubrum |
|Moist (macerated) ||Hyperkeratosis of webspace with maceration of stratum corneum ||T. mentagrophytes |
|Moccasin (chronic hyperkeratotic or dry) ||Keratoderma ||Most often caused by T. rubrum, especially in atopic individuals; also Epidermophyton floccosum |
|Inflammatory or bullous (vesicular) ||Blisters in nonoccluded skin ||Least common type; usually caused by T. mentagrophytes var. mentagrophytes (granular). Resembles an allergic contact dermatitis |
|Ulcerative ||An extension of interdigital type into dermis due to maceration and secondary (bacterial) infection ||T. rubrum, E. floccosum, T. mentagrophytes, C. albicans |
|Dermatophytid ||Presents as a vesicular eruption of the 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 ||T. mentagrophytes, T. rubrum |
Epidemiology and Etiology
Three genera of dermatophytes (“skin plants”): Trichophyton, Microsporum, Epidermophyton. More than 40 species are currently recognized; approximately 10 spp. are common causes of human infection.
Trichophyton rubrum is the most common cause of epidermal dermatophytosis and onychomycosis in industrialized nations. Currently, 70% of the U.S. population experience at least one episode of T. rubrum infection (usually tinea pedis). Soldiers wearing occlusive boots in tropical climates developed “jungle rot”—extensive tinea pedis with secondary bacterial infection. In U.S. adults, T. rubrum is the most common cause of dermatophytic folliculitis.
Tinea capitis. Etiology in children varies geographically. Trichophyton tonsurans: Most common cause in North America and Europe. Previously, M. audouinii, T. violaceum: Europe, Asia, and Africa.
Children have scalp infections (Trichophyton, Microsporum). Young and older adults have intertriginous infections. The incidence of onychomycosis is correlated directly with age; in the United States, up to 50% of individuals aged 75 years have onychomycosis.
Adult blacks may have a lower incidence of dermatophytosis. Tinea capitis is more common in black children.
Some species have a worldwide distribution; others are restricted to particular continents or regions. However, T. concentricum, the cause of tinea imbricata, is endemic to the South Pacific and parts of South America. T. rubrum was endemic to Southeast Asia, Western Africa, and Australia but now occurs commonly in North America and Europe.
Dermatophyte infections can be acquired from three sources:
Most commonly from another person [usually by fomites, less so by direct skin-to-skin contact (tinea gladiatorum)]
From animals such as puppies or kittens.
Least commonly from soil.
Classification of Dermatophytes
Based on their ecology, dermatophytes classified:
Anthropophilic: Person-to-person transmission by fomites and by direct contact.
Zoophilic: Animal-to-human by direct contact or by fomites.
Atopic diathesis: Cell-mediated immune deficiency for T. rubrum. Topical immunosuppression by application of glucocorticoids: tinea incognito. Systemic immunocompromised: Patients have a higher incidence and more intractable dermatophytoses; follicular abscesses and granulomas may occur (Majocchi granuloma).
In vivo, dermatophytes grow only on or within keratinized structures and, as such, involve the following:
Epidermal dermatophytosis. Tinea facialis, tinea corporis, tinea cruris, tinea manus, tinea pedis.
Dermatophytoses of nail apparatus. Tinea unguium (toenails, fingernails). Onychomycosis (more inclusive term, including nail infections caused by dermatophytes, yeasts, and molds).
Dermatophytoses of hair and hair follicle. Dermatophytic folliculitis, Majocchi granuloma, tinea capitis, tinea barbae.
Dermatophytes synthesize keratinases that digest keratin and sustain existence of fungi in keratinized structures. Cell-mediated immunity and antimicrobial activity of polymorphonuclear leukocytes restrict dermatophyte pathogenicity. Host factors that facilitate dermatophyte infections: atopy, topical and systemic glucocorticoids, ichthyosis, collagen vascular disease. Local factors favoring dermatophyte infection: sweating, occlusion, occupational exposure, geographic location, high humidity (tropical or semitropical climates). The clinical presentation of dermatophytoses depends on several factors: site of infection, immunologic response of the host, and species of fungus. Dermatophytes (e.g., T. rubrum) that initiate little inflammatory response are better able to establish chronic infection. Organisms such as Microsporum canis cause an acute infection associated with a brisk inflammatory response and spontaneous resolution. In some individuals, infection can involve the dermis, as in kerion and Majocchi granuloma.
