In 1952, an outbreak of fatal liver disease in dogs occurred in the southeastern United States. The disease, termed hepatitis X, was characterized by icterus, lethargy, anorexia, petechiae, melena, epistaxis, and hematemesis. Affected dogs died one
to 14 days after clinical presentation.1-4 The postmortem findings of hepatitis X were noted to be similar to those in swine and cattle after ingestion of moldy corn.5 Further investigation revealed that the disease resulted from exposure to aflatoxins produced by the fungus Aspergillus species. In 1959, the role of aflatoxins in hepatitis X was confirmed when a group of dogs acquired the disease after being
fed purified aflatoxin B1.6
Since the identification of aflatoxins, poisonings have been described in many species, including people, dogs, poultry, swine,
and other livestock. Aflatoxicosis inflicts varying degrees of hepatic damage depending on the species, exposure (dose and
duration), and the animal's nutritional status (protein and vitamin intake).7-10 Of the four natural aflatoxins—B1, B2, G1, and G2—aflatoxin B1 is the most toxic. In addition to having mutagenic and immunosuppressive effects, it is a potent carcinogen that has been
linked to hepatic cell carcinoma in people.9,11
Studies on aflatoxicosis in dogs have focused on its diagnosis and the pathologic changes that occur after aflatoxin exposure.
No antidotes for the toxins exist, and few studies have addressed the care and management of dogs with aflatoxicosis. This
article focuses on the therapeutic management of canine aflatoxicosis, drawing from treatments used in other cases of hepatotoxicosis
or hepatic failure.
ROUTE OF EXPOSURE
Most cases of aflatoxicosis occur when animals ingest moldy corn, peanuts, or other foods susceptible to contamination by
Aspergillus flavus or Aspergillus parasiticus.7,8,12 Preventive measures can be taken by pet food manufacturers through careful monitoring of aflatoxin concentrations in food
and proper storage of food in a clean, dry area.
Outbreaks of aflatoxicosis continue to occur. In December 2005, several acute outbreaks of hepatic failure in dogs across
the United States raised suspicion of a food-related toxicosis. Postmortem examination of the affected dogs revealed severe
liver damage suggestive of aflatoxicosis. Affected dogs consumed food produced by a single manufacturer. Analysis of the pet
food confirmed contamination with aflatoxins. The manufacturer issued a recall, and the FDA released an alert, but over the
course of the next few weeks more than 100 dogs became intoxicated and died.13,14
Dogs with aflatoxicosis often have a vague initial presentation because of the insidious onset of the disease. Signs include
anorexia, lethargy, vomiting, and jaundice. Hematochezia, melena, and hematemesis are sometimes present, as well as mucosal
or more widespread petechiae and ecchymoses. Patients may have peripheral edema or ascites. Polyuria and polydipsia may also
be noted. In some cases of toxicity, acute death occurs before clinical signs are noted. The disease is progressive, and the
case fatality rate is high.
The signs of aflatoxicosis are consistent with liver failure; they are not specific for an aflatoxin etiology.4,13,15-18 Other differential diagnoses for acute liver failure include drug toxicosis (e.g. acetaminophen, ketoconazole, carprofen), biotoxins (e.g. blue-green algae, Amanita species mushrooms, cycad palm seed), heavy metal toxicosis, infectious diseases (e.g.
Clostridium species infection, infectious canine hepatitis, systemic fungal infections), and massive ischemia (e.g. arterial or venous occlusion).
CBC, SERUM CHEMISTRY, AND CLOTTING PROFILE FINDINGS
Patients may have mild to moderate anemia and, in cases of disseminated intravascular coagulation (DIC), may be thrombocytopenic.
Hematologic parameters are otherwise unremarkable. Liver enzyme activities (alanine transaminase, alkaline phosphatase, aspartate
transaminase, gamma-glutamyltransferase ) and total bilirubin concentrations are elevated, and cholesterol and albumin concentrations
are decreased. Coagulation profiles are often markedly abnormal, with prolonged activated partial thromboplastin times and
prothrombin times and decreased antithrombin and protein C concentrations.4,13,18