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Ringworm (Dermatophytosis) in Dogs and Cats


Sandra R. Merchant

, DVM, DACVD, School of Veterinary Medicine, Louisiana State University

Last full review/revision May 2013 | Content last modified Jun 2013

Ringworm in dogs is caused mainly by Microsporum canis (70% of cases), but also by M gypseum (20%) and Trichophyton mentagrophytes (10%); in cats, 98% are caused by M canis. The Wood’s lamp is useful in establishing a tentative diagnosis of dermatophytosis in dogs and cats but cannot be used to exclude this type of infection. Definitive diagnosis is established by DTM culture (see Dermatophytosis). Detection of infection in asymptomatic carrier animals is facilitated by brushing the coat with a new toothbrush and then inoculating a culture plate with the collected hair and scale by pressing the bristles to the surface of the medium.

The clinical appearance of ringworm in cats is quite variable. Kittens are affected most commonly. Typical lesions consist of focal alopecia, scaling, and crusting; most are located around the ears and face or on the extremities. Cats with clinically inapparent infections can serve as a source of infection to other cats or people. Occasionally, dermatophytosis in cats causes feline miliary dermatitis and is pruritic. Cats with generalized dermatophytosis occasionally develop cutaneous ulcerated nodules, known as dermatophyte granulomas or pseudomycetomas. Devon Rex cats can have a maculopapular hyperpigmented, crusted disease that histopathologically is an eosinophilic/mastocytic dermatitis.

Lesions in dogs are classically alopecic, scaly patches with broken hairs. Dogs may also develop regional or generalized folliculitis and furunculosis with papules and pustules. A focal nodular form of dermatophytosis in dogs is the kerion reaction. Generalized ringworm in adult dogs is uncommon and is usually accompanied by immunodeficiency, especially endogenous or iatrogenic hyperadrenocorticism. Differential diagnoses for classic ringworm lesions in dogs include demodicosis, bacterial folliculitis, and seborrheic dermatitis.

Dermatophytosis in dogs and shorthaired cats may be self-limiting, but resolution can be hastened by treatment. Another primary objective of therapy is to decrease environmental contamination and prevent spread of infection to other animals and people. Although no controlled studies exist that prove clipping of the hair coat shortens the duration of infection, clinical studies support this recommendation, at least for cats with long hair and/or generalized dermatophytosis, even if it initially worsens or spreads the lesions. Environmental decontamination with bleach (1:10 dilution) or enilconazole solution (0.2%) is effective.

Whole-body topical therapy may hasten a clinical cure (if not a mycologic cure) and decrease environmental contamination. Based on in vitro and in vivo studies, whole-body lime sulfur dips (1:16), 0.2% enilconazole rinses, 2% miconazole, and a combined 2% miconazole/chlorhexidine shampoo were found to be antifungal. These may be appropriate for adjunctive therapy. Enilconazole rinse is not currently available in the USA in a formulation approved for dogs and cats. Topical use of enilconazole may have been the cause of hypersalivation, idiopathic muscle weakness, and slightly increased serum ALT concentration in one study. Local lesions can be treated effectively with topical miconazole or clotrimazole.

For chronic or severe cases and for ringworm in longhaired breeds of cats and Yorkshire Terriers, systemic treatment is indicated. Itraconazole, fluconazole, terbinafine, ketoconazole, and griseofulvin have all been used successfully. The microsized formulation of griseofulvin can be used in dogs (25–100 mg/kg, daily or in divided doses) and in cats (25–50 mg/kg, daily in divided doses) and is best absorbed when given with a fatty meal. The ultramicrosized formulations should be used at lower dosages (10–15 mg/kg/day). There is no veterinary-labeled griseofulvin currently approved for use in dogs and cats in the USA. Cats may develop bone marrow suppression, especially neutropenia, at higher doses as idiosyncratic reactions. This is more common in feline immunodeficiency virus–positive cats. In both dogs and cats, GI upset is a fairly common sequela of griseofulvin administration.

Other effective treatments include itraconazole (5–10 mg/kg/day, or pulse therapy 5–10 mg/kg/day for 28 days then on an alternate-week regimen [1 week on, 1 week off]), ketoconazole (5–10 mg/kg/day), terbinafine (30–40 mg/kg/day), and fluconazole (5–10 mg/kg/day). Fluconazole may be the least effective of these drugs. Terbinafine was found to be at levels higher than the minimum inhibitory concentration on the hair of treated animals for 5.3 wk after 2 wk of daily therapy. This may indicate its potential for use as a pulse therapy drug after 2 wk of daily administration. None of these drugs is approved for use in domestic animals in the USA. In addition, ketoconazole is often a cause of anorexia in cats and is not used as often in this species. Systemic and topical treatments for dermatophytosis should be continued until a negative brush culture is obtained. A brush culture is usually submitted after a minimum of 1 mo of therapy or when clinical lesions are minimal to resolved. In chronic disease and/or challenging environments, the endpoint of treatment may more appropriately be two or three consecutive negative fungal cultures obtained at weekly or biweekly intervals. Efficacy of lufenuron either to treat or prevent M canis infection has not been confirmed in controlled studies.

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