Pemphigus Foliaceus Associated to Sebaceous Adenitis in an Akita Dog: A Case Report
M.R. Farias1; R. Friesen1; J. Werner2
Pemphigus foliaceus (PF) is an autoimmune skin disease due to production of antibodies against autoantigen Desmoglein 1, a component of desmosomes in the superficial layers of the epidermis and epithelium of hair follicles. PF causes loss of intercellular cohesion that leads to acantholysis and formation of subcorneal or infragranular vesicles and bullae. The literature states that PF can be spontaneous, drug-related or associated with chronic dermatopathies. In the case reported herein a ten years old Akita male dog, with a one-year history of granulomatous sebaceous adenitis (GSA) diagnosed by skin biopsies was brought to the clinic. The dog presented (besides the signs of GSA) diffuse papular-pustular lesions centered in hair-follicles, multiple irregular pustules in the skin of the neck, dorsal and abdominal thoracic regions, and intense pruritus. Cytologic examination of material aspirated from the pustules revealed acantholytic keratinocytes surrounded by neutrophils (Tzank's cells). No bacteria were observed. A skin biopsy of the pustular lesions was then performed and examined histologically. The epidermis and epithelium of hair follicles showed subcorneal and infragranular pustules containing abundant acantholytic keratinocytes and neutrophils. The epithelium beneath the pustules showed signs of active acantholysis. The pustules were covered by kerato-leukocytic crusts containing many degenerated free keratinocytes. A diagnosis of PF was made based on the histopathological findings and the patient started to receive prednisone and azathioprine. The pustular lesions and pruritus disappeared completely but recurred after a while. Further recurrences were avoided by association of prednisone, azathioprine, cyclosporine and ketoconazole. Concurrent GSA was controlled continuously by topic emollient therapy. Chronic dermatopathies like GSA and allergic dermatitis may precipitate PF, but the exact pathogenic mechanisms are unknown. PF associated to allergic dermatopathies, especially those associated to arthropod saliva, are probably due to antigenic stimulation by keratinocytes modified by chronic inflammation and aggression to the skin. There are no theories to explain the association to GSA, whose pathogenesis also is undetermined. What is clear though is that the presence of concurrent chronic dermatopathies makes the control of PF more difficult, requiring the association of multiple therapies and causing the prognosis to be guarded or uncertain.