Update on malassezia dermatitis in dogs and cats (Proceedings)

Article

Malassezia yeasts and Malassezia dermatitis have been the subject of almost innumerable publications and anecdotes since the early 1990s. The condition is diagnosed commonly in the dog and uncommonly in the cat.

Malassezia yeasts and Malassezia dermatitis have been the subject of almost innumerable publications and anecdotes since the early 1990s. The condition is diagnosed commonly in the dog and uncommonly in the cat. This presentation will focus on what has been published since the submission of the sixth edition of Muller & Kirk's Small Animal Dermatology in 2001.

Thanks to the advances in molecular biology, the genus Malassezia has undergone extensive investigation and revision. The genus currently contains 13 species: one lipid-dependent, M. pachydermatis; and 12 lipid-independent, M. caprae, M. dermatis, M. equina, M. furfur, M. globosa, M. japonica, M. nana, M. obtusa, M. restricta, M. slooffiae, M. sympodialis, and M. yamatoensis. M. pachydermatis remains the most commonly isolated and studied in dogs and cats.

Dogs

M. pachydermatis is most commonly isolated, in decreasing order of frequency, from interdigital skin, ears, claw folds, mouth, groin, conjunctiva, axilla, perineum, anus, and circumanal glands of atopic dogs.27 The highest yeast counts are found on lesional skin.

M. pachydermatis produces a large number of substances which may be important in the production of disease: acid phosphatase, alkaline phosphatase, chondroitin-sulfatase, esterase, galactosidase, glucosidase, hyaluronidase, lecithinase, leucine arylamidase, lipoxygenase, peroxidase, phosphoamidase, phosphohydrolase, phospholipase, protease, and urease.16 Multiple M. pachydermatis genotypes and subgenotypes were isolated from healthy dogs or dogs with skin lesions, and those from lesional skin contained significantly higher phospholipase activity.

The variability in adhesive capacity of M. pachydermatis and M. sympodialis to canine, feline, and human corneocytes did not explain the marked difference in Malassezia flora in these three species.7 The in vitro growth of M. pachydermatis was inhibited at pH 1 to 3 and 9 to 10.

M. pachydermatis applied to the skin of healthy dogs produced mild, transient lesions; when the yeast was applied under occlusion, the lesions were more severe, lasted longer, but still spontaneously resolved. Fungal culture was positive much more commonly than cytology when sampling healthy and inflamed skin. Cultures from adhesive tape samples were positive twice as frequently as those from dry swabs.

There was no significant difference in anti-Malassezia IgE levels between atopic dogs with or without Malassezia dermatitis and/or otitis. Neither were there significant differences in anti-Malassezia IgE levels (commercial ELISA test) between atopic dogs with or without Malassezia dermatitis and healthy dogs.18 Passive transfer of type-1 hypersensitivity reactivity confirmed the functionality of anti-Malassezia IgE.

Intradermal test reactions to M. pachydermatis antigen were 4 times more frequently immediate than delayed. Intradermal tests (commercial M. pachydermatis antigen) were positive (immediate reactions) in all atopic dogs with Malassezia dermatitis, 31% of atopic dogs without Malassezia dermatitis, and no healthy dogs. Lymphocyte blastogenesis to M. pachydermatis antigen was positive in atopic dogs with or without Malassezia dermatitis. Patch tests using M. pachydermatis antigen were more often positive in basset hounds with Malassezia dermatitis than in healthy basset hounds and healthy beagles.

Proteins of 45, 52, 56, and 63 kDA were recognized by over 50% of the atopic dogs with Malassezia dermatitis, thus qualifying as major allergens. Results of this study were not in total agreement with those from previous studies. Differences could be due to the fact that there is variation in antigenic expression in different growth phases of M. pachydermatis.

In vitro susceptibility testing of strains of M. pachydermatis from dogs showed that all were susceptible to azoles: ketoconazole > itraconazole > fluconazole. Ketoconazole and itraconazole were equally effective for systemic treatment of Malassezia dermatitis, and there was no difference in efficacy between ketoconazole at 5 mg/kg q24h and 10 mg/kg q24h. There was no difference in the efficacy of itraconazole when administered daily or for two consecutive days/week.Ketoconazole and terbinafine were equally effective for reducing population sizes of Malassezia and for the treatment of Malassezia dermatitis.

M. pachydermatis was 11 times more likely to be demonstrated by PCR on the hands of owners of atopic dogs with Malassezia dermatitis or otitis.

Cats

Malassezia spp. (mostly M. pachydermatis) were demonstrated (ear canal, anus, claw fold, axilla, and groin were sampled) in 90% of Devon Rex, 50% of domestic shorthair, and 39% of Cornish Rex cats. M. slooffiae (mostly clawbed) and M. nana (mostly ear canal) were occasionally isolated. Frequency of isolation and population sizes of Malassezia spp. (mostly M. pachydermatis) were greater in "seborrheic" Devon Rex than in healthy Devon Rex or domestic shorthair cats.1 The prevalence of Malassezia spp. in clawfolds was greater in Devon Rex (100%; 8.6/oil immersion) than non-Devon Rex (61%; 0.59/oil immersion). The frequency of isolation and population sizes of Malassezia sp. were not significantly different in healthy cats and cats with diabetes mellitus, hyperthyroidism, and neoplasia.

Results of a retrospective histopathological study suggested that the finding of Malassezia yeasts in surface keratin was often associated with the presence of systemic disease (e.g., paraneoplastic alopecia, thymoma). Malassezia yeasts were demosntrated in allergic cats (atopic dermatitis, food allergy) and treatment with itraconazole or ketoconazole resulted in reduced pruritus and dermatitis. Itraconazole administration produced reduced Malassezia counts and dermatitis in "seborrheic" Devon Rex cats.

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