Aflatoxicosis is a disease caused by the consumption of aflatoxins. Aflatoxins are secondary mold metabolites produced by some strains of Aspergillus flavus and Aspergillus parasiticus. The four most common aflatoxins are B1, B2, G1, and G2. Contaminated grains and grain byproducts are the most common sources of aflatoxin. Corn silage may also be a source of aflatoxins, because the ensiling process does not destroy toxins already present in silage.
   Aflatoxins are metabolized in ruminants by the liver and are excreted in the bile. Aflatoxin B1 is the most potent mycotoxin (toxic substance produced by a mold) to affect cattle. B1 increases the apparent protein requirement of cattle and is a potent carcinogen (cancer causing agent). When significant quantities of B1 are consumed, the metabolite M1 appears in milk within 12 hours. Research suggests M1 is not as carcinogenic or mutagenic as B1, but it does appear to be as toxic as its parent compound.


    Beef and dairy cattle are more susceptible to aflatoxicosis than sheep or horses, although other mycotoxicoses occur in these species, such as facial eczema in sheep and leukoencephalomalacia in horses. Young animals of all species are more susceptible than mature animals to the effects of aflatoxin. Pregnant and growing animals are less susceptible than young animals, but more susceptible than mature animals.

   Feed refusal, reduced growth rate and decreased feed efficiency are the predominant signs of chronic aflatoxin poisoning. In addition, listlessness, weight loss, rough hair coat and mild diarrhea may occur. Anemia along with bruises and subcutaneous hemorrhage are also symptoms of aflatoxicosis. The disease may also impair reproductive efficiency, including abnormal estrous cycles (too short and too long) and abortions. Other symptoms include impaired immune system response, increased susceptibility to disease, and rectal prolapse.


    Clinical laboratory findings vary with the animal species, level of aflatoxin in the ration, and the duration of feeding. There are no consistent diagnostic changes in hematocrit, hemoglobin, and differential cell counts in animals fed aflatoxin. Leukocytosis may occur in animals with secondary bacterial infections. Serum bilirubin levels may be elevated and typically serum protein levels are decreased.

    Lesions observed at necropsy related to either acute or chronic liver disease are dependent upon the level of aflatoxin and the duration of feeding. A majority of acute liver damage observed has been the result of experimentally high doses, while chronic liver damage is a more common field observation. The liver is usually pale tan, yellow or orange. Hepatic fibrosis and edema of the gallbladder may also be observed.


   The diagnosis of aflatoxicosis is often difficult because of the variation in clinical signs, gross pathological conditions and the presence of infectious diseases due to the suppression of the immune system. On the farm, more than one mold or toxin may be present in the contaminated feed, which often makes definitive diagnosis of aflatoxicosis difficult.

   The prognosis of aflatoxicosis depends upon the severity of liver damage. Once overt symptoms are noticed than prognosis is poor. Treatment should be directed at the severely affected animals in the herd and further poisoning prevented.


   Aflatoxicosis is typically a herd rather than an individual cow problem. If aflatoxicosis is suspected, the ration should be analyzed immediately. If aflatoxins are present, the source should be eliminated immediately. Levels of protein in the ration and vitamins A,D,E,K and B should be increased as the toxin binds vitamins and affects protein synthesis. Good management practices to alleviate stress are essential to reduce the risk of secondary infections. Secondary infections must receive immediate attention and treatment.


   Aflatoxicosis can only be prevented by feeding rations free of aflatoxin. Preventing aflatoxin contamination is outlined in fact Sheet 444, but since preventing contamination is not always possible, here are a few keys facts to remember when dealing with contaminated feeds in animal rations:

  -  The recommended feeding level is 0 parts per billion (ppb).

  -  The level of aflatoxin an animal can tolerate will depend upon the age and sex of the animal, its health status, and overall management level of the farm.

  -  To avoid contamination of milk, lactating dairy cattle should not receive more than 20 ppb in the total ration.

-  Calves should not receive milk from cows fed in excess of 20 ppb.

  -  Beef cattle should not receive more than 400 ppb in the total ration. Weanlings should not receive more than 100 ppb in their total ration.

   -  Poultry and swine are more sensitive to aflatoxin contamination and should not receive more than 20 ppb aflatoxin in the total ration.

    These are only suggested guidelines. This does not suggest that feeding at these levels or below will reduce or eliminate the potential for aflatoxicosis. There are no clear-cut safe feeding levels. To feed at a level other than 0 ppb is a risk assumed by the person making the decision to do so.


    Aflatoxins are highly toxic to livestock, poultry and people. Even fed at nonfatal levels, aflatoxin can seriously impair animal health and productivity. For lactating dairy cattle, do not exceed 20 ppb aflatoxin in rations to avoid exceeding the food and Drug Administration level of 0.5 ppb in milk. Aflatoxin is just one of many mycotoxins that can adversely affect animal health and productivity.