Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005–2006)

Diane M. Dereszynski Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Sharon A. Center Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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John F. Randolph Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Marjory B. Brooks Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Alice G. Hadden Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Kiran S. Palyada Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Sean P. McDonough Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Joanne Messick Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Tracy Stokol Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Karyn L. Bischoff Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Stuart Gluckman Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Sara Y. Sanders Departments of Clinical Sciences, Population Medicine and Diagnostic Sciences, and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; and Mendon Village Animal Hospital, 1380B Pittsford-Mendon Rd, Mendon, NY 14506.

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Abstract

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.

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