With the exceptions of tinea capitis and tinea unguium, which typically require systemic antifungal treatment, most tinea infections are diagnosed and treated in a similar fashion, and carry a similar prognosis.
The dictum “if it scales scrape it” is the guiding principle in diagnosing fungal infection. A simple KOH preparation revealing hyphae is diagnostic for dermatophytic or candidal infection. The clinical presentation is usually sufficient to distinguish between these two cases. Scales can also be cultured, either to distinguish between dermatophytic and candidal infection, or in cases of high clinical suspicion and a negative KOH test. Biopsy is not indicated. A Wood’s light exam is of no use in dermatophytic skin infection. However, it will cause fluorescence of infected scalp hairs in some varieties of tinea capitis.
Topical antifungal agents are the mainstay of treatment for localized dermatophytic infections. Imidazole agents, such as clotrimazole (e.g. Lotrimin) and miconazole (e.g. Micatin) are available over-the-counter, while others (e.g. econazole]) require a prescription. Other drugs (non-imidazoles) include naftitine (e.g. Naftin), terbinafine (e.g. Lamisil), and ciclopirox olamine (e.g. Loprox). The medication needs to be applied for 1 to 2 weeks after the lesions have cleared. For difficult to treat infections, such as refractory tinea pedis, suppressive therapy with an antifungal powder should be considered. For widespread disease or disease resistant to topical treatments, systemic therapy is required. Systemic therapy is also required for scalp or nail involvement. Effective oral antifungal agents include: griseofulvin, ketoconazole (e.g. Nizoral), itraconazole (e.g. Sporanox), fluconazole (e.g. Diflucan), and terbinafine (e.g. Lamisil). Note that Mycolog (active agent in Nystatin) is not effective against dermatophytic infections; it is only active against candida albicans.
Many acute dermatophytic infections resolve without treatment—probably due to cellular immunity provoked by dermatophyte antigens— but most benefit from a course of therapy. The degree of inflammation is, in fact, dependent on the character of the immune response. Persistent infections are attributed to a lack of immune response, either due to dermatophyte-specific immune deficiency, or because dermatophyte antigens remain superficial and fail to gain access to the vasculature. Dermatophyte infections do not penetrate beyond the epidermis. Complications, including secondary bacterial infection, are uncommon. However, interdigital tinea pedis can sometimes create a port of entry for bacteria, leading to lower extremity cellulitis.