|
Dermatophytoses
are fungal infections of keratin in the skin and nails (nail infection
is called tinea unguium—see Nail Disorders: Onychomycosis). Symptoms and signs vary by site of infection.
Diagnosis is by clinical appearance and by examination of skin scrapings
on potassium hydroxide wet mount. Treatment varies by site but always
involves topical or oral antifungal drugs.
Dermatophytes are molds that require keratin for nutrition and must live on stratum corneum, hair, or nails to survive. Human infections are caused by Epidermophyton, Microsporum, and Trichophyton spp. These differ from candidiasis in that they are rarely if ever invasive. Transmission is person-to-person, animal-to-person, and rarely, soil-to-person. The organism may persist indefinitely. Most people do not develop clinical infection; those who do may have impaired T-cell responses from an alteration in local defenses (eg, from trauma with vascular compromise) or from primary (hereditary) or secondary (eg, diabetes, HIV) immunosuppression.
Symptoms and Signs
Symptoms and signs vary by site (skin, hair, nails). Organism virulence and host susceptibility and hypersensitivity determine severity. Most often, there is little or no inflammation; asymptomatic or mildly itching lesions with a scaling, slightly raised border remit and recur intermittently. Occasionally, inflammation is more severe and manifests as sudden vesicular or bullous disease (usually of the foot) or as an inflamed boggy lesion of the scalp (kerion).
Diagnosis
Diagnosis is based on clinical appearance and site of infection and confirmed by skin scrapings and demonstration of hyphae on potassium hydroxide (KOH) wet mount. Identification of specific organisms by culture is unnecessary except for scalp infection (where an animal source may be identified and treated) and nail infection (which may be caused by a nondermatophyte). Culture may also be useful when overlying inflammation and bacterial infection are severe and/or accompanied by alopecia.
Differential diagnosis includes
Treatment
Topical antifungals are generally adequate (see Table 1: Fungal Skin Infections: Options for Treatment of Superficial Fungal Infections* ). In general, OTC terbinafine is best; econazole or ciclopirox may be better if candidal infection cannot be excluded. Oral antifungals are used for most nail and scalp infections, resistant skin infections, and patients unwilling or unable to adhere to prolonged topical regimens; doses and duration differ by site of infection.
Corticosteroid creams can be used to help relieve itching and pain for the first few days. Low-dose hydrocortisone can be applied separately, or more potent corticosteroids may be added to the antifungal cream. Oral corticosteroids are occasionally used for treatment of severe inflammatory lesions.
Tinea
Barbae
Tinea barbae
(barber's itch) is a dermatophyte infection of the beard area most
often caused by Trichophyton mentagrophytes or T.
verrucosum.
Tinea barbae presents as superficial annular lesions, but deeper infection similar to folliculitis may occur. It may also occur as an inflammatory kerion that can result in scarring hair loss. Diagnosis is by KOH wet mount, culture, or biopsy.
Treatment is micronized griseofulvin 500 mg to 1 g po once/day until 2 to 3 wk after clinical clearance. Terbinafine 250 mg po once/day and itraconazole 200 mg po once/day have also been used. If the lesions are severely inflamed, a short course of prednisone should be added (to lessen symptoms and perhaps reduce the chance of scarring), starting with 40 mg po once/day (for adults) and tapering the dose over 2 wk.
Tinea
Capitis
Tinea capitis
(scalp ringworm) is a dermatophyte infection of the scalp.
Tinea capitis mainly affects children, is contagious, and can be epidemic. Trichophyton
tonsurans is the most common cause in the US, followed by Microsporum canis and M.
audouinii; other Trichophyton sp (eg, T. schoenleinii, T.
violaceum) are common elsewhere.
Tinea capitis causes the gradual appearance of round patches of dry scale, alopecia, or both. T.
tonsurans infection causes “black dot ringworm,” in which hair shafts break at the scalp surface; M.
audouinii infection causes “gray patch ringworm,” in which hair shafts break above the surface, leaving short stubs. Tinea capitis less commonly manifests as diffuse scaling, like dandruff, or in a diffuse pustular pattern.
Kerion:
Dermatophyte infection occasionally leads to formation of a kerion, which is a large, boggy, inflammatory scalp mass caused by a severe inflammatory reaction to the dermatophyte. A kerion may have pustules and crusting and can be mistaken for an abscess. A kerion may result in scarring hair loss.
Diagnosis
Tinea capitis is diagnosed by clinical appearance and by KOH wet mount of plucked hairs or of hairs and scale obtained by scraping or brushing. Spore size and appearance inside (endothrix) or outside (ectothrix) the hair shaft distinguish organisms and can help guide treatment. Blue-green fluorescence during Wood's light examination is diagnostic for infection with M. canis and M.
audouinii and can distinguish tinea from erythrasma.
Differential diagnosis of tinea capitis includes
Treatment
Children are treated with micronized griseofulvin suspension 10 to 20 mg/kg po once/day (doses vary by several parameters, but maximum dose is generally 1 g/day) or, if > 2 yr, with ultramicronized griseofulvin 5 to 10 mg/kg (maximum 750 mg/day) po once/day or in 2 divided doses with meals or milk for 4 to 6 wk or until all signs of infection are gone. Terbinafine also may be used; children < 20 kg are given 62.5 mg once/day; those 20 to 40 kg, 125 mg once/day, and those > 40 kg, 250 mg once/day. An imidazole or ciclopirox cream should be applied to the scalp to prevent spread, especially to other children, until tinea capitis is cured; selenium sulfide 2.5% shampoo should also be used at least twice/wk. Children may attend school during treatment.
