chapter 32 MalasseziaDermatitis..................................
DEFINITION/OVERVIEW
Malasseziapachydermatis(syn.Malassezia canis,Pityrosporumcanis,andPityrosporum
pachydermatis): normal yeast commensal of the skin, ears, and mucocutaneous areas.
Malasseziaovergrowth syndrome (MOG)/Malasseziadermatitis – clinical disease due
to overgrowth and colonization of a commensal organism causing dermatitis, cheilitis,
paronychia, and otitis in dogs and cats.ETIOLOGY/PATHOPHYSIOLOGY
M. pachydermatisis nonlipid dependent; several species isolated from the cat and dog
are lipid dependent (M. sympodialis,M. globosa,M. nana,M. slooffiae,M. restricta,and
M. furfur).Malasseziaspecies do not invade the skin beneath the stratum corneum.
Malasseziamay have a symbiotic relationship with commensal staphylococci; both
yeast and bacterial numbers in diseased areas are typically excessive.
Dermatitis likely results from inflammatory or hypersensitivity reactions to yeast
products and antigens; the causes of the transformation from harmless commensal
to pathogen are poorly understood but seem related to allergy, seborrheic conditions,
and possibly congenital and hormonal factors.Malasseziaproduce many enzymes (e.g., lipases and proteases) which contribute to
cutaneous inflammation by altering the lipidic cutaneous protective barrier (epider-
mal lipid barrier), changing cutaneous pH, and causing eicosanoid release and com-
plement activation.Malasseziamay be a primary allergen initiating a type I (immediate) hypersensitivity;
skin testing withMalasseziaextract results in an immediate hypersensitivity reaction
in sensitized individuals; a delayed hypersensitivity pathway is also proposed.Malassezia-specific IgG and IgE are higher in atopic dogs compared to normal dogs;
yeast may play a role in the pathogenesis of atopic dermatitis.
Malasseziadermatitis is usually secondary to an underlying cause (e.g., allergy).
Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Dermatology, Third Edition.
Karen Helton Rhodes and Alexander H. Werner.
©2018 John Wiley & Sons, Inc. Published 2018 by John Wiley & Sons, Inc.
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