Dermatophytes: KOH preparation Multiple, septated, tubelike structures (hyphae or mycelia) and spore formation in scales from an individual with tinea pedis.
Skin: Collect scale with a no. 15 scalpel blade, edge of a glass microscope slide, brush (tooth or cervical brush). Scales are placed on center of microscope slide, swept into a small pile, and covered with a coverslip. Recent application of cream/ointment or powder often makes identification of fungal element difficult/impossible.
Nails: Keratinaceous debris is collected with a no. 15 scalpel blade or small curette. Distal lateral subungual onychomycosis (DLSO): debride from the undersurface of nail of most proximally involved site or nail bed; avoid nail plate. Superficial white onychomycosis: superficial nail plate. Proximal subungual onychomycosis (PSO): undersurface of proximal nail plate; obtain sample by using a small punch biopsy tool, boring through involved nail plate to undersurface; obtain keratin from undersurface of the involved nail plate.
Hair: Remove hairs by epilation of broken hairs with a needle holder or forceps. Place on microscope slide and cover with glass coverslip. Skin scales from involved hairy site can be obtained with a brush (tooth or cervical).
Preparation of sample potassium hydroxide 5–20% solution is applied at the edge of coverslip. Capillary action draws solution under 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 chlorazol 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.
Specimens collected from scaling skin lesions, hair, and nails. Scale and hair from the scalp are best harvested with 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. Repeat cultures recommended monthly.
Dermatopathology DLSO. PAS or methenamine silver stains are more sensitive than KOH preparation or fungal culture in identification of fungal elements in DLSO.
Topical agents for epidermal dermatophytoses: Imidazoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole, sulconazole, sertaconazole); allylamines (naftifine, terbinafine); naphthionates (tolnaftate); substituted pyridine (ciclopirox olamine).
Systemic Antifungal Agents
Terbinafine 250-mg tablet. Allylamine. Most effective oral antidermatophyte antifungal; low efficacy against other fungi. Approved for onychomycosis in the United States.
Itraconazole 100-mg capsules; oral solution (10 mg/mL): Intravenous. Triazole. Needs acid gastric pH for dissolution of capsule. Raises levels of digoxin and cyclosporine. Approved for onychomycosis in the United States.
Fluconazole 100-, 150-, 200-mg tablets; oral suspension (10 or 40 mg/mL); 400 mg IV.
Ketoconazole 200-mg tablets. Needs acid gastric pH for dissolution of tablet. Take with food or cola beverage; antacids and H2 blockers reduce absorption. The most hepatotoxic of azole drugs; hepatotoxicity occurs in an estimated one of every 10,000–15,000 exposed persons. Not approved for treatment of dermatophyte infections in the United States.
Dermatophytoses of Epidermis
Epidermal dermatophytoses are the most common dermatophytic infection. May be associated with dermatophytic infection of hair/hair follicles and/or the nail apparatus. Synonym: Ringworm.
ICD-9: 110.4 ○ ICD-10: B35.3
Dermatophytic infection of the feet.
Clinical Findings. Erythema, scaling, maceration, and/or bulla formation. Infections at other sites such as tinea cruris usually associate initial tinea pedis.
Course. Provides breaks in the integrity of the epidermis through which bacteria such as S. aureus or group A streptococcus (GAS) can invade, causing skin or soft-tissue infection.
Synonyms. Athlete’s foot. Jungle rot.
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.
Late childhood or young adult life. Most common, 20–50 years.
Hot, humid climate; occlusive footwear; hyperhidrosis.
Duration: months to years to lifetime. Often, prior history of tinea pedis, and tinea unguium of toenails. Usually asymptomatic. Pruritus. Pain with secondary bacterial infection (Fig. 25-30).
