Veterinaria

Journal of Veterinary Diagnostic Investigation
http://vdi.sagepub.com/ Aflatoxicosis in Nine Dogs after Exposure to Contaminated Commercial Dog Food
Shelley Joy Newman, Joanne R. Smith, Kate A. Stenske, Leslie B. Newman, John R. Dunlap, Paula M. Imerman and Claudia A. Kirk J VET Diagn Invest 2007 19: 168 DOI: 10.1177/104063870701900205 The online version of this article can be found at:http://vdi.sagepub.com/content/19/2/168

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J Vet Diagn Invest 19:168–175 (2007)

Aflatoxicosis in nine dogs after exposure to contaminated commercial dog food
Shelley Joy Newman,1 Joanne R. Smith,Kate A. Stenske, Leslie B. Newman, John R. Dunlap, Paula M. Imerman, Claudia A. Kirk
Abstract. The purpose of this study was to characterize light and electron microscopic findings from 9 dogs that had consumed aflatoxin-contaminated commercial dog food from recalled batches. Four dogs died and 5 were euthanized after signs of liver failure. Analysis of feed and liver samples confirmed exposure toaflatoxin. Of the 9 dogs, 8 had classic signs of liver failure, and 1 had signs of liver failure. Enlarged, pale yellow livers were seen macroscopically at necropsy in the dogs with subacute hepatopathy, and cirrhosis was noted in the dog with chronic hepatopathy. Histopathologic findings included hepatic lipidosis, portal fibroplasia, and biliary hyperplasia, which supported a diagnosis ofsubacute toxic hepatopathy in the 8 symptomatic animals. Marked lobular atrophy, bridging portal fibrosis, and regenerative hepatocellular nodules characterized the dog with chronic hepatopathy. Electron microscopy revealed marked hepatocellular lipid vacuolation and early fibroplasia in the dogs with acute hepatopathy and marked fibrosis and regeneration in the dog with chronic hepatopathy. Analysis offeed for aflatoxin consistently revealed high levels of aflatoxin B1 (range of 223–579 ppb), and hepatic tissue contained elevated levels of aflatoxin B1 metabolite M1 (0.6–4.4 ppb). Although dogs are not commonly affected by aflatoxicosis, they are highly susceptible and can present with classic signs of acute or chronic hepatopathy. Characteristic gross, histologic, and electron microscopicchanges help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis. Key words: Aflatoxin; canine; hepatopathy; liver; toxicity.

Introduction Aflatoxicosis has been documented in humans, cats, dogs, rodents, pet birds, cattle, and poultry after exposure to feed contaminated with amycotoxinproducing fungus.4,6,10,12–15 Aflatoxin outbreaks are more common in livestock than in dogs. The last large canine outbreak in the United States was in 1998.6 The current case series resulted from an outbreak associated with mycotoxin-contaminated corn processed into dry commercial dog food.18 This outbreak affected animals throughout the eastern United States in late 2005 through early 2006.Although a previous publication included some of the same dogs,18 the
From the Department of Pathology, University of Tennessee, College of Veterinary Medicine, Room A201, 2407 River Dr., Knoxville, TN, 37996-4542 (Newman); the Department of Small Animal Clinical Sciences, UTCVM, 2407 River Dr., Knoxville, TN, 37996 (Smith, Stenske, Kirk), the Bishop Animal Hospital, Benton, TN 37037 (L. B....