Dermatophyte infections - Practical Therapeutics

Author: Barry L. Hainer
Date: Jan 1, 2003

The dryness of the skin's outer layer discourages colonization by microorganisms, and the shedding of epidermal cells keeps many microbes from establishing residence. (1) However, the skin's mechanisms of protection may fail because of trauma, irritation, or maceration. Furthermore, occlusion of the skin with nonporous materials can interfere with the skin's barrier function by increasing local temperature and hydration. (2) With inhibition or failure of the skin's protective mechanisms, cutaneous infection may occur.

Microsporum, Trichophyton, and Epidermophyton species are the most common pathogens in skin infections. Less frequently, superficial skin infections are caused by nondermatophyte fungi (e.g., Malassezia furfur in tinea [pityriasis] versicolor) and Candida species. This article reviews the diagnosis and treatment of common dermatophyte infections.

Dermatophytoses

Because dermatophytes require keratin for growth, they are restricted to hair, nails, and superficial skin. Thus, these fungi do not infect mucosal surfaces. Dermatophytoses are referred to as "tinea" infections. They are also named for the body site involved.

Some dermatophytes are spread directly from one person to another (anthropophilic organisms). Others live in and are transmitted to humans from soil (geophilic organisms), and still others spread to humans from animal hosts (zoophilic organisms). Transmission of dermatophytes also can occur indirectly from fomites (e.g., upholstery, hairbrushes, hats).

Anthropophilic organisms are responsible for most fungal skin infections. Transmission can occur by direct contact or from exposure to desquamated cells. Direct inoculation through breaks in the skin occurs more often in persons with depressed cell-mediated immunity. Once fungi enter the skin, they germinate and invade the superficial skin layers.

In patients with dermatophytoses, physical examination may reveal a characteristic pattern of inflammation, termed an "active" border (Figure 1). The inflammatory response is usually characterized by a greater degree of redness and scaling at the edge of the lesion or, occasionally, blister formation. Central clearing of the lesion may be present and distinguishes dermatophytoses from other papulosquamous eruptions such as psoriasis or lichen planus, in which the inflammatory response tends to be uniform over the lesion (Figure 2).

The location of the lesions also can help identify the pathogen. A dermatophytosis can most likely be ruled out if a patient has mucosal involvement with an adjacent red, scaly skin rash. In this situation, the more probable diagnosis is a candidal infection such as perleche (if single or multiple fissures are present in the corners of the mouth) or vulvovaginitis or balanitis (if lesions are present in the genital mucosa).

Potassium hydroxide (KOH) microscopy aids in visualizing hyphae and confirming the diagnosis of dermatophyte infection. Other diagnostic modalities include Wood's lamp examination, fungal culture, and skin or nail biopsy (Table 1). (2,3)

Tinea Capitis

Tinea capitis, the most common dermatophytosis in children, is an infection of the scalp and hair shafts. (4) Transmission is fostered by poor hygiene and overcrowding, and can occur through contaminated hats, brushes, pillowcases, and other inanimate objects. After being shed, affected hairs can harbor viable organisms for more than one year.

Tinea capitis is characterized by irregular or well-demarcated alopecia and scaling. When swollen hairs fracture a few millimeters from the scalp, "black dot" alopecia is produced. Tinea scalp infection also may result in a cell-mediated immune response termed a "kerion," which is a boggy, sterile, inflammatory scalp mass. Cervical and occipital lymphadenopathy may be prominent.

Before 1950, most tinea capitis cases in North America were caused by fluorescent Microsporum species (bright blue-green). Today, about 90 to 95 percent of tinea scalp infections in adults and children are caused by Trichophyton tonsurans, which does not fluoresce. (4,5) Therefore, Wood's lamp examination has become a less useful diagnostic test for tinea capitis.

Tinea capitis is generally identified by the presence of branching hyphae and spores on KOH microscopy (Table 1). If hyphae and spores are not visualized, Wood's lamp examination can be performed. If KOH microscopy and Wood's lamp examinations are negative, fungal culture may be considered when tinea capitis is strongly suspected.

Alternatively, clinical features can point to the diagnosis. In one study, (6) tinea capitis was confirmed by culture in 92 percent of children who had at least three of the following clinical features: scalp scaling, scalp pruritus, occipital adenopathy, and diffuse, patchy, or discrete alopecia.

When scaling and inflammation are prominent, other diagnoses to consider include seborrheic dermatitis (no hair loss), atopic dermatitis (lesions in flexural folds of the neck, arms, or legs), and psoriasis (nail changes and silvery scales on the knees or elbows). When alopecia is prominent, diagnoses to rule out include alopecia areata (complete, rather than patchy, hair loss), traction alopecia (history of tight hair braiding), and trichotillomania (hairs of differing lengths and a history of obsessive hair manipulation).

Topical treatment is not effective for tinea capitis. Systemic antifungal therapy is required to penetrate the hair follicles. Griseofulvin (Grisactin, Gris-PEG) is the only agent that the U.S. Food and Drug Administration (FDA) has labeled for the treatment of tinea capitis. Although griseofulvin remains the gold standard, (7) it is a less than ideal agent for several reasons (8,9): resistant organisms require dosage increases to effect a cure; treatment must be continued for six to 12 weeks; relapse rates are high because of rapid clearance of the drug from the skin with the cessation of therapy; and the liquid form for young children is a bitter-tasting solution.

