Clinical Manifestations

Tinea capitis is a dermatophyte infection of the scalp most often caused by Trichophyton tonsurans, occasionally by Microsporum canis, and, much less commonly, by other Microsporum and Trichophyton spp. It is particularly common in black children age 4-14 yr. In Microsporum and some Trichophyton infections, the spores are distributed in a sheath-like fashion around the hair shaft (ectothrix infection), whereas T. tonsurans produces an infection within the hair shaft (endothrix). Endothrix infections may continue past the anagen phase of hair growth into telogen and are more chronic than infections with ectothrix organisms that persist only during the anagen phase. T. tonsurans is an anthropophilic species acquired most often by contact with infected hairs and epithelial cells that are on such surfaces as theater seats, hats, and combs. Dermatophyte spores may also be airborne within the immediate environment, and high carriage rates have been demonstrated in noninfected schoolmates and household members. Microsporum canis is a zoophilic species that is acquired from cats and dogs.

The clinical presentation of tinea capitis varies with the infecting organism. Endothrix infections such as those caused by T. tonsurans create a pattern known as “black-dot ringworm,” characterized initially by many small circular patches of alopecia in which hairs are broken off close to the hair follicle (Fig. 658-3). Another clinical variant manifests as diffuse scaling, with minimal hair loss secondary. It strongly resembles seborrheic dermatitis, psoriasis, or atopic dermatitis (Fig. 658-4). T. tonsurans may also produce a chronic and more diffuse alopecia. Lymphadenopathy is common (Fig. 658-5). A severe inflammatory response produces elevated, boggy granulomatous masses (kerions), which are often studded with pustules (Fig. 658-6A). Fever, pain, and regional adenopathy are common, and permanent scarring and alopecia may result (Fig. 658-6B). The zoophilic organism M. canis or the geophilic organism Microsporum gypseum also may cause kerion formation. The pattern produced by Microsporum audouinii, the most common cause of tinea capitis in the 1940s and 1950s, is characterized initially by a small papule at the base of a hair follicle. The infection spreads peripherally, forming an erythematous and scaly circular plaque (ringworm) within which the infected hairs become brittle and broken. Numerous confluent patches of alopecia develop, and patients may complain of severe pruritus. M. audouinii infection is no longer common in the USA. Favus is a chronic form of tinea capitis that is rare in the USA and is caused by the fungus Trichophyton schoenleinii. Favus starts as yellowish red papules at the opening of hair follicles. The papules expand and coalesce to form cup-shaped, yellowish, crusted patches that fluoresce dull green under a Wood lamp.

Figure 658-3 Black-dot ringworm with hairs broken off at the scalp.

Figure 658-4 Tinea capitis mimicking seborrheic dermatitis.

Figure 658-5 Lymphadenopathy associated with tinea capitis.

Figure 658-6 A, Kerion. Boggy granulomatous mass of the scalp. B, Scarring after kerion.

Differential Diagnosis

Tinea capitis can be confused with seborrheic dermatitis, psoriasis, alopecia areata, trichotillomania, and certain dystrophic hair disorders. When inflammation is pronounced, as in kerion, primary or secondary bacterial infection must also be considered. In adolescents, the patchy, moth-eaten type of alopecia associated with secondary syphilis may resemble tinea capitis. If scarring occurs, discoid lupus erythematosus and lichen planopilaris must also be considered in the differential diagnosis.

The important diagnostic procedures for the various dermatophyte diseases include examination of infected hairs with a Wood lamp, microscopic examination of KOH preparations of infected material, and identification of the etiologic agent by culture. Hairs infected with common Microsporum spp. fluoresce a bright blue-green. Most Trichophyton-infected hairs do not fluoresce.

Microscopic examination of a KOH preparation of infected hair from the active border of a lesion discloses tiny spores surrounding the hair shaft in Microsporum infections and chains of spores within the hair shaft in T. tonsurans infections. Fungal elements are not usually seen in scales. A specific etiologic diagnosis of tinea capitis may be obtained by planting broken off infected hairs on Sabouraud medium with reagents to inhibit growth of other organisms. Such identification may require 2 wk or more.

