Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B₁ in Poultry

This review is a comprehensive introduction to the effects of poultry exposure to the toxic and carcinogenic mycotoxin aflatoxin B₁ (AFB₁). The relationship between AFB₁ sensitivity and metabolism, major direct and indirect effects of AFB₁, recent studies of gene expression and transcriptome responses to exposure, and mitigation strategies to reduce toxicity are discussed. Exposure to AFB₁ primarily occurs by consumption of contaminated corn, grain or other feed components. Low levels of residual AFB₁ in poultry feeds can cause reduction in growth, feed conversion, egg production, and compromised immune functions, resulting in significant economic costs to producers. Thus, AFB₁ acts as a “force multiplier” synergizing the adverse effects of microbial pathogens and other agents, and factors detrimental to poultry health. Domestic turkeys (Meleagris gallopavo) are one of the most sensitive animals known to AFB₁ due, in large part, to a combination of efficient hepatic bioactivation by cytochromes P450 1A5 and 3A37, and deficient hepatic glutathione-S-transferase (GST)-mediated detoxification. Because of their sensitivity, turkeys are a good model to investigate chemopreventive treatments and feed additives for their ability to reduce AFB₁ toxicity. Transcriptome analysis (RNA-seq) of turkey poults (liver and spleen) has identified AFB₁-induced gene expression changes in pathways of apoptosis, carcinogenesis, lipid regulation, antimicrobial activity, cytotoxicity and antigen presentation. Current research focuses on further identifying the molecular mechanisms underlying AFB₁ toxicity with the goal of reducing aflatoxicosis and improving poultry health.