Peer-reviewed veterinary case report
Signs and survival in 72 dogs after eating aflatoxin-contaminated food
By Dereszynski, Diane M et al.·Published in Journal of the American Veterinary Medical Association·2008·Department of Clinical Sciences, United States·View original on PubMed →
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Original publication title: Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005-2006).
- Species:
- dog
Plain-English summary
A group of 72 dogs developed serious liver problems after eating contaminated dog food that contained aflatoxins, a type of toxin produced by mold. Symptoms included loss of appetite, lethargy, vomiting, yellowing of the skin (jaundice), and diarrhea. Despite aggressive treatment, many of the dogs did not survive, especially those showing severe symptoms. The study found that low levels of certain proteins in the blood could indicate a higher risk of death. Unfortunately, common tests for liver damage were not reliable early on, making it difficult to predict which dogs would recover.
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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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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/18447777/