Diagnosis and treating of Malassezia dermatitis (Proceedings)

Malassezia is a genus of lipophilic yeast found as a commensal of the skin and mucosal surfaces that may cause skin disease in a variety of mammalian species.  In normal dogs these organisms are present in very small numbers on the skin (fold areas-lip, vulvar, axillae, interdigital), oral and anal mucosal surfaces, in the ear canals and anal sacs.  In contrast to Candida, MD is not associated w/recent antibiotic administration, in fact, there appears to be a symbiotic relationship between the surface staphylococcal organisms and the yeast.  It is theorized that the organisms produce growth factors and micro-environmental changes (eg inflammation) that are beneficial to each so it is not uncommon to see concurrent infections w/Malassezia and staphylococcus.  Since there doesn't seem to be an identifiable difference in virulence and/or adhesion in Malassezia organisms found on affected skin vs unaffected skin- why do animals develop Malassezia dermatitis (MD)? It appears that the host response to Malassezia seems to be the explanation of why some dogs develop MD. Both type I and type IV hypersensitivity reactions have been identified in dogs w/MD.  With Malassezia overgrowth, there are a variety of events that occur that can contribute to cutaneous inflammation including metabolism of the surface free fatty acids (Malassezia produces lipases) that changes the cutaneous pH, causes inflammatory eicosanoid release and decreases normal cutaneous barrier function.  Complement activation activation may also occur due to the percutaneous absorption of Malassezia antigen.  Disorders that affect the barrier function of the skin (eg pruritic skin disease) or the cutaneous lipid content (eg hypothyroidism) are risk factors for developing MD

Signalment

There is no age or sex predilection

History

Frequently when MD occurs the clinical and/or therapeutic features of the underlying disease changes.  Pruritus that was seasonal becomes nonseasonal; the distribution of the pruritus changes, responsiveness to previously effective antibiotic and/or glucocorticoid therapy is decreased.  Any allergic animal whose pruritus (intensity or distribution) or the therapeutic responsiveness of the pruritus changes suddenly should be evaluated for MD, pyoderma or parasites.

Clinical findings

May include lichenification, erythema, greasy exudate, dry scale, papules, plaques, alopecia or hyperpigmentation.  A moist dermatitis with a musty odor is frequently present.  Pruritus may vary from mild to intense and erythema may be present with minimal pruritus especially interdigitally.

The lesions may be focal or generalized and the distribution of the lesions overlaps with other pruritic diseases.  Areas affected include interdigitally, intertriginous areas, face, nail folds, perioral (lateral muzzle), pinna and flexor surface of the elbow

Diagnosis

Identifying Malassezia organisms budding yeast in the shape of Planter's peanuts or a footprint) from affected area is necessary to establish a diagnosis of MD.  Direct impression smear is the most common method used for sampling affected areas.  If the skin is quite dry a scalpel blade is used to collect a sample. It is important to examine multiple fields since the number of organisms per oil field can vary a lot (do 20-25 fields that contain keratinocytes).  Samples are stained w/3 step Diff-Quik.  The question is “how many is too many organisms?”  A previous report found that normal dogs had 1 yeast per 2700 oil field.  On cytology if you find ANY field that has more 1 organism OR if you find 1 organism every 1-3 fields (1000X) then you should treat it. 

MD may cause a folliculitis that is clinically identical to staph pyoderma.  Therefore if there are follicular papules, epidermal collarettes or lichenification you can't assume that there is a bacterial component to the skin disease w/o cytology (of course skin scrapings +/- dermatophyte culture should be performed)

An interesting question is "Why can't I find yeast when I'm sure the dog has Malassezia dermatitis?" Obviously site selection has significant impact.  Because Malassezia is a surface organism whose numbers may be decreased by the animal's licking multiple sites need to be sampled. 

Treatment

Since MD is a secondary disease in order to prevent recurrence you must identify and treat the underlying disease.  As previously mentioned any disease that disrupts the barrier function, the lipid content of the skin surface, the cutaneous microclimate or host defense mechanisms may predispose the animal to MD.  These include hypersensitivities (atopy, cutaneous adverse food reactions), ectoparasites (demodex, sarcoptes, and fleas), endocrinopathies (hypothyroidism, hyperadrenocorticism), metabolic epidermal necrosis, cutaneous T-cell lymphoma, and excessive skin folds.  Bassett hounds are genetically predisposed to having a higher number of Malassezia organisms on their skin, making them a greater risk for developing MD.

Unless the MD is very focal, the author prefers both topical and systemic therapy.  This is so when the dog is rechecked, it is certain that the MD is resolved and any remaining pruritus is a result of the underlying hypersensitivity reaction.  The most common shampoo the author uses contains at least 3% chlorhexidene or contains 2% chlorhexidene combined w/an azole.  This is then followed by a leave on conditioner containing 2% miconazole.  Frequency of application varies from daily to 3x/week depending on the severity and extensiveness of the lesions. 

Ketoconazole (200 mg tabs) 5-10 mg/kg sid is the systemic drug of choice.  If the dog doesn't tolerate ketoconazole, itraconazole 5 mg/kg given 2 consecutive days/week is also effective, albeit more expensive. If the dog has liver disease or is very small fluconazole (comes in 50 mg tabs) – 5-10 mg/kg daily would be a good choice since fluconazole is not metabolized or excreted by the liver.  As in treating superficial bacterial pyoderma, treatment should be continued for 14 days beyond clinical resolution BASED ON YOUR examination (not a phone call) w/a minimum treatment time of 21 days.  Please note that griseofulvin is ineffective against Malassezia.

Be sure to evaluate the dog for concurrent superficial bacterial pyoderma since MD and pyoderma occur simultaneously in dogs.  In cases of concurrent superficial bacterial pyoderma, antibiotic therapy should be used simultaneously.

References

Scott DW, Miller WH, and Griffin CE. Fungal Skin Diseases. In: Muller & Kirk's Small Animal Dermatology, 6th ed. Philadelphia: WB Saunders Co, 2001; 363-374.

Farver K, Morris DO, Shofer F, et al.  Humoral measurement of type-1 hypersensitivity reactions to a commercial Malassezia allergen Vet Dermatol August 2005;16(4):261-8

Morris DO. Malassezia dermatitis and otitis. In: Campbell KA, ed. Veterinary Clinics of North America: Small Animal Practice. Philadelphia: W.B. Saunders Co., 1999; 1303-1310.

Matousek JL, Campbell KL. Malassezia Dermatitis. Compend Sm Anim Prac 2002; 24:224-231.

Kennis RA, Rosser EJ, Olivier NB, et al.  Quantity and distribution of Malassezia organisms on the skin of clinically normal dogs  J Am Vet Med Assoc. April 1996;208(7):1048-51.

Cafarchia C, Gallo S,  Romito D, et al.   Frequency, body distribution, and population size of Malassezia species in healthy dogs and in dogs with localized cutaneous lesions J Vet Diagn Invest. July 2005;17(4):316-22.

Pinchbeck LR, Hillier A, Kowalski JJ, et al. Comparison of pulse administration versus once daily administration of itraconazole for the treatment of Malassezia pachydermatis dermatitis and otitis in dogs. J Am Vet Med Assoc 2002; 220:1807-1812.

Chen T, Hill PB The biology of Malassezia organisms and their ability to induce immune responses and skin disease.  Vet Dermatol. February 2005;16(1):4-26