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Find information on animal health topics, written for the veterinary professional.


By Gary D. Osweiler, DVM, MS, PhD, Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University

Aflatoxins are produced by toxigenic strains of Aspergillus flavus and A parasiticus on peanuts, soybeans, corn (maize), and other cereals either in the field or during storage when moisture content and temperatures are sufficiently high for mold growth. Usually, this means consistent day and night temperatures >70°F. The toxic response and disease in mammals and poultry varies in relation to species, sex, age, nutritional status, and the duration of intake and level of aflatoxins in the ration. Earlier recognized disease outbreaks called “moldy corn toxicosis,” “poultry hemorrhagic syndrome,” and "Aspergillus toxicosis” may have been caused by aflatoxins.

Aflatoxicosis occurs in many parts of the world and affects growing poultry (especially ducklings and turkey poults), young pigs, pregnant sows, calves, and dogs. Adult cattle, sheep, and goats are relatively resistant to the acute form of the disease but are susceptible if toxic diets are fed over long periods. Experimentally, all species of animals tested have shown some degree of susceptibility. Dietary levels of aflatoxin (in ppb) generally tolerated are ≤50 in young poultry, ≤100 in adult poultry, ≤50 in weaner pigs, ≤200 in finishing pigs, <50 in dogs, <100 in calves, and <300 in cattle. Approximately two times the tolerable levels stated is likely to cause clinical disease, including some mortality. Dietary levels as low as 10–20 ppb result in measurable metabolites of aflatoxin (aflatoxin M1 and M2) being excreted in milk; feedstuffs that contain aflatoxins should not be fed to dairy cows. Acceptable regulatory values in milk may range from 0.05 ppb to 0.5 ppb in different countries; individual state or federal regulatory agencies should be consulted when contamination occurs.

Aflatoxins are metabolized in the liver to an epoxide that binds to macromolecules, especially nucleic acids and nucleoproteins. Their toxic effects include mutagenesis due to alkylation of nuclear DNA, carcinogenesis, teratogenesis, reduced protein synthesis, and immunosuppression. Reduced protein synthesis results in reduced production of essential metabolic enzymes and structural proteins for growth. The liver is the principal organ affected. High dosages of aflatoxins result in hepatocellular necrosis; prolonged low dosages result in reduced growth rate, immunosuppression, and liver enlargement.

Clinical Findings:

In acute outbreaks, deaths occur after a short period of inappetence; other acute signs include vomiting, depression, hemorrhage, and icterus. Subacute outbreaks are more usual, with unthriftiness, weakness, anorexia, reduced growth and feed efficiency, and occasional sudden deaths. Laboratory changes in most species are related to liver damage, coagulopathy, and impaired protein synthesis. Specific laboratory changes include increased AST, ALT, and alkaline phosphatase; hypothrombinemia, prolonged prothrombin and activated partial thromboplastin times, hyperbilirubinemia, hypocholesterolemia, hypoalbuminemia, and variable thrombocytopenia. Generally, aflatoxin concentrations in feed twice the tolerable levels given above are associated with acute aflatoxicosis. Recently, acute and fatal aflatoxicosis with many of these signs and laboratory changes has been documented in dogs. Frequently, there is a high incidence of concurrent infectious disease, often respiratory, that responds poorly to the usual drug therapy. Dairy cattle experience inappetence, and ruminants may have decreased ruminal contractions at high concentrations (>1,000 ppb) of aflatoxins. Liver damage can lead to reduced clotting factor synthesis with acute to chronic hemorrhage. Subclinical effects are reduced growth rate and feed efficiency, hypoproteinemia, and reduced resistance to some infectious diseases despite vaccination.


In acute cases, there are widespread hemorrhages and icterus. The liver is the major target organ. Microscopically, the liver is enlarged and shows marked fatty accumulations and massive centrilobular necrosis and hemorrhage. In subacute cases, the hepatic changes are not so pronounced, but the liver is somewhat enlarged and firmer than usual. There may be edema of the gallbladder. Microscopically, the liver shows periportal inflammatory response and proliferation and fibrosis of the bile ductules; the hepatocytes and their nuclei (megalocytosis) are enlarged. The GI mucosa may show glandular atrophy and associated inflammation. Rarely, there may be tubular degeneration and regeneration in the kidneys. Prolonged feeding of low concentrations of aflatoxins may result in diffuse liver fibrosis (cirrhosis) and, rarely, carcinoma of the bile ducts or liver.


Disease history, laboratory data, necropsy findings, and microscopic examination of the liver should indicate the nature of the hepatotoxin, but hepatic changes are somewhat similar in Senecio poisoning (see Pyrrolizidine Alkaloidosis). The presence and levels of aflatoxins in the feed should be determined. Acutely affected animals have increases in liver enzymes (alkaline phosphatase, AST, or ALT), bilirubin, serum bile acids, and prothrombin time. Chronic exposure can cause hypoproteinemia (including decrease in both albumin and globulin). Aflatoxin M1 (principal metabolite of aflatoxin B1) can be detected in urine, liver, kidney, or milk of lactating animals if toxin intakes are high. Aflatoxin residues in organs and dairy products generally are eliminated within 1–3 wk after exposure ends.


Contaminated feeds can be avoided by monitoring batches for aflatoxin content. Local crop conditions (drought, insect infestation) should be monitored as predictors of aflatoxin formation. Young, newly weaned, pregnant, and lactating animals require special protection from suspected toxic feeds. Dilution with noncontaminated feedstuffs is one possibility, but this may not be acceptable on a regulatory basis. Cleaning to remove lightweight or broken grains will often substantially reduce mycotoxin concentration in remaining grain. Ammoniation reduces aflatoxin contamination in grain but is not currently approved by the FDA for use in food animals in the USA because of uncertainty about by-products produced.

Numerous products are marketed as anticaking agents to sequester or "bind" aflatoxins and reduce absorption from the GI tract. One effective binder for aflatoxins is hydrated sodium calcium aluminosilicates (HSCAS), which reduce the effects of aflatoxin when fed to pigs or poultry at 10 lb/ton (5 kg/tonne). They also provide substantial protection against dietary aflatoxin. HSCAS reduce aflatoxin M1 in milk by ~50% but do not eliminate residues of aflatoxin M1 in milk from dairy cows fed aflatoxin B1. Other adsorbents (sodium bentonites, polymeric glucomannans) have shown variable but partial efficacy in reducing low-level aflatoxin residues in poultry and dairy cattle. To date, the FDA has not licensed any product for use as a "mycotoxin binder" in animal feeds.