Two patterns: dry scaling (Fig. 26-26); maceration, scaling, fissuring of toe webs (Fig. 26-27). Hyperhidrosis common. Most common site: between fourth and fifth toes. Infection may spread to adjacent areas of feet.
Tinea pedis: interdigital dry type The interdigital space between the toes shows erythema and scaling; the toenail is thickened, indicative of associated distal subungual onychomycosis.
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.
Well-demarcated scaling with erythema with minute papules on margin, fine white scaling, and hyperkeratosis (Figs. 26-28 and 26-29) (confined to heels, soles, lateral borders of feet). Distribution: Sole, involving area covered by a ballet slipper. One or both feet may be involved with any pattern; bilateral involvement more common.
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.
Tinea pedis: moccasin type A 63-year-old male with scaling feet for years. Sharply marginated erythema of the medial foot with a mild keratoderma. Tinea corporis was also present on the forearms and dorsum of hands.
Vesicles or bullae filled with clear fluid (Fig. 26-30). Pus usually indicates secondary infection with S. aureus infection or GAS. After rupturing, erosions with ragged ringlike border. May be associated with “id” reaction (autosensitization or dermatophytid). Distribution: Sole, instep, webspaces.
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.
Extension of interdigital tinea pedis onto plantar and lateral foot (Fig. 26-30). May be secondarily by S. aureus.
Erythrasma, pitted keratolysis
Psoriasis, eczematous dermatitis (dyshidrotic, atopic, allergic contact), pitted keratolysis.
Inflammatory/bullous type. Bullous impetigo, allergic contact dermatitis, dyshidrotic eczema, bullous disease.
Direct Microscopy (Fig. 26-24). In bullous type, examine scraping from the inner aspect of bulla roof for detection of hyphae.
Negative fluorescence usually rules out erythrasma in interdigital infection. Erythrasma and interdigital tinea pedis may coexist.
Dermatophytes can be isolated in 11% of normal-appearing interspaces and 31% of macerated toe webs. Candida spp. may be copathogens in webspaces. In individuals with macerated interdigital space, S. aureus, P. aeruginosa, and diphtheroids are commonly isolated. S. aureus causes secondary infection.
Demonstration of hyphae on direct microscopy, isolation of dermatophyte on culture.
Tends to be chronic. May provide portal of entry for soft-tissue infections, especially in patient’s venous stasis. Without secondary prophylaxis, recurrence is the rule.
ICD-9: 110.2 ○ ICD-10: B35.2
Chronic dermatophytosis of the hand(s).
Often unilateral, most commonly on the dominant hand.
Usually associated with tinea pedis.
Frequently symptomatic. Pruritus. Dyshidrotic type: Episodic symptoms of pruritus.
Well-demarcated scaling patches, hyperkeratosis, fissures on palmar hand (Fig. 26-31). Borders well demarcated; central clearing. May extend onto dorsum of hand with follicular papules, nodules, and pustules with dermatophytic folliculitis. Dyshidrotic type: Papules, vesicles, bullae (uncommon on the margin of lesion) on palms and lateral fingers, similar to lesions of bullous tinea pedis. Secondary changes: Lichen simplex chronicus, prurigo nodules, secondary S. aureus infection. Distribution: Diffuse hyperkeratosis of the palms with pronounced involvement of palmar creases or patchy scaling on the dorsa and sides of fingers; 50% of patients have unilateral involvement. Usually associated with tinea pedis (Fig. 26-32) and tinea cruris. If chronic, often associated with tinea unguium of fingernails and toenails (Fig. 26-32).
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.
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.
Atopic dermatitis, lichen simplex chronicus, allergic contact dermatitis, irritant contact dermatitis, psoriasis vulgaris.
Chronic, does not resolve spontaneously. After treatment, recurs unless onychomycosis of fingernails, feet, and toenails is eradicated. Fissures and erosions provide portal of entry for bacterial infections.
Must eradicate tinea unguium of fingernails as well as toenails; also tinea pedis and tinea cruris, otherwise, tinea manuum will recur.
