Daniel O. Morris,     Philadelphia, Pennsylvania

Pathogenesis

Malassezia yeast colonizes the skin and external ear canals of animals in very low numbers. Overt “infection,” sometimes referred to as “overgrowth,” is defined by increased numbers of the yeast on the skin surface in conjunction with inflammation. In a diseased state alterations in the microclimate of the surface of the skin contribute to increased susceptibility to yeast infection. Primary diseases that cause increased moisture, altered surface lipids, or disruption of stratum corneum barrier function encourage secondary overgrowth of the organism. Pruritic inflammatory diseases (allergic and parasitic) result in microclimate changes caused by scratching (disruption of barrier function), licking (added moisture), and increased production of sebum. Endocrinopathies, especially hyperadrenocorticism, directly cause alterations in sebum characteristics and stratum corneum function. Metabolic diseases that result in hyperkeratosis (such as zinc-responsive dermatosis, hepatocutaneous syndrome/superficial necrolytic dermatitis of dogs, and thymoma-associated dermatosis of cats) also appear to be risk factors. Secondary MD also is associated with primary (idiopathic) seborrhea of dogs and cats and paraneoplastic alopecia caused by internal carcinomas in cats.

In some dogs with AD, antigens produced by M. pachydermatis may be recognized by the immune system as allergens (i.e., MH), in which case a highly inflammatory and pruritic response can be mounted to relatively low numbers of yeast organisms, so that the line between cytologic definitions of colonization and infection is blurred. However, many dogs with MH also have overt infection, as defined cytologically by overgrowth of yeast on the skin surface (see the section on cytologic analysis later in the chapter for guidelines). MH has not yet been studied or defined in cats with allergic skin disease, although MD does appear to contribute to the pruritic threshold of some cats with AD.

Zoonosis

M. pachydermatis has been documented to cause life-threatening fungemia in people, especially in patients in critical condition receiving parenteral lipid infusions, such as neonates in the intensive care unit (ICU). In one case, the source of infection was shown to be a pet dog owned by a nurse who worked in the ICU (Chang et al, 1998). This observation suggested that M. pachydermatis could represent an emerging infectious zoonotic pathogen. An epidemiologic survey conducted by the author’s clinical research group has shown that M. pachydermatis can be isolated very commonly from the hands of dog owners, regardless of whether their dogs have MD or healthy skin (Morris et al, 2005). However, the public health significance appears to be extremely low, considering the commonness of mechanical carriage by dog owners coupled with the paucity of fungemia cases reported in the human literature.

Clinical Signs

Several excellent reviews describing the clinical presentations of MD and MO in dogs and cats are available (Matousek and Campbell, 2002; Morris, 1999; Muse, 2000). Some key points are included here.

Although MD usually is intensely pruritic, the only primary lesion produced is erythema. Secondary lesions, including alopecia, excoriations, seborrheic plaques, lichenification, maceration, and hyperpigmentation, are common and cannot be distinguished reliably from staphylococcal pyoderma without cytologic examination. Therefore one should look for the yeast on the surface of any pruritic skin lesion.

The clinical appearance of the skin in cases of MD is highly variable. It may be either dry and flaky (seborrhea sicca) or tacky or greasy (seborrhea oleosa). In rare cases M. pachydermatis can cause a folliculitis that mimics staphylococcal folliculitis, dermatophytosis, and demodicosis.

The distribution pattern of canine MD is variable, but MD most commonly affects some combination of the face (especially periocular and perioral skin), feet (interdigital spaces and claw folds), intertriginous areas (axillae, groin-inguinal area, facial folds, vulvar and mammary folds), and perineum. Generalized cases of MD may occur in chronic cases of allergic dermatitis. Similar distributions occur in cats. Malassezia overgrowth can provoke an overwhelming pruritic response in atopic dogs that can occur acutely and be misconstrued as increased exposure to aeroallergens. Resolution of the yeast infection can reduce the pruritic threshold of an atopic dog by as much as 75% to 100% in some cases, depending on concurrent exposure to other allergens. Therefore undiagnosed MD is one of the most common reasons for perceived failure in the management of atopic dogs.

Malassezia pododermatitis may occur with or without more widespread MD. The feet are the most common single body area affected in allergic dogs. Patients with interdigital Malassezia pododermatitis are brought to the veterinarian because of paw licking or chewing. Paronychia (inflammation of the claw beds) also may occur as the sole presenting sign of MD and often causes claw biting. Physical examination usually reveals a reddish-brown staining of the proximal claw or a waxy exudate in the claw fold, with inflammation of the surrounding soft tissue.

In any dog with a known endocrine or metabolic disease, MD must be ruled out (by surface cytologic analysis) if pruritus, cutaneous inflammation, or even noninflammatory seborrhea is present.

Malassezia yeast also play an important role in cases of ceruminous otitis externa, in which it is highly proinflammatory. Some cases appear to be primary and associated only with moisture trapping (especially in swimming dogs).

Diagnosis

Diagnosis of MD and MO is made by microscopic examination of surface cytologic specimens. Diagnosis of MH in dogs is made by intradermal testing with a commercial M. pachydermatis extract.