Superficial Dermatophyte Infections of the Skin


Acknowledgments

The authors wish to acknowledge the work of previous edition authors Gregory Raugi and Thao U. Nguyen.

Abstract

Fungal infections of the skin can be divided into superficial and deep infections. The vast majority are superficial and are caused by dermatophytes, which invade only fully keratinized tissues (stratum corneum, hair, and nails). They are classified into three genera: Epidermophyton, Microsporum, and Trichophyton . Less frequent causes include nondermatophyte fungi (e.g., Malassezia furfur in tinea versicolor) and Candida species. In naming clinical dermatophyte infections, traditionally tinea precedes the Latin name of the involved body region. Superficial fungal infections are divided into tinea barbae, tinea capitis, tinea corporis, tinea faciei, tinea manus, tinea pedis, tinea cruris, tinea unguium, tinea versicolor, and cutaneous candidiasis.

Disease Burden

Dermatophyte infections are among the most common dermatologic conditions and are frequently refractory to treatment, leading to recurrence. In 2010, fungal skin diseases were the fourth most common of all diseases worldwide. The prevalence varies across the age spectrum; men are more likely to be affected than women. With the exception of tinea capitis, which primarily affects prepubertal children, the vast majority of dermatophytoses occur in adult hosts. Although dermatophytes rarely undergo deep local invasion and systemic dissemination, they can cause considerable morbidity, particularly in immunocompromised hosts.

Pathogenesis and Risk Factors

Dermatophytes are not endogenous pathogens. Transmission can occur directly from person to person (anthropophilic organisms), animal to person (zoophilic organisms), and soil to person (geophilic organisms) as well as from fomites like hair brushes and hats. Infective spores in dermal scales and hair can remain viable for months to years. Once the infectious elements of the fungus (arthroconidia) enter the skin, they germinate and invade the superficial skin layers. Dermatophytosis may cause defects in the skin barrier, which serve as a portal of entry to bacterial infections such as cellulitis. Disease severity is affected by several factors: sebum (which has an inhibitory effect on dermatophytes), the cutaneous barrier, genetic susceptibility to certain fungal infections, and the host’s immune system.

Clinical Features

Tinea Barbae

Tinea barbae, also known as tinea sycosis and barber’s itch , is an uncommon infection that involves the terminal hairs and skin in the beard and mustache area of adult men. The lesions can be divided into deep and superficial. The deep type, sometimes known as tinea barbae profunda, tends to be more severe, nodular, and suppurative and is often caused by zoophilic dermatophytes, namely Trichophyton mentagrophytes and Trichophyton verrucosum . The superficial type may cause crusted, partially bald patches with folliculitis; Trichophyton rubrum and Trichophyton violaceum are usually the causative organisms. Reversible alopecia may sometimes be seen accompanying these lesions. Farm workers are most often affected because the causative organisms are usually zoophilic dermatophytes. Autoinoculation may also occur after minor trauma or from a razor blade while shaving. The use of topical steroids may play a role as well.

The differential diagnosis includes bacterial folliculitis (due to Staphylococcus aureus ), furuncle or carbuncle, perioral dermatitis, pseudofolliculitis barbae, contact dermatitis, and herpes simplex. The clinical diagnosis can be confirmed using microscopy to examine potassium hydroxide (KOH) of plucked hair or a biopsy specimen.

Tinea barbae is treated with systemic antifungal therapy. Common regimens in adults include terbinafine 250 mg/day, itraconazole 200 mg/day, griseofulvin 500 mg twice daily, and fluconazole 150 mg once weekly. Treatment is continued for 2 to 3 weeks after lesion resolution. Topical agents are helpful only as adjunctive therapy.

Tinea Capitis

Tinea capitis is an infection of the scalp and hair shafts. It is most common in children and more common in boys than girls. Poor hygiene and overcrowding can foster transmission, which can occur through inanimate objects such as hats, brushes, and pillowcases. In the United States, 90% to 95% of tinea scalp infection is caused by the anthropophilic dermatophyte Trichophyton tonsurans , which does not fluoresce. Before 1950, fluorescent Microsporum species were the most common cause. KOH, fungal culture, and Wood lamp examination can be used for diagnostic testing. Tinea capitis begins with a small papule, which spreads to form scaly, irregular, or well-demarcated areas of alopecia. “Black dot” alopecia is produced when swollen hairs fracture a few millimeters from the scalp. Cervical and occipital lymphadenopathy may be prominent. A boggy, sterile inflammatory mass known as a kerion may also be seen, which can result in permanent alopecia if not treated promptly.

There are many scalp and hair conditions that lead to scaling or alopecia (scarring and nonscarring) that are not caused by fungal infections. When scaling and inflammation are prominent, diagnoses to be ruled out include atopic dermatitis, seborrheic dermatitis, and psoriasis. When alopecia is prominent, other diagnoses to consider include alopecia areata, traction alopecia, and trichotillomania.

Systemic antifungal therapy is required to penetrate the hair follicles. Griseofulvin 20 to 25 mg/kg/day for 8 weeks is commonly recommended ( Fig. 22.1 ). Several other agents—including itraconazole, terbinafine, and fluconazole—have been reported as effective and safe. They allow a shorter course of treatment and can be used in patients with griseofulvin allergy or in recalcitrant cases. Terbinafine may be more effective in cases due to T. tonsurans, whereas griseofulvin is likely more effective in cases due to M. canis. Preventive measures are also important, because the disease is contagious; all individuals residing with the infected patient should be evaluated and appropriately treated. Adjunctive topical therapy with antifungal shampoo, such as 2% ketoconazole or 2.5% selenium sulfide, may be useful to decrease shedding of viable fungi and spores.

Clinical Vignette

A 52-year-old man presented with an itchy rash on his left wrist, which had been present for 3 months. He had treated it with over-the-counter hydrocortisone with minimal improvement, and the lesions appeared to be spreading. His skin exam was notable for a 5-cm area of affected skin containing erythematous scaly papules with admixed pustules. KOH examination of the affected area reveals fungal hyphae. A diagnosis of Majocchi granuloma, a superficially invasive dermatophyte infection usually caused by T. rubrum , was made. Patients with Majocchi granuloma often have a history of corticosteroid use, minor trauma, immunosuppression, and/or of onychomycosis or tinea corporis. A KOH examination is not always positive; if it is negative, a skin biopsy with fungal staining may be required to make the diagnosis. Systemic antifungal treatment is necessary. Example regimens include terbinafine 250 mg PO daily for 4 weeks.

Fig. 22.1, Managing tinea capitis.

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