Aflatoxin is a product of several species of fungus in the genera Aspergillus (e.g., A. flavus and A. parasiticus) and Penicillium, which may grow on a variety of crops including corn, peanuts, cottonseed, walnuts and pecans. It can be produced in the field before harvest or during food storage. Contaminated corn is believed to have been the source of aflatoxin in the recent serious dog food-related outbreak.

Aflatoxin especially targets the liver where it is activated by enzymes. The toxic adduct avidly binds with DNA and proteins, altering the metabolic abilities of involved hepatocytes. 100 parts per billion (ppb) aflatoxin in dog food has been associated with canine illness; this is the equivalent of 100 kernals of corn in a filled, 45-foot silo, 16 feet in diameter!

The onset of clinical signs is insidious and may be delayed for 3 weeks or longer after exposure. Signs remain vague initially and can progress to inappetence, lethargy, vomiting and weight loss. Other signs include polyuria/polydipsia, mild jaundice, hematochezia, melena, hematemesis, bruising, abdominal distention, modified transudate progressing to a hemorrhagic body cavity, effusions, and peripheral edema. Severely affected animals may succumb to severe gastrointestinal blood loss, hepatic encephalopathy and severe hypogylcemia.

Based on current understanding, the minimum data base for detecting exposure to aflatoxin is a dietary review, thorough physical examination, CBC, biochemistry profile and urinalysis. Decreased concentrations of antithrombin III and protein C are reported to be an early indicator of aflatoxicosis. Liver damage from aflatoxin exposure may still be present even if results of laboratory tests are within normal limits.

Hematology profile is usually normal, but may show neutropenia, anemia and/or thrombocytopenia; biochemistry profile shows variable mild to moderate increases in ALT, moderately low cholesterol, high total bilirubin (between 5-9 mg/dL); coagulation profile shows high APTT and PT, and significantly lowered antithrombin and protein C activity; urinalysis reveals dilute urine and granular casts as toxicity escalates. On liver cytology there is microvesicular fatty vacuolation, and liver histopathology reveals hepatocellular fatty vacuolation and perivenular inflammation. As the condition progresses, there may be acute onset of portal hypertension, abdominal effusion, and bleeding into the distal small intestine and colon.

In acute cases, histopathology reveals hemorrhage and necrosis with dissociation of hepatic cords. More chronic lesions include lipidosis, biliary hyperplasia and portal fibrosis with infiltrates of lymphocytes and macrophages. Foci of necrosis are also noted.