Oral agents eradicate dermatophytoses of hands, feet, and nails: Terbinafine: 250 mg daily for 14 days. Itraconazole: 200 mg daily for 7 days. Fluconazole: 150–200 mg daily for 2–4 weeks. Note: Eradication of fingernail onychomycosis requires longer use.
ICD-9: 110.3 ○ ICD-10: B35.6
Months to years duration. Often, history of long-standing tinea pedis and prior history of tinea cruris.
Large, scaling, well-demarcated dull red/tan/brown plaques (Fig. 26-33). Central clearing. Papules, pustules may be present at margins: dermatophytic folliculitis. Treated lesions: lack scale; postinflammatory hyperpigmentation in darker-skinned persons. In atopics, chronic scratching may produce secondary changes of lichen simplex chronicus. Distribution. Groins and thighs; may extend to buttocks (Figs. 26-34 and 26-35). Scrotum and penis are rarely involved.
Tinea cruris (inguinalis): acute A 80-year-old female with pruritic inguinal rash for several weeks. She was being treated with prednisone for polymyalgia rheumatica. Typical inflamed rings and arcs are seen on the proximal thigh and adjacent inguinal area.
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.
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.
Erythrasma, Candida intertrigo, intertriginous psoriasis, tinea, or pityriasis versicolor.
After eradication minimize reinfection with shower shoes and antifungal powders;
ICD-9: 110.5 ○ ICD-10: B35.4
Dermatophyte infections of the trunk, legs, arms, and/or neck, excluding the feet, hands, and groin.
Etiology. Most commonly caused by T. rubrum. M. canis lesions are often inflammatory or bullous. T. tonsurans caused tinea corporis in parents of black children with tinea capitis.
Scaling, sharply marginated plaques. Peripheral enlargement and central clearing (Figs. 26-36, 26-37, 26-38, 26-39) produce annular configuration with concentric rings or arcuate lesions; fusion of lesions produces gyrate patterns. Single and occasionally scattered multiple lesions. Psoriasiform plaques. Lesions of zoophilic infection (contracted from animals) are more inflammatory, with marked vesicles, pustules, crusting at margins. Papules, nodules, pustules: dermatophytic folliculitis, i.e., Majocchi granuloma.
Tinea corporis: tinea incognito An 80-year-old male with a rash on buttocks for 1 year. Erythematous 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.
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. Corticosteroid has been applied to the site. Tinea corporis was associated with tinea pedis and onychomycosis (see inset).
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.
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.
Allergic contact dermatitis, atopic dermatitis, annular erythemas, psoriasis, seborrheic dermatitis, pityriasis rosea, pityriasis alba, tinea versicolor, erythema migrans, subacute lupus erythematosus, cutaneous T cell lymphoma.
See “Direct Microscopy (Fig. 26-24),” and culture.
Dermatophytosis of the glabrous facial skin. Well-circumscribed erythematous patch. More commonly misdiagnosed than any other dermatophytosis.
Synonym: Tinea faciei
Etiology. T. tonsurans associated with tinea capitis in black children and their parents. T. mentagrophytes, T. rubrum most commonly; also M. audouinii, M. canis.
Well-circumscribed macule to plaque of variable size; elevated border and central regression (Figs. 26-40 and 26-41). Scaling is often minimal. Pink to red; in black patients, hyperpigmentation. Any area of face but usually not symmetric.
Tinea facialis A 5-year-old girl with inflammatory lesion on the periorbital skin. Papules are dermatophytic folliculitis of vellus hairs. The site has previously been treated with hydrocortisone cream.
Tinea facialis A 83-year-old immunosuppressed 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 present on the left eyebrow. The tumor on the left neck is B-cell lymphoma; this lesion regressed when prednisone was tapered.
Seborrheic dermatitis, contact dermatitis, erythema migrans, lupus erythematosus, polymorphous light eruption, phototoxic drug eruption, lymphocytic infiltrate.
See “Direct Microscopy,” and culture.
Epidermal dermatophytosis, often associated with dermatophytic folliculitis.
Occurs after the topical application of a glucocorticoid preparation to a site colonized or infected by dermatophyte.
