WHO Model Prescribing Information: Drugs Used in Skin Diseases
(1997; 132 pages) [French] [Spanish] View the PDF document
Table of Contents
View the documentPreface
View the documentIntroduction
Open this folder and view contentsParasitic infections
Open this folder and view contentsInsect and arachnid bites and stings
Close this folderSuperficial fungal infections
View the documentDermatophyte infections
View the documentPityriasis (tinea) versicolor
View the documentCandidosis
Open this folder and view contentsSubcutaneous fungal infections
Open this folder and view contentsBacterial infections
Open this folder and view contentsViral infections
Open this folder and view contentsEczematous diseases
Open this folder and view contentsScaling diseases
Open this folder and view contentsPapulosquamous diseases
View the documentCutaneous reactions to drugs
Open this folder and view contentsPigmentary disorders
Open this folder and view contentsPremalignant lesions and malignant tumours
Open this folder and view contentsPhotodermatoses
Open this folder and view contentsBullous dermatoses
View the documentAlopecia areata
View the documentUrticaria
Open this folder and view contentsConditions common in children
View the documentAcne vulgaris
View the documentPruritus
View the documentTropical ulcers
Open this folder and view contentsAntimicrobial drugs
Open this folder and view contentsAntifugal drugs
Open this folder and view contentsAntiseptic agents
Open this folder and view contentsKeratoplastic and keratolytic agents
Open this folder and view contentsScabicides and pediculicides
Open this folder and view contentsAnti-inflammatory and antipruritic drugs1
Open this folder and view contentsAntiallergics and drugs used in anaphylaxis
Open this folder and view contentsUltraviolet radiation-blocking agents (sunscreens)
Open this folder and view contentsMiscellaneous drugs
Open this folder and view contentsAnnex
View the documentSelected WHO Publications of Related Interest
View the documentBack cover
 

Dermatophyte infections

Ringworm (tinea) is caused by dermatophytes of three genera: Epidermophyton, Trichophyton and Microsporum. Different species have different primary hosts and some are free-living in the soil. Infection of humans is favoured by heat, humidity and poor hygiene.

The lesions produced by each species have a characteristic cutaneous distribution. The typical erythematous annular lesions with raised scaly edges on glabrous skin are readily confused with those of psoriasis and other annular or circular erythematous scaly dermatitic lesions such as nummular eczema. The characteristic lesions have an expanding border and central clearing. However, many lesions are atypical, particularly in the tropics, and when the diagnosis is in doubt, scrapings from the edge of a lesion should be placed on a glass slide with 10% aqueous potassium hydroxide and examined microscopically for fungal filaments.

Treatment

Both benzoic acid and methylrosanilinium chloride (gentian violet) solution are cheap, effective fungistatic compounds. Repeated application of a mixture of benzoic acid and salicylic acid (Whitfield’s ointment), which is keratolytic, is also widely used to clear minor skin lesions. Creams and powders containing an imidazole, undecylenic acid or tolnaftate are more likely to cure long-established lesions, but these are more expensive. However, extensive and generalized infections of the skin and hair should be treated systemically for several weeks with griseofulvin. Much longer courses of treatment are required when the nails are affected. Ketoconazole is a more effective systemic fungicide, but close monitoring of liver function is required throughout treatment, particularly if treatment is prolonged. Itraconazole and terbinafine may prove to be safer than ketoconazole and are at least as effective in the treatment of resistant cases of ringworm, including onychomycosis. However, these drugs are expensive.

Scalp ringworm (tinea capitis) typically appears as a patch of scaling alopecia, or a swollen inflammatory area (kerion). Mild forms may resolve spontaneously at puberty. Inflamed lesions should be treated orally with griseofulvin at a dose of 10 mg/ kg daily in two divided doses, up to a maximum of 1 g daily for at least 6 weeks. In severe cases, treatment may need to be continued for up to 3 months. Topical application of an imidazole cream or benzoic acid + salicylic acid ointment may accelerate clearing of scaly lesions, but does not affect the infection within the hair. While a kerion may appear to be secondarily infected, the kerion represents an inflammatory response to the infection, and antibiotics are usually not indicated unless there is severe secondary infection. Scarring may result from a kerion, owing to the destruction of the hair follicles.

Ringworm of the trunk (tinea corporis) is caused by either T. rubrum or the fungi that cause scalp ringworm. Lesions can often be cleared by topical application of benzoic acid + salicylic acid ointment or an imidazole cream, but in some cases a 4-week course of orally administered griseofulvin is required. Itraconazole, 200 mg daily for 15-30 days, or terbinafine, 250 mg daily for 1-2 weeks, is also effective.

Foot ringworm (tinea pedis or athlete’s foot), a common dermatophyte infection, is caused by many dermatophyte species. Lesions frequently first appear in the fourth interdigital web, which is nearly always involved. While tinea pedis responds to topical and oral antifungal therapy, recurrences are common, particularly in T. rubrum infections or when the toenails are involved. Therefore, tinea pedis is usually treated with topical agents. Benzoic acid + salicylic acid ointment or an imidazole cream should be applied twice daily to all infected areas and the toe clefts for at least 4 weeks. If there is a history of recurrence, a powder containing an antifungal agent should be used prophylactically. Severe weeping lesions respond to frequent footbaths of 0.5% aqueous gentian violet solution or 1:10000 potassium permanganate, and systemic antifungals assist clearing. If oral therapy is used, griseofulvin administered at 10 mg/kg daily as a single dose to a maximum of 1 g daily for 4 weeks is usually helpful. However, in patients with associated infections of the nails, treatment needs to be extended for 12-18 months and, even then, the results are often disappointing. Terbinafine, 250 mg daily for 1-2 weeks, or itraconazole, 400 mg daily for 7 consecutive days per month for 3 months, is more effective than griseofulvin, but more expensive. These infections should first be confirmed by laboratory examination since Candida and Scopulariopsis spp., which are unresponsive to griseofulvin, also infect nails.

Ringworm of the groin (tinea cruris) is usually limited to the skin of the inner thigh in contact with the scrotum. Flexural eczema, often secondarily infected with Candida spp. or bacteria, occurs in the same site. It is usually treated with preparations containing a mixture of an antifungal and a steroid, but tinea cruris should be treated with an antifungal alone since corticosteroids worsen ringworm infections. An imidazole cream applied daily for 2 weeks is usually effective. Lesions unresponsive to topical preparations can usually be cleared with a 4-week course of griseofulvin, as described above.

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