Aflatoxin is a product of serveral species of fungus in the genus Aspergillus (e.g.,A. flavus and A. parasiticus, 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.

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. The first signs usually are vague and include inappetence, nausea and lethargy. As the syndrome advances, vomiting and diarrhea progressivley become blood tinged. The development of jaundice indicates substantial liver injury; this sign develops in the most severely affected dogs. Terminal signs involve the development of an abdominal effusion (modified transudate) and severe hemorrhage into the distal small bowel and colon. Signs of a diffuse coagulopathy also may develop that may be severe enough to be confused with warfarin rodenticide exposure (clinical signs). Severely affected animals may succumb to severe gastrointestinal blood loss, hepatic encephalopathy and severe hypogylcemia.

We hope the following will prove helpful in providing a reference point to you clients. 100 parts per billion(ppb) aflatoxin in dog food has been associated with canine illess. This is the equivalent of 100 kernals of corn in a filled, 45-foot silo, 16 feet in diameter

The onset of clinical signs may be delayed for 3 weeks or longer after exposure.  Based on our current understanding, the minimum data base for detecting exposure to aflatoxin is a biochemistry profile and determination of antithrombin and protein C activity.  However, because dogs with suspected aflatoxin exposure can have a chronic underlying disease that has been mistaken for aflatoxicosis, it is recommended that ill dogs have a full baseline hemogram, biochemical profile, and urinalysis along with the antithrombin and protein C tests.  If an animal is not showing clinical signs, and the intent is to “screen for aflatoxin effects on the liver”, then it is recommended that a biochemical profile and the antithrombin and protein C tests be conducted weekly for a minimum of 3 weeks.  In lieu of a biochemical profile, one could use ALT activity, cholesterol, and total bilirubin as a minimum data base.  Low cholesterol has been an early change.  ALT activity is not usually as elevated as expected with other liver abnormalities.  Normal blood results do not rule out liver damage from aflatoxin exposure.

Information regarding the tests you may want to submit is listed below. 

If animals die, we recommend a complete necropsy.  Whole body (refrigerated, not frozen) or a complete set of fixed tissues including liver (in 10% neutral-buffered formalin) should be submitted to the AHDC for a diagnosis.  The histologic lesions in the liver are unique for aflatoxin because diffuse lipidosis caused by this toxin is otherwise rarely found in dogs.

The Toxicology Laboratory of the AHDC offers aflatoxin testing on pet food.  Because the delay between exposure and clinical signs may be several weeks, contaminated feed may be used up by the time the animal presents with clinical signs.  Samples should be taken from different areas of the bag, combined, and submitted in a clean, dry container.  Please note that low aflatoxin concentrations in the food do not rule out exposure. 

For additional details regarding sample submissions to the AHDC, please refer to our sample submission web page at www.diagcenter.vet.cornell.edu/subreq/ or call 607-253-3900