Variably inflamed patches. Occurs when an inflammatory dermatophytosis is mistaken for psoriasis or an eczematous dermatitis (Figs. 26-35, 26-36, 26-37, 26-38 and 26-40). Involved sites often have exaggerated features of epidermal dermatophytoses, being a deep red or violaceous. Scaling often not apparent. Papules or pustule within involved sites is dermatophytic folliculitis. Epidermal atrophy caused by chronic glucocorticoid application may be present.
Systemic antifungal therapy may be indicated due to deep involvement of the hair apparatus. See Sampling.
Dermatophytes are capable of invading hair follicles and hair shafts, causing:
Two types of hair involvement are seen (see Fig. 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).
ICD-9: 110.5 ○ ICD-10: B35.0
Dermatophytic trichomycosis of the scalp, predominantly in preadolescent children.
Clinical presentations vary widely:
Scaling and broken-off hairs
Severe, painful inflammation with painful, boggy nodules that drain pus (kerion) and result in scarring alopecia
Synonyms: Ringworm of the scalp, tinea tonsurans
Epidemiology and Etiology
Toddlers and school-age children (6–10 years of age) most commonly affected. Much more common in blacks than in whites in the United States. Etiology varies from country to country and from region to region. Species change in time due to immigration. Infections can become epidemic in schools and institutions, especially with overcrowding. United States: Random fungal cultures in urban study detected a 4% infection rate and a 12.7% colonization rate among black children.
United States and Western Europe. 90% of cases of tinea capitis caused by T. tonsurans. Less commonly, M. canis.
Eastern and Southern Europe, North Africa. T. violaceum
Person-to-person, animal-to-person, via fomites. Spores are present on asymptomatic carriers, animals, or inanimate objects.
Scalp hair traps fungi from the environment or fomites. Asymptomatic colonization is common. Trauma assists inoculation. Dermatophytes initially invade stratum corneum of scalp, which may be followed by hair shaft infection. Spread to other hair follicles then occurs.
Ectothrix infection. Occurs outside hair shaft. Hyphae fragment into arthroconidia, leading to cuticle destruction. Caused by Microsporum spp. (M. audouinii and M. canis) (Fig. 26-42).
Endothrix infection. Occurs within hair shaft without cuticle destruction (Fig. 26-42). Arthroconidia found within hair shaft. Caused by Trichophyton spp. (T. tonsurans in North America; T. violaceum in Europe, Asia, parts of Africa).
“Black dot” tinea capitis. Variant of endothrix resembling seborrheic dermatitis.
Kerion. Variant of endothrix with boggy inflammatory plaques.
Favus. Variant of endothrix with arthroconidia and airspaces within hair shaft. Very uncommon in Western Europe and North America. In some parts of the world (Middle East, South Africa), however, it is still endemic.
Scaling. Diffuse or circumscribed alopecia. Occipital or posterior auricular adenopathy.
“Gray patch” tinea capitis (Fig. 26-43). Partial alopecia, often circular in shape, showing numerous broken-off hairs, dull gray from their coating of arthrospores. Fine scaling with fairly sharp margin. Hair shaft becomes brittle, breaking off at or slightly above scalp. Small patches coalesce, forming larger patches. Inflammatory response minimal, but massive scaling. Several or many patches, randomly arranged, may be present. Microsporum species may show green fluorescence with Wood’s lamp. Differential diagnosis: Seborrheic dermatitis, psoriasis, atopic dermatitis, lichen simplex chronicus, and alopecia areata.
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.
“Black Dot” Tinea Capitis
Broken-off hairs near 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 scalp. Tends to be diffuse and poorly circumscribed. Low-grade folliculitis may be present. Resembles seborrheic dermatitis. Usually caused by T. tonsurans, T. violaceum. Differential diagnosis: Seborrheic dermatitis, psoriasis, atopic dermatitis, lichen simplex chronicus, chronic cutaneous lupus erythematosus, alopecia areata.
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.