Treatment

Oral administration of griseofulvin microcrystalline (20 mg/kg/24 hr) is the recommended treatment for all forms of tinea capitis. It may be necessary for 8-12 wk and should be terminated only after fungal culture results are negative. Treatment for 1 month after a negative culture result minimizes the risk of recurrence. Adverse reactions to griseofulvin are rare but include nausea, vomiting, headache, blood dyscrasias, phototoxicity, and hepatotoxicity. Oral itraconazole is useful in instances of griseofulvin resistance, intolerance, or allergy. Itraconazole is given for 4-6 wk at a dosage of 3-5 mg/kg/24 hr with food. Capsules are preferable to the syrup, which may cause diarrhea. Terbinafine is also effective at a dosage of 3-6 mg/kg/24 hr for 4-6 wk or possibly in pulse therapy, although it has limited activity against M. canis. Neither itraconazole nor terbinafine is approved by the U.S. Food and Drug Administration (FDA) for treatment of dermatophyte infections in the pediatric population. Topical therapy alone is ineffective, but it may be an important adjunct because it may decrease the shedding of spores. Asymptomatic dermatophyte carriage in family members is common. One in 3 families have at least 1 member who is a carrier. Therefore, treatment of both patient and potential carriers with a sporicidal shampoo may hasten clinical resolution. Vigorous shampooing with a 2.5% selenium sulfide, zinc pyrithione, or ketoconazole shampoo is helpful. It is not necessary to shave the scalp.

Clinical Manifestations

Tinea corporis, defined as infection of the glabrous skin, excluding the palms, soles, and groin, can be caused by most of the dermatophyte species, although T. rubrum and Trichophyton mentagrophytes are the most prevalent etiologic organisms. In children, infections with M. canis are also common. Tinea corporis can be acquired by direct contact with infected persons or by contact with infected scales or hairs deposited on environmental surfaces. M. canis infections are usually acquired from infected pets.

The most typical clinical lesion begins as a dry, mildly erythematous, elevated, scaly papule or plaque that spreads centrifugally and clears centrally to form the characteristic annular lesion responsible for the designation ringworm (Fig. 658-7). At times, plaques with advancing borders may spread over large areas. Grouped pustules are another variant. Most lesions clear spontaneously within several months, but some may become chronic. Central clearing does not always occur (Fig. 658-8), and differences in host response may result in wide variability in the clinical appearance—for example, granulomatous lesions called Majocchi granuloma due to penetration of organisms along the hair follicle to the level of the dermis, producing a fungal folliculitis and perifolliculitis (Fig. 658-9), and the kerion-like lesions referred to as tinea profunda. Majocchi granuloma is more common after inappropriate treatment with topical corticosteroids, especially the superpotent class.

Figure 658-7 Annular plaque of tinea corporis with central clearing.

Figure 658-8 Minimal central clearing with tinea corporis.

Figure 658-9 Follicular papule and pustule in Majocchi granuloma after use of a superpotent topical steroid.

Differential Diagnosis

Many skin lesions, both infectious and noninfectious, must be differentiated from the lesions of tinea corporis. Those most frequently confused are granuloma annulare, nummular eczema, pityriasis rosea, psoriasis, seborrheic dermatitis, erythema chronicum migrans, and tinea versicolor. Microscopic examination of KOH wet mount preparations and cultures should always be performed when fungal infection is considered. Tinea corporis usually does not fluoresce with a Wood lamp.

Treatment

Tinea corporis usually responds to treatment with one of the topical antifungal agents (e.g., imidazoles, terbinafine, naftifine) twice daily for 2-4 wk. In unusually severe or extensive disease, a course of therapy with oral griseofulvin microcrystalline may be required for 4 wk. Itraconazole has produced excellent results in many cases with a 1- to 2-wk course of oral therapy.

Clinical Manifestations

Tinea cruris, or infection of the groin, occurs most often in adolescent males and is usually caused by the anthropophilic species Epidermophyton floccosum or Trichophyton rubrum, but occasionally by the zoophilic species T. mentagrophytes.

The initial clinical lesion is a small, raised, scaly, erythematous patch on the inner aspect of the thigh. This spreads peripherally, often developing numerous tiny vesicles at the advancing margin. It eventually forms bilateral, irregular, sharply bordered patches with hyperpigmented scaly centers. In some cases, particularly in infections with T. mentagrophytes, the inflammatory reaction is more intense and the infection may spread beyond the crural region. The penis is usually not involved in the infection, an important distinction from candidosis. Pruritus may be severe initially but abates as the inflammatory reaction subsides. Bacterial superinfection may alter the clinical appearance, and erythrasma or candidosis may coexist. Tinea cruris is more prevalent in obese persons and in persons who perspire excessively and wear tight-fitting clothing.

Differential Diagnosis

The diagnosis of tinea cruris is confirmed by culture and by demonstration of septate hyphae on a KOH preparation of epidermal scrapings. The disorder must be differentiated from intertrigo, allergic contact dermatitis, candidosis, and erythrasma. Bacterial superinfection must be precluded when there is a severe inflammatory reaction.

