Malaseb

Malassezia Associated Seborrheic Dermatitis

Seborrhea is a defect in keratinization resulting in augmented scale formation, excessive greasiness of the skin and haircoat and sometimes by secondary inflammation. Seborrhea may be inherited (primary Seborrhea) or, as is more frequently the case, caused by external or internal pathogens (secondary Seborrhea). When secondary Seborrhea is present, the patient should be tested for Malassezia. While Malassezia is a yeast commonly found on the skin and in the ears of dogs and cats in small numbers, recent research has found that Malassezia pachydermatis as well as Staphylococcus play a significant role in Seborrheic dermatitis, especially when oily, scaly, erythematous and pruritic skin is present. Malassezia dermatitis occurs in dogs of any age, sex, and breed. About 40% of the dogs with Malassezia dermatitis have Staphylococcal pyoderma.

Until recently Seborrhea was considered an abnormality of epidermal maturation. But recent research has discovered that yeast and bacterial infections cause Seborrheic dermatitis and that scale and sebum are a protective response of the skin. Sebum is an oil-water mixture of electrolytes, fatty acids and secreted antibodies that regulates the water content of the epidermis, carries protective bioactives to the surface and provides the fluid medium in which they can act. Keratinocytes are continuously being shed from the surface and are regenerated from the basal cells. This increased shedding and scale formation is the natural response of the skin to insults. By shedding kertinocytes and thickening the epidermis (lichenification) to avoid penetration, the body protects itself from potential allergens and toxins.

When a pathogen overwhelms the skin’s protective mechanisms the patient will develop an allergy, resulting in disruption to the skin barrier function and leakage of body fluids through the damaged epidermis. To control fluid loss and scale formation, the sebaceous glands will increase the sebum flow as a protective reaction. An increase of cutaneous commensals such as Malassezia and Staph result from the excess sebum. Secreted antibodies and excess nutrients on the skin surface are diluted by the exudate. Malassezia and Staph are normally shed onto the skin from the nose, mouth, ears and peripheral carriage sites, without taking hold. But with the new environment created by the excess sebum, Malassezia and Staph proliferate and adhere to the skin surface, with their protease and lipase enzymes altering the sebum to their ecological advantage. An infection has developed once the skin’s protective mechanisms are overwhelmed.