Inflammatory mass in which remaining hairs are loose. Characterized by boggy, purulent, inflamed nodules, and plaques (Fig. 26-45). Usually painful; drains pus from multiple openings, like honeycomb. Hairs do not break off but fall out and can be pulled without pain. Follicles may discharge pus; sinus formation; mycetoma-like grains. Thick crusting with matting of adjacent hairs. A single plaque is usual, but multiple lesions may occur with involvement of entire scalp. Frequently, associated lymphadenopathy is present. Usually caused by zoophilic (T. verrucosum, T. mentagrophytes var. mentagrophytes) or geophilic species. Heals with scarring alopecia.
Kerion A 5-year-old black boy with an inflammatory mass on the scalp unresponsive to oral antibiotics. 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.)
Latin for honeycomb. Early cases show perifollicular erythema and matting of hair. Later, thick yellow adherent crusts (scutula) composed of skin debris and hyphae that are pierced by remaining hair shafts (Fig. 26-46). Fetid odor. Shows little tendency to clear spontaneously. Often results in scarring alopecia. Differential diagnosis: Impetigo, ecthyma, crusted scabies.
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.
T. tonsurans does not fluoresce.
Skin scales contain hyphae and arthrospores. Ectothrix: arthrospores can be seen surrounding the hair shaft in cuticle. Endothrix: spores within hair shaft. Favus: loose chains of arthrospores and airspaces in hair shaft (Fig. 26-42).
Growth of dermatophytes usually seen in 10–14 days.
Rule out bacterial infection, usually S. aureus or GAS.
Chronic untreated kerion and favus, especially if secondarily infected with S. aureus, result in scarring alopecia. Regrowth of hair is the rule if treated with systemic antifungal agents (see Sampling).
ICD-9: 110.0 ○ ICD-10: B35.0
T. verrucosum, T. mentagrophytes var. mentagrophytes, most commonly. May be acquired through animal exposure. T. rubrum an uncommon cause.
Pustular folliculitis (Fig. 26-47), i.e., hair follicles surrounded by red inflammatory papules, pustules, nodules, or plaques. Involved hairs are loose and easily removed. With less follicular involvement, there are scaling, circular, reddish patches (tinea facialis) in which hair is broken off at the surface. Papules may coalesce to inflammatory plaques topped by pustules.
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 pedis, 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.
Kerion: boggy purulent nodules and plaques as with tinea capitis (Fig. 26-48). Beard and moustache areas, rarely, eyelashes, eyebrows.
Tinea barbae with kerion and tinea facialis Confluent, painful papules, nodules, and pustules on the upper lip (kerion). Epidermal dermatophytosis (tinea facialis) with sharply marginated 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 involvement, tinea facialis versus follicular inflammation, tinea barbae), depending on whether glabrous skin or hairy skin was infected (see also Fig. 26-23).
Regional lymphadenopathy, especially if of long duration and if superinfected.
S. aureus folliculitis, furuncle, carbuncle, acne vulgaris, rosacea, pseudofolliculitis.
Topical agents ineffective. Systemic antifungal therapy required (see Sampling).
See “Infectious Folliculitis” in Section 31.
Dermatophytic folliculitis with foreign-body granuloma occurring in response to keratin in dermis and immune reaction to dermatophyte.
Etiology. Most commonly T. rubrum, T. tonsurans
Risk Factors. Topical glucocorticoid application. Host defense defects
Follicular type with local immunosuppression (topical glucocorticoid use)
Subcutaneous nodular type with systemic immunocompromised (Fig. 26-49). Solitary or multiple
Majocchi granuloma A 55-year-old diabetic male renal transplant recipient with painful nodules on left lower thigh. Eroded papules with crusting above the knee. Tinea pedis and onychomycosis were also present. T. rubrum was isolated on dermatophyte culture. He was treated with voriconazole.
Any hair-bearing area; scalp, face, forearms (Fig. 26-50), dorsum of hands/feet, shaved legs.
Majocchi granuloma A 87-year-old male with two nodules on the L-forearm for 6 weeks. Initial impression was cutaneous malignancies. Diagnosis of Majocchi granuloma was made on lesional biopsy. Systemic terbinafine was given.