Treatment

Patients should be advised to wear loose cotton underwear. Topical treatment with an imidazole is recommended for severe infection, especially because these agents are effective in mixed candidal-dermatophytic infections.

Clinical Manifestations

Tinea pedis (athlete’s foot), infection of the toe webs and soles of the feet, is uncommon in young children but occurs with some frequency in preadolescent and adolescent males. The usual etiologic agents are T. rubrum, T. mentagrophytes, and E. floccosum.

Most commonly, the lateral toe webs (3rd to 4th and 4th to 5th interdigital spaces) and the subdigital crevice are fissured, with maceration and peeling of the surrounding skin (Fig. 658-10). Severe tenderness, itching, and a persistent foul odor are characteristic. These lesions may become chronic. This type of infection may involve overgrowth by bacterial flora, including Kytococcus sedantarius, Brevibacterium epidermidis, and gram-negative organisms. Less commonly, a chronic diffuse hyperkeratosis of the sole of the foot occurs with only mild erythema (Fig. 658-11). In many cases, two feet and one hand are involved. This type of infection is more refractory to treatment and tends to recur. An inflammatory vesicular type of reaction may occur with T. mentagrophytes infection. This type is most common in young children. The lesions involve any area of the foot, including the dorsal surface, and are usually circumscribed. The initial papules progress to vesicles and bullae that may become pustular (Fig. 658-12). A number of factors, such as occlusive footwear and warm, humid weather, predispose to infection. Tinea pedis may be transmitted in shower facilities and swimming pool areas.

Figure 658-10 Interdigital tinea pedis.

Figure 658-11 Diffuse, minimally erythematous tinea pedis.

Figure 658-12 Vesicobullous tinea pedis.

Differential Diagnosis

Tinea pedis must be differentiated from simple maceration and peeling of the interdigital spaces, which is common in children. Infection with Candida albicans and various bacterial organisms (erythrasma) may cause confusion or may coexist with primary tinea pedis. Contact dermatitis, vesicular foot dermatitis, atopic dermatitis, and juvenile plantar dermatitis also simulate tinea pedis. Fungal mycelia can be seen on microscopic examination of a KOH preparation or by culture.

Treatment

Treatment for mild infections includes simple measures such as avoidance of occlusive footwear, careful drying between the toes after bathing, and the use of an absorbent antifungal powder such as zinc undecylenate. Topical therapy with an imidazole is curative in most cases. Each of these agents is also effective against candidal infection. Several weeks of therapy may be necessary, and low-grade, chronic infections, particularly those caused by T. rubrum, may be refractory. In refractory cases, oral griseofulvin therapy may effect a cure, but recurrences are common.

Clinical Manifestations

Tinea unguium is a dermatophyte infection of the nail plate. It occurs most often in patients with tinea pedis, but it may occur as a primary infection. It can be caused by a number of dermatophytes, of which T. rubrum and T. mentagrophytes are the most common.

The most superficial form of tinea unguium (i.e., white superficial onychomycosis) is due to T. mentagrophytes. It manifests as irregular single or numerous white patches on the surface of the nail unassociated with paronychial inflammation or deep infection. T. rubrum generally causes a more invasive, subungual infection that is initiated at the lateral distal margins of the nail and is often preceded by mild paronychia. The middle and ventral layers of the nail plate, and perhaps the nail bed, are the sites of infection. The nail initially develops a yellowish discoloration and slowly becomes thickened, brittle, and loosened from the nail bed (Fig. 658-13). In advanced infection, the nail may turn dark brown to black and may crack or break off.

Figure 658-13 Hyperkeratotic nail in onychomycosis.

Differential Diagnosis

Tinea unguium must be differentiated from various dystrophic nail disorders. Changes due to trauma, psoriasis, lichen planus, eczema, and trachyonychia can all be confused with tinea unguium. Nails infected with C. albicans have several distinguishing features, most prominently a pronounced paronychial swelling. Thin shavings taken from the infected nail, preferably from the deeper areas, should be examined microscopically with KOH and cultured. Repeated attempts may be required to demonstrate the fungus. Histologic evaluation of nail clippings with special stains for dermatophytes can be diagnostic.

The long half-life of itraconazole in the nail has led to promising trials of intermittent short courses of therapy (double the normal dose for 1 wk of each month for 3-4 mo). Oral terbinafine is also used for the treatment of onychomycosis. Terbinafine once daily for 12 weeks is more effective than itraconazole pulse therapy. Griseofulvin and application of topical fungistatic agents to the nail bed are often ineffective and are not recommended.