Aflatoxicosis in Nine Dogs after Exposure to Contaminated Commercial Dog Food

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 to aflatoxin. 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 of subacute 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 of feed 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 microscopic changes help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis.

A retrospective study of oral prednisolone treatment in canine chronic hepatitis

“…The stage (acute-chronic-cirrhosis) reflects the degree of fibrosis and the extent of disruption of the normal lobular architecture. Known aetiologies include viruses, toxins, and drugs (Watson 2004;Boomkens et al 2005;Rallis et al 2005;Decaro et al 2005;Newman et al 2007;Wagner et al 2007). Hepatic accumulation of copper is a major cause of chronic hepatitis in many breeds (Labrador retriever, Dalmatian, Dobermann, spaniel breeds, West Highland terriers, Bedlington terriers) and may account for about 35% of all cases of hepatitis in a referral hospital population (Van den Ingh et al 1988;Brewer et al 1992;Honeckman 2003;Mandigers et al 2005;Hoffmann et al 2006;Spee et al 2006;Poldervaart et al 2009;Smedley et al 2009).…”

Aflatoxicose em cães na região Sul do Rio Grande do Sul

“…Casos coletivos de aflatoxicose são relatados com frequência e chamam atenção principalmente pelo número elevado de animais que morre em consequência da intoxicação, geralmente com evolução aguda ou subaguda (Newman et al 2007, Dereszynski et al 2008, Arnot et al 2012, Wouters et al 2013. No presente trabalho o caso avaliado do surto apresentou-se, também, com lesões agudas.…”

“…Wouters et al (2013) mencionam que o uso de alimento à base de milho aumenta o risco da ocorrência de aflatoxicose e, portanto, a cirrose hepática pode ser muitas vezes consequência desta micotoxicose, pela prática da alimentação de cães com polenta ou outros derivados de milho. Além disso, os cães são extremamente sensíveis à ação dessas toxinas (Newmann et al 2007, Dereszynski et al 2008) e, no Brasil, o limite máximo permitido de micotoxinas para alimentação animal é 50 ppb e, em cães, a dose tóxica é 60 ppb (Newberne & Butler 1969, Stenske et al 2006, Newman et al 2007). …”

A Review of Class I and Class II Pet Food Recalls Involving Chemical Contaminants from 1996 to 2008

“…In October and November of 1998, a recall was initiated for 1,362,516 bags of 54 pet food brands and treats made by Doane Products Co., Inc. due to aflatoxin contamination [8]. The aflatoxin contamination of the pet food was attributed to a contaminated batch of corn which was not [13,14]. Clinical signs in affected dogs included anorexia, lethargy, vomiting, jaundice, and diarrhea [15].…”

“…Analysis of the feed yielded aflatoxin B 1 in range of 223-579 ppb. In livers of affected dogs, the concentration of aflatoxin M 1 metabolite of aflatoxin B 1 was determined to be in the range of 0.6-4.4 ppb [13,14]. The two pet food aflatoxin adulteration events happened because there was inadequate testing of raw materials, particularly corn, which went into manufacturing of pet food.…”