Occurrence and clinical manifestations of aflatoxicosis

Abstract

The modern age of mycotoxicology began a quarter of a century ago when a mold contaminated batch of Brazilian peanut meal was incorporated into poultry ration by an English feed manufacturer and resulted in the deaths of 100,000 turkeys, 14,000 ducklings, and thousands of partridge and pheasant poults. Because the causative agent was unknown, the disease was initially called Turkey ‘X’ disease [9]. The rapid series of experimental observations that were made led to the discovery of the aflatoxins, and these coumarin-type compounds have become one of the most investigated groups of toxins in history. Today we know many of the conditions that favor growth of the toxin-producing fungi and that optimize production of aflatoxins by the fungi. We know the levels of contamination that will produce both acute and chronic toxicity problems in many domestic and laboratory species. We have extensive information on the tissue distribution and excretion patterns of aflatoxins administered by various routes. We know structures and rates of formation of many of the biotransformation products, and we have a substantial amount of evidence that one of these metabolites, the highly reactive 2,3-oxide, is responsible for both the acute effects and the carcinogenic activity of aflatoxin B₁ Recent work on the formation and the nature of aflatoxin-DNA adducts has begun to reveal the qualitative, quantitative and kinetic properties underlying the molecular basis for aflatoxin-induced carcinogenesis [29]. In this review I will attempt to (i) briefly describe some factors that influence the occurrence of aflatoxin contamination, (ii) describe the clinical symptoms that occur in aflatoxicosis and the criteria required in order to establish aflatoxin as the probable causative agent, and (iii) discuss aflatoxin as a threat not only to domestic animals but to human populations as well.