Chapter 658 Cutaneous Fungal Infections
Tinea Versicolor
A common, innocuous, chronic fungal infection of the stratum corneum, tinea versicolor is caused by the dimorphic yeast Malassezia globosa. The synonyms Pityrosporum ovale and Pityrosporum orbiculare were used previously to identify the causal organism.
Etiology
M. globosa is part of the indigenous flora, predominantly in the yeast form, and is found particularly in areas of skin that are rich in sebum production. Proliferation of filamentous forms occurs in the disease state. Predisposing factors include a warm, humid environment, excessive sweating, occlusion, high plasma cortisol levels, immunosuppression, malnourishment, and genetically determined susceptibility. The disease is most prevalent in adolescents and young adults.
Clinical Manifestations
The lesions of tinea versicolor vary widely in color. In white individuals, they are typically reddish brown, whereas in black individuals they may be either hypopigmented or hyperpigmented. The characteristic macules are covered with a fine scale. They often begin in a perifollicular location, enlarge, and merge to form confluent patches, most commonly on the neck, upper chest, back, and upper arms (Fig. 658-1). Facial lesions are common in adolescents; lesions occasionally appear on the forearms, dorsum of the hands, and pubis. There may be little or no pruritus. Involved areas do not tan after sun exposure. A papulopustular perifollicular variant of the disorder may occur on the back, chest, and sometimes the extremities.
Differential Diagnosis
Examination with a Wood lamp discloses a yellowish gold fluorescence. A potassium hydroxide (KOH) preparation of scrapings is diagnostic, demonstrating groups of thick-walled spores and myriad short, thick, angular hyphae resembling macaroni and meatballs. Skin biopsy, including culture and special stains for fungi (periodic acid–Schiff), are often necessary to make the diagnosis in cases of primarily follicular involvement. Microscopically, organisms and keratinous debris can be seen within dilated follicular ostia.
Tinea versicolor must be distinguished from dermatophyte infections, seborrheic dermatitis, pityriasis alba, and secondary syphilis. Tinea versicolor may mimic nonscaling pigmentary disorders, such as postinflammatory pigmentary change, if a patient has removed the scales by scrubbing. M. globosa folliculitis must be distinguished from the other forms of folliculitis.
Treatment
Many therapeutic agents can be used to treat this disease successfully. The causative agent, a normal human saprophyte, is not eradicated from the skin, however, and the disorder recurs in predisposed individuals. Appropriate topical therapy may include one of the following: a selenium sulfide suspension applied overnight for 1 wk followed by 1 night per wk for 4 wk; an imidazole or terbinafine cream may be used twice daily for 2-4 wk. Oral therapy may be more convenient and may be achieved successfully with ketoconazole or fluconazole, 400 mg, repeated in 1 wk, or itraconazole, 200 mg/24 hr for 5-7 days. Recurrent episodes continue to respond promptly to these agents. Maintenance therapy with selenium sulfide applied overnight once a week may be used.
Dermatophytoses
Dermatophytoses are caused by a group of closely related filamentous fungi with a propensity for invading the stratum corneum, hair, and nails. The 3 principal genera responsible for infections are Trichophyton, Microsporum, and Epidermophyton.
Etiology
Trichophyton spp. cause lesions of all keratinized tissue, including skin, nails, and hair. T Trichophyton rubrum is the most common dermatophyte pathogen. Microsporum spp. principally invade the hair, and the Epidermophyton spp. invade the intertriginous skin. Dermatophyte infections are designated by the word tinea followed by the Latin word for the anatomic site of involvement. The dermatophytes are also classified according to source and natural habitat. Fungi acquired from the soil are called geophilic. They infect humans sporadically, inciting an inflammatory reaction. Dermatophytes that are acquired from animals are zoophilic. Transmission may be through direct contact or indirectly by infected animal hair or clothing. Infected animals are frequently asymptomatic. Dermatophytes acquired from humans are referred to as anthropophilic. These infestations range from chronic low-grade to acute inflammatory disease. Epidermophyton infections are transmitted only by humans, but various species of Trichophyton and Microsporum can be acquired from both human and nonhuman sources.
Epidemiology
Host defense has an important influence on the severity of the infection. Disease tends to be more severe in individuals with diabetes mellitus, lymphoid malignancies, immunosuppression, and states with high plasma cortisol levels, such as Cushing syndrome. Some dermatophytes, most notably the zoophilic species, tend to elicit more severe, suppurative inflammation in humans. Some degree of resistance to re-infection is acquired by most infected persons and may be associated with a delayed hypersensitivity response. No relationship has been demonstrated, however, between antibody levels and resistance to infection. The frequency and severity of infection are also affected by the geographic locale, the genetic susceptibility of the host, and the virulence of the strain of dermatophyte. Additional local factors that predispose to infection include trauma to the skin, hydration of the skin with maceration, occlusion, and elevated temperature.
Occasionally, a secondary skin eruption, referred to as a dermatophytid or “id” reaction, appears in sensitized individuals and has been attributed to circulating fungal antigens derived from the primary infection. The eruption is characterized by grouped papules (Fig. 658-2) and vesicles and, occasionally, by sterile pustules. Symmetric urticarial lesions and a more generalized maculopapular eruption also can occur. Id reactions are most often associated with tinea pedis but also occur with tinea capitis.
Tinea Capitis
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.
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