FDA's Bad Bug Book
Aflatoxicosis is poisoning that results from ingestion of aflatoxins in contaminated food or feed. The aflatoxins are a group of structurally related toxic compounds produced by certain strains of the fungi Aspergillus flavus and A. parasiticus. Under favorable conditions of temperature and humidity, these fungi grow on certain foods and feeds, resulting in the production of aflatoxins. The most pronounced contamination has been encountered in tree nuts, peanuts, and other oilseeds, including corn and cottonseed. These toxins are usually found together in various foods and feeds in various proportions.
Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the liver in a number of animal species; no animal species is resistant to the acute toxic effects of aflatoxins; hence it is logical to assume that humans may be similarly affected. Animal species respond differently in their susceptibility to the chronic and acute toxicity of aflatoxins. The toxicity can be influenced by environmental factors, exposure level, and duration of exposure, age, health, and nutritional status of diet. In each species, the liver is the primary target organ of acute injury. The relative susceptibility of humans to aflatoxins is not known, even though epidemiological studies in Africa and Southeast Asia, where there is a high incidence of hepatoma, have revealed an association between cancer incidence and the aflatoxin content of the diet. These studies have not proved a cause-effect relationship, but the evidence suggests an association.
One of the most important accounts of aflatoxicosis in humans occurred in more than 150 villages in adjacent districts of two neighboring states in northwest India in the fall of 1974. According to one report of this outbreak, 397 persons were affected and 108 persons died. In this outbreak, contaminated corn was the major dietary constituent, and aflatoxin levels of 0.25 to 15 mg/kg were found. The patients experienced high fever, rapid progressive jaundice, edema of the limbs, pain, vomiting, and swollen livers. One investigator reported a peculiar and very notable feature of the outbreak: the appearance of signs of disease in one village population was preceded by a similar disease in domestic dogs, which was usually fatal. Histopathological examination of humans showed extensive bile duct proliferation and periportal fibrosis of the liver together with gastrointestinal hemorrhages. A 10-year follow-up of the Indian outbreak found the survivors fully recovered with no ill effects from the experience.
A second outbreak of aflatoxicosis was reported from Kenya in 1982. There were 20 hospital admissions with a 60% mortality; daily aflatoxin intake was estimated to be at least 38 ug/kg body weight for an undetermined number of days.