RESUMO
OBJECTIVE: To characterize clinical signs, clinicopathologic features, treatments, and survival in dogs with naturally acquired foodborne aflatoxicosis. DESIGN: Retrospective case series. ANIMALS: 72 dogs that consumed aflatoxin-contaminated commercial dog food. PROCEDURES: Medical records of affected dogs were reviewed. Between December 2005 and March 2006, dogs were identified as having foodborne aflatoxin hepatotoxicosis on the basis of the history of consumption of contaminated food or characteristic histopathologic lesions (subject dog or a recently deceased dog in the same household or kennel). Recorded information included signalment, clinical features, clinicopathologic test results, treatments, and survival. Data were analyzed by survival status. RESULTS: Most dogs were of large breeds from breeding kennels. No significant differences were found in age or weight between 26 (36%) survivor dogs and 46 (64%) nonsurvivor dogs. Severity of clinical signs varied widely; 7 dogs died abruptly. In order of onset, clinical features included anorexia, lethargy, vomiting, jaundice, diarrhea (melena, hematochezia), abdominal effusion, peripheral edema, and terminal encephalopathy and hemorrhagic diathesis. Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia. Cytologic hepatocellular lipid vacuolation was confirmed in 11 dogs examined. In comparisons of clinicopathologic test results between survivor and nonsurvivor dogs, only granular cylindruria (7/21 dogs) consistently predicted death. Best early markers of aflatoxicosis were low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia. Despite aggressive treatment, many but not all severely affected dogs died. CONCLUSIONS AND CLINICAL RELEVANCE: Serum liver enzyme activities and bilirubin concentration were unreliable early markers of aflatoxin hepatotoxicosis in dogs. Hypocholesterolemia and decreased plasma protein C and antithrombin activities may function as exposure biomarkers.
Assuntos
Aflatoxinas/intoxicação , Doenças do Cão/patologia , Doenças Transmitidas por Alimentos/veterinária , Fígado/patologia , Aflatoxinas/análise , Ração Animal/análise , Animais , Antitrombinas/metabolismo , Biomarcadores/sangue , Colesterol/sangue , Doenças do Cão/sangue , Doenças do Cão/mortalidade , Cães , Feminino , Contaminação de Alimentos/análise , Doenças Transmitidas por Alimentos/sangue , Doenças Transmitidas por Alimentos/mortalidade , Doenças Transmitidas por Alimentos/patologia , Fígado/enzimologia , Masculino , Proteína C/metabolismo , Estudos Retrospectivos , Análise de SobrevidaRESUMO
Previously reported cases of congenital cutaneous mast cell tumours in calves were characterized by multiple discrete nodules. The calf presented herein is, to the authors' knowledge, the first documented case of congenital diffuse cutaneous mastocytosis. The entire skin was thickened and wrinkled with particularly prominent skin folds on the head, ventrum, and legs. Histological examination of two haired skin specimens (eyelid, muzzle margin) revealed that the dermis was diffusely infiltrated by sheets of neoplastic mast cells.