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, <100 in calves, and <300 in cattle. Dietary levels as low as 10–20 ppb may 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; individual 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 doses of aflatoxins result in severe hepatocellular necrosis; prolonged low dosages result in reduced growth rate and liver enlargement.
In acute outbreaks, deaths occur after a short period of inappetence. Subacute outbreaks are more usual, and unthriftiness, weakness, anorexia, and sudden deaths can occur. Generally, aflatoxin concentrations in feed >1,000 ppb are associated with acute aflatoxicosis. Frequently, there is a high incidence of concurrent infectious disease, often respiratory, that responds poorly to the usual chemotherapy. Dairy cattle experience inappetence, and ruminants may have decreased ruminal contractions at high concentrations (>1 ppm) of aflatoxins. Liver damage can lead to reduced clotting factor synthesis with acute to chronic hemorrhage.
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. In the kidneys, there rarely may be tubular degeneration and regeneration. Prolonged feeding of low concentrations of aflatoxins may result in diffuse liver fibrosis (cirrhosis) and carcinoma of the bile ducts or liver.
Disease history, necropsy findings, and microscopic examination of the liver should indicate the nature of the hepatotoxin, but hepatic changes are somewhat similar in Senecio poisoning (p 2722). 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, or kidney or in 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 non-contaminated feedstuff is one possibility. Ammoniation of grain reduces contamination but is not currently approved for use in food animals because of uncertainty about byproducts produced.
Hydrated sodium calcium aluminosilicates (HSCAS) reduce the effects of aflatoxin when fed to pigs or poultry; at 10 lb/ton (5 kg/tonne), they provided substantial protection against dietary aflatoxin. HSCAS reduces aflatoxin M1 by ~50% but does 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.
Last full review/revision March 2012 by Gary D. Osweiler, DVM, MS, PhD, DABVT