Tinea capitis, or "ringworm" of the scalp, presents itself as one or more sharply marginated plaques of partial alopecia. Inflammation and scale are present, but often these two changes are quite minimal. The recognition of broken hairs (stubble and black dots at the follicular orifices) is the best clue to correct diagnosis.
Nearly all cases occur in children, but the diagnosis should be considered in any adult presenting with evidence of localized alopecia . Kerion formation is a complication that occurs in about 10% of cases. This represents a sensitization phenomenon whereby the fungi induce a remarkably brisk inflammatory reaction with resulting pustulation, crusting, and edema formation. Wood's lamp examination does not reveal fluorescence in the most common forms of tinea capitis or in kerion formation. Unfortunately, KOH preparations are difficult for the inexperienced to interpret. For this reason, any suspected diagnosis requires the plucking of infected hairs for fungal culture.
Course and Prognosis
Tinea capitis and zoophilic tinea corporis usually resolve spontaneously after 6 to 12 months of activity. Tinea pedis, tinea cruris, and anthropophilic tinea corporis continue indefinitely. There are, however, periods of relative quiescence and exacerbation. All of these fungal diseases respond well to treatment, but with the exception of tinea capitis and zoophilic tinea corporis infections, recurrence following treatment is rather likely.
Pathogenesis
Tinea pedis, tinea cruris, and anthropophilic tinea corporis are most commonly caused by Trichophyton rulnum. Trichophyton interdigitate and Epidermophhyton floccoswn infections are also seen. Generally, one cannot predict the causative organism on the basis of clinical appearance. Zoophilic tinea corporis can be caused by Microsporum canis, Trichophyton mentagrophytes, and Trichophyton verrucosum. Tinea capitis is caused by Trichophyton tonsurans in 90% of cases.
The likelihood of inoculation with any of these fungi is enhanced if cuts and scratches are present on the skin. Clinical evidence of infection following inoculation is enhanced by the presence of warmth and moisture, such as occurs in the groin and under footwear. Depression of cell-mediated immune responsiveness, as in atopic patients, is a major predisposing factor for the development of T. rubrum infection.
Therapy
Tinea cruris and those cases of tinea pedis that involve only the web spaces can be treated with any of the topical antifungal agents. Other forms of tinea pedis usually require the use of griseofulvin. Mild cases of tinea corporis also respond well to topical agents. Extensive disease and those cases with a component of follicular involvement are best treated with griseofulvin. Tinea capitis requires the use of griseofulvin. Orally administered ketoconazole therapy is rarely appropriate for either tinea corporis or capitis. Kerion on nation, if present, can be treated with intralesional steroid injections or with a short burst of systemically administered steroids.
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