Tinea pedis or athlete’s foot is the most common fungal infection. It is seen most in those who wear occlusive footwear because shoes promote warmth and sweating, which encourage fungal growth. Tinea must be differentiated from allergic and irritant contact dermatitis (see Chapter 160). In several studies, application of the allylamine terbinafine bid resulted in a higher cure rate than twice-daily application of the imidazole clotrimazole, and at a quicker rate (1 week vs. 4 weeks).

All superficial dermatophytes of the skin, except those involving the scalp, beard, face, hands, feet, groin, and nails, are known as tinea corporis, or ringworm of the body. Contact with pets is often the source of the infection. Systemic diseases (e.g., diabetes, leukemia, acquired immunodeficiency disease [AIDS]) predisposes patients to tinea corporis.

Candidiasis and erythrasma may resemble tinea cruris, but candidal lesions are usually more moist, red, and tender (see Chapter 165). Pustules may be seen within the indistinct border, and satellite lesions may be scattered over adjacent skin. Candidiasis also may involve the scrotum or penis, which are usually spared by tinea. Candida organisms may be treated topically with naftifine (Naftin), ciclopirox (Loprox), or clotrimazole (Lotrimin, Mycelex).

Erythrasma is a skin infection caused by Corynebacterium minutissimum, a gram-positive bacterium. The rash characteristically consists of asymptomatic, reddish-brown, superficial dull patches with well-defined margins and no central clearing. The peripheral edge is not usually any more raised than the center (Figure 181-5, A). When illuminated with an ultraviolet Wood lamp, the infected skin glows with coral-pink fluorescence (Figure 181-5, B). Erythrasma is treated with oral erythromycin, 250 mg qid × 14 days.

Figure 181-5 A and B, Erythrasma appears as red-brown patches of the groin or axilla that fluoresce coral-pink under Wood light examination. (From White G, Cox N: Diseases of the skin, ed 2. St Louis, 2006, Mosby.)

Tinea versicolor is a misnomer, because it is not caused by a dermatophyte fungus but by lipophilic yeast. Pityriasis versicolor is the more correct name. It is asymptomatic, and its presentation to an acute care facility usually is incidental to some other problem. There is, however, no reason to ignore this chronic superficial skin infection, which causes cosmetically unpleasant irregular patches of varying pigmentation that tend to be lighter than the surrounding skin in the summer and darker than the surrounding skin in the winter. Wood light examination sometimes reveals a white or yellow fluorescence (Figure 181-6).

Figure 181-6 A, Tinea versicolor on the upper back of a young adult. B, Wood light examination of the same patient. (From White G, Cox N: Diseases of the skin, ed 2. St Louis, 2006, Mosby.)

Differential diagnosis includes tinea corporis, pityriasis alba, pityriasis rosea, vitiligo, leprosy, and secondary syphilis.

Prescribe a 2.5% selenium sulfide lotion (Selsun) to be applied as lather, leave on 10 to 15 minutes, then wash off daily for 10 to 14 days and then qhs monthly, or use three to five times weekly for 2 to 4 weeks (which also should be followed with monthly re-treatments). Alternatively, use terbinafine 1% solution (spray) twice daily for 1 week or ketoconazole (Nizoral) cream 2% daily for 2 weeks, or ketoconazole or fluconazole (Diflucan) as a single 300-mg oral dose to be repeated in 4 weeks. Also, itraconazole can be taken 200 mg qd × 3 to 7 days. (See the PDR for adverse side effects and interactions.) Superficial scaling should resolve in a few days, and the pigmentary changes will slowly clear over a period of several months. Tinea versicolor has a recurrence rate of 80% after 2 years; patients are therefore likely to need periodic re-treatment or preventive maintenance.

Tinea capitis is mainly a disease of infants, children, and young adolescents, usually involving black or Hispanic preschoolers. Tinea capitis presents in numerous ways: The primary lesions may be scales, papules, pustules, plaques, or nodules on the scalp. Inflammation and secondary infection lead to secondary processes, such as alopecia, erythema, exudate, and edema (Figure 181-7). A kerion forms as a result of increased cell-mediated immune response, demonstrated by an inflamed, exudative, nodular, boggy swelling with associated hair loss and cervical lymphadenopathy (Figure 181-8). Tinea capitis can be diagnosed on KOH examination of extracted hair. Culture must involve the extracted hair, not simply scales.

Figure 181-7 Tinea capitis. (From Bolognia J, Jorizzo J, Rapini R: Dermatology. St Louis, 2003, Mosby.)

Figure 181-8 Kerion with swollen regional lymph nodes. (From White G, Cox N: Diseases of the skin, ed 2. St Louis, 2006, Mosby.)

Oral antifungals are the mainstay of treatment for tinea capitis. Griseofulvin is the only drug approved by the United States Food and Drug Administration for use in children, although other medications have been used. Terbinafine (Lamisil) is now considered the primary drug of choice for the treatment of tinea capitis. Prescribe 250 mg qd × 4 to 8 weeks. Prescribe 6 to 12 mg/kg/day qd × 4 to 8 weeks for children. Griseofulvin is given as 20 to 25 mg/kg/day qd × 8 weeks (or 2 weeks beyond cure), or liquid microsized griseofulvin (Grifulvin V), 15 to 25 mg/kg every day for 8 weeks. Ketoconazole shampoo and cream can be used to reduce fungal shedding. To prevent spread to other family members, contaminated combs and brushes should be cleaned, and family members can use selenium sulfide lotion or shampoo for 5 to 10 minutes (then rinse) three times per week.

Onychomycosis (also known as tinea unguium) is an infection of the nail plate or nail bed that interferes with normal nail function (Figure 181-9). Patients with this infection often have concomitant fungal infections at other sites. Because onychomycosis requires expensive prolonged therapy (6 weeks for fingernail infections and 12 weeks for toenail infections), the diagnosis should be confirmed before treatment is initiated. This can be achieved by clipping off the distal edge of the affected nail, placing it in formalin along with attached subungual debris, and sending it for periodic acid–Schiff staining with histologic examination in a hospital or reference laboratory.

Figure 181-9 Tinea unguium or subungual onychomycosis. (From White G, Cox N: Diseases of the skin, ed 2. St Louis, 2006, Mosby.)

Terbinafine, at a dosage of 250 mg per day for 12 weeks, has a better mycologic cure rate than “pulse” therapy, in which 500 mg of terbinafine is given once daily for 7 days of each of 2 months (fingernails) or 4 months (toenails). It should be noted, though, that follow-up must be arranged with a patient’s primary doctor or dermatologist. Long-term dosage with this drug has caused some significant liver disease. Terbinafine is considered the drug of choice for dermatophyte onychomycosis, with greater mycologic cure rates, less serious and fewer drug interactions, and a lower cost than continuous itraconazole therapy. Adjunct débridement may improve the clinical and complete cure rates compared with terbinafine alone.

Newer oral antifungal agents have greatly improved the management of dermatomycoses, but not without consequence. Some are very expensive, have side effects and organ toxicity that may or may not be tolerable, and have significant adverse drug interactions. Laboratory monitoring is recommended during treatment with all oral antifungal medications. Liver function tests for itraconazole should be done at baseline, at 1 month, and if any signs or symptoms of liver dysfunction present. Terbinafine use warrants liver function tests at baseline, at 6 weeks, if signs or symptoms present, and then 4 weeks later. In general, one should monitor patients more closely if taking medications that impair renal or hepatic function.