Adults are treated with terbinafine 250 mg po once/day for 2 to 4 wk, which is more effective for endothrix infections, or itraconazole 200 mg once/day for 2 to 4 wk or 200 mg bid given for 1 wk, followed by 3 wk without the drug (pulsed) for 2 to 3 mo.
For severely inflamed lesions and for kerion, a short course of prednisone should be added (to lessen symptoms and perhaps reduce the chance of scarring), starting with 40 mg po once/day (1 mg/kg for children) and tapering the dose over 2 wk.
Tinea Corporis
Tinea corporis
(body ringworm) is a dermatophyte infection of the face, trunk,
and extremities.
Common causes are T.
mentagrophytes, T. rubrum, and M. canis.
Tinea corporis causes pink-to-red annular patches and plaques with raised scaly borders that expand peripherally and tend to clear centrally. A variant form appears as nummular scaling patches studded with small papules or pustules.
Differential diagnosis includes
Treatment
Treatment of mild-to-moderate lesions is an imidazole, ciclopirox , naftifine , or terbinafine in cream, lotion, or gel. The drug should be rubbed in bid continuing at least 7 to 10 days after lesions disappear, typically at about 2 to 3 wk.
Extensive and resistant lesions occur in patients infected with T. rubrum and in people with debilitating systemic diseases. For such cases, the most effective therapy is oral itraconazole 200 mg once/day or terbinafine 250 mg once/day for 2 to 3 wk.
Tinea
Cruris
Tinea cruris
(jock itch) is a dermatophyte infection of the groin.
Common organisms include T.
rubrum or T. mentagrophytes. The primary risk factors are associated with a moist environment (ie, warm weather, wet and restrictive clothing, obesity causing constant apposition of skin folds). Men are affected more than women because of apposition of the scrotum and thigh.
Typically, a pruritic, ringed lesion extends from the crural fold over the adjacent upper inner thigh. Infection may be bilateral. Lesions may be complicated by maceration, miliaria, secondary bacterial or candidal infection, and reactions to treatment. In addition, scratch dermatitis and lichenification can occur. Recurrence is common because fungi may repeatedly infect susceptible people. Flare-ups occur more often during summer.
Differential diagnosis includes
Scrotal involvement is usually absent or slight; by contrast, the scrotum is often inflamed in candidal intertrigo or lichen simplex chronicus.
Treatment
Treatment is with topical antifungal cream or lotion. Choices include terbinafine , miconazole , clotrimazole , ketoconazole , econazole , naftifine , and ciclopirox applied bid for 10 to 14 days. Itraconazole 200 mg po once/day or terbinafine 250 mg po once/day for 3 to 6 wk may be needed in patients who have refractory, inflammatory, or widespread infections.
Tinea
Pedis
Tinea pedis
(athlete's foot) is a dermatophyte infection of the feet.
Tinea pedis is the most common dermatophytosis because moisture from foot sweating facilitates fungal growth. Tinea pedis may occur as any of 4 clinical forms or in combination:
Chronic
hyperkeratotic tinea pedis due to T. rubrum causes a distinctive pattern of lesion, manifesting as scaling and thickening of the soles, which often extends beyond the plantar surface in a moccasin distribution. Differential diagnosis is sterile maceration (due to hyperhidrosis and occlusive footgear), contact dermatitis (due to type IV delayed hypersensitivity to various materials in shoes, particularly adhesive cement, thiuram compounds in footwear that contains rubber, and chromate tanning agents used in leather footwear), irritant dermatitis, and psoriasis.
Chronic intertriginous tinea pedis is characterized by scaling, erythema, and erosion of the interdigital and subdigital skin of the feet, most commonly affecting the lateral 3 toes.
Acute ulcerative tinea pedis (most often caused by T. mentagrophytes, var. interdigitale) typically begins in the 3rd and 4th interdigital spaces and extends to the lateral dorsum and/or the plantar surface of the arch. These toe web lesions are usually macerated and have scaling borders. Secondary bacterial infection, cellulitis, and lymphangitis are common complications.
Vesiculobullous tinea pedis, in which vesicles develop on the soles and coalesce into bullae, is the less common result of a flare of interdigital tinea pedis; risk factors are occlusive shoes and environmental heat and humidity.
Diagnosis
Diagnosis is usually obvious based on clinical examination and review of risk factors.
Treatment
The safest treatment is topical antifungals, but recurrence is common and treatment must often be prolonged. Alternatives that provide a more durable response include itraconazole 200 mg po once/day for 1 mo (or pulse therapy with 200 mg bid 1 wk/mo for 1 to 2 mo) and terbinafine 250 mg po once/day for 2 to 6 wk. Concomitant topical antifungal use may reduce recurrences.
Moisture reduction on the feet and in footwear is necessary for preventing recurrence. Permeable or open-toe footwear and sock changes are important especially during warm weather. Interdigital spaces should be manually dried after bathing. Drying agents are also recommended; options include antifungal powders (eg, miconazole ), gentian violet, Burow's solution (5% aluminum subacetate) soaks bid, and 20 to 25% aluminum chloride hexahydrate powder once/day.
Dermatophytid
Reaction
Dermatophytid
is an inflammatory reaction to dermatophytosis at a cutaneous site
distant from the primary infection.
Dermatophytid (identity or “id”) reactions are protean; they are not related to localized growth of the fungus but rather are an inflammatory reaction elsewhere on the body. Lesions are typically pruritic but may manifest as
Distribution may be extensive. Diagnosis is by KOH wet mounts that are negative at the site of the id reaction and positive at the distant site of dermatophyte infection.
Treatment of the primary infection cures dermatophytid; pending cure, topical corticosteroids and/or antipruritics (eg, hydroxyzine 25 mg qid) can be used to relieve symptoms.
Last full review/revision August 2008 by A. Damian Dhar, MD, JD
Content last modified August 2008
| 
