Immunopathogenesis of canine chronic ulcerative stomatitis.

Canine Chronic Ulcerative Stomatitis is a spontaneously occurring inflammatory disease of the oral mucosa. An immune-mediated pathogenesis is suspected though not yet proven. We have recently reported on the clinical and histologic features, and identification of select leukocyte cell populations within the lesion. A clinical and histologic similarity to oral lichen planus of people was proposed. In the present study, these initial observations are extended by examining lesions from 24 dogs with clinical evidence of chronic ulcerative stomatitis. Because dogs with chronic ulcerative stomatitis often have concurrent periodontal disease, we wondered if dental plaque/biofilm may be a common instigator of inflammation in both lesions. We hypothesized that dogs with chronic ulcerative stomatitis would exhibit a spectrum of pathologic changes and phenotype of infiltrating leukocytes that would inform lesion pathogenesis and that these changes would differ from inflammatory phenotypes in periodontitis. Previously we identified chronic ulcerative stomatitis lesions to be rich in FoxP3+ and IL17+ cells. As such, we suspect that these leukocytes play an important role in lesion pathogenesis. The current study confirms the presence of moderate to large numbers of FoxP3+ T cells and IL17+ cells in all ulcerative stomatitis lesions using confocal immunofluorescence. Interestingly, the majority of IL17+ cells were determined to be non-T cells and IL17+ cell frequencies were negatively correlated with severity on the clinical scoring system. Three histologic subtypes of ulcerative stomatitis were determined; lichenoid, deep stomatitis and granulomatous. Periodontitis lesions, like stomatitis lesions, were B cell and plasma cell rich, but otherwise differed from the stomatitis lesions. Direct immunofluorescence results did not support an autoantibody-mediated autoimmune disease process. This investigation contributes to the body of literature regarding leukocyte involvement in canine idiopathic inflammatory disease pathogenesis.

Establishing a canine superficial pyoderma model.

AIMS: Pyoderma, predominantly associated with Staphylococcus pseudintermedius, is a common skin infection of dogs that typically requires long-lasting treatments, complicated by increasing antimicrobial resistance. To investigate new treatment strategies, we aimed at establishing a dog model of pyoderma that closely mimics the natural disease. METHODS AND RESULTS: We inoculated six laboratory beagles with a methicillin-susceptible strain of S. pseudintermedius. One millilitre of approximately 107 , 108 , 109 CFU per ml was topically applied onto clipped and tape stripped area of dog skin, which was then treated with a dermaroller (microneedle size: 500 µm) immediately after administration. Dogs were monitored daily, suspect pustules were cultured for S. pseudintermedius and evaluated by cytological and histopathological methods. After 24 h, all dogs developed papules and pustules at all three bacterial inoculation sites, which worsened over the next 48 h. Cytological samples of all skin lesions revealed neutrophils with intracellular cocci. Histopathology confirmed subcorneal neutrophilic pustular dermatitis with intralesional cocci and acantholytic keratinocytes, consistent with superficial pyoderma. Staphylococcus pseudintermedius was isolated from pustules of all dogs and confirmed to be the inoculating strain. The results were replicated in all dogs after a wash out period of 6 weeks. CONCLUSIONS: These data demonstrate the feasibility of establishing a dog model of pyoderma. SIGNIFICANCE AND IMPACT OF THE STUDY: The new model can be used to evaluate novel prevention and treatment options for canine pyoderma.