Compared with griseofulvin, ketoconazole (Nizoral) is no more effective and has the potential for adverse hepatic effects and drug interactions. (10) In one study involving a small number of children, treatment with itraconazole (Sporanox), in a dosage of 3 to 5 mg per kg per day for four weeks, resulted in clinical and mycologic cure rates of 90 to 100 percent. (11) [Evidence level B, nonrandomized clinical trial] Fluconazole (Diflucan) and terbinafine (Lamisil) are promising agents; randomized, comparative studies with griseofulvin should clarify their role in the treatment of tinea capitis. (12) One randomized trial (13) in patients with tinea capitis caused by Trichophyton species showed that treatment with terbinafine, fluconazole, or itraconazole for two weeks was as effective as six weeks of griseofulvin therapy.

Adjunctive topical therapy with selenium sulfide (e.g., Exsel), ketoconazole, or povidone iodine (Betadine) lotion or shampoo (applied for five minutes twice weekly) is useful to decrease shedding of viable fungi and spores (12,14,15); over-the-counter 1 percent selenium sulfide shampoo works as well as the prescription 2.5 percent strength. (15) [Reference 15: Evidence level A, randomized controlled trial (RCT)]

Tinea Corporis

Tinea corporis, or ringworm, typically appears as single or multiple, annular, scaly lesions with central clearing, a slightly elevated, reddened edge, and sharp margination (abrupt transition from abnormal to normal skin) on the trunk, extremities, or face (Figure 1). The border of the lesion may contain pustules or follicular papules. Itching is variable.

The diagnosis of tinea corporis is based on clinical appearance and KOH examination of skin scrapings from the active edge. The differential diagnosis includes nummular eczema, pityriasis rosea, Lyme disease, tinea versicolor, contact dermatitis, granuloma annulare, and psoriasis (Figure 2).

Previous topical corticosteroid use can alter the appearance of the lesions, so that raised edges with central clearing are not present. Corticosteroid use may also be a factor in the development of Majocchi's granuloma, a deep follicular tinea infection that usually involves the legs and is more common in women. (3)

Treatment of tinea corporis usually consists of measures to decrease excessive skin moisture and the use of topical antifungal creams (Table 2). (16-19) Rarely, widespread infections may require systemic therapy.

Tinea Barbae

Tinea barbae involves the skin and coarse hairs of the beard and mustache area. This dermatophyte infection occurs in adult men and hirsute women. Because the usual cause is a zoophilic organism, farm workers are most often affected. Tinea barbae may cause scaling, follicular pustules, and erythema (Figure 3).

(18.) Shear NH, Einarson TR, Arikian SR, Doyle JJ, van Assche D. Pharmacoeconomic analysis of topical treatments for tinea infections. Int J Dermatol 1998;37:64-71.

(19.) Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea infections. Am Fam Physician 1998;58:163-74,177-8.

(20.) Zuber TJ, Baddam K. Superficial fungal infection of the skin. Where and how it appears help determine therapy. Postgrad Med 2001;109(1):117-20,123-6,131-2.

(21.) Goldstein AO, Smith KM, Ives TJ, Goldstein B. Mycotic infections. Effective management of conditions involving the skin, hair, and nails. Geriatrics 2000;55:40-2,45-7,51-2.

(22.) Gupta AK, Jain HC, Lynde CW, Watteel GN, Summerbell RC. Prevalence and epidemiology of unsuspected onychomycosis in patients visiting dermatologists' offices in Ontario, Canada--a multicenter survey of 2,001 patients. Int J Dermatol 1997; 36:783-7.

(23.) Rodgers P, Bassler M. Treating onychomycosis. Am Fam Physician 2001;63:663-72,677-8.

(24.) Lawry MA, Haneke E, Strobeck K, Martin S, Zimmer B, Romano PS. Methods for diagnosing onychomycosis: a comparative study and review of the literature. Arch Dermatol 2000;136:1112-6.

(25.) Mehregan DR, Gee SL. The cost effectiveness of testing for onychomycosis versus empiric treatment of onychodystrophies with oral antifungal agents. Cutis 1999;64:407-10.

(26.) Gupta AK, Fleckman P, Baran R. Ciclopirox nail lacquer topical solution 8% in the treatment of toenail onychomycosis. J Am Acad Dermatol 2000;43(4 suppl):S70-80.

(27.) Harrell TK, Necomb WW, Replogle WH, King DS, Noble SL. Onychomycosis: improved cure rates with itraconazole and terbinafine. J Am Board Fam Pract 2000;13:268-73.

Members of various family practice departments develop articles for "Practical Therapeutics." This article is one in a series coordinated by the Department of Family Medicine at the Medical University of South Carolina. Guest editor of the series is William J. Hueston, M.D.

BARRY L. HAINER, M.D., is professor of family medicine and director of the clinical services division in the Department of Family Medicine at the Medical University of South Carolina, Charleston. Dr. Hainer received his medical degree from Georgetown University School of Medicine, Washington, D.C., and completed a family medicine residency at the Medical University of South Carolina.

Address correspondence to Barry L. Hainer, M.D., Department of Family Medicine, Medical University of South Carolina, P.O. Box 250192, Charleston, SC 29425 (e-mail: hainerbl@musc.edu). Reprints are not available from the author.

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