Aflatoxicosis

Aflatoxins are metabolites produced by fungi growing on spoiled feeds. Increased humidity and warm temperatures are associated with fungal growth. The most important aflatoxin toxicosis is associated with the ingestion of Aspergillus spp.

Aspergillus flavus, A. nomius, and A. parasiticus are the most commonly recognized species that produce aflatoxins. Other less common aflatoxin producing species include A. niger, A. ruber, A. wentii, Penicillium citrinum, and P. frequentans.


Epidemiology

Aflatoxicosis has been reported in most countries and on many spoiled feeds, especially corn, sorghum grain, cottonseed meal, harvested peanuts, peanuts in shells, moldy bread, or rarely on a standing crop, e.g., ears of sweet corn.

The mycotoxin is not destroyed by milling of the grain.

Animal Risk Factors
All animal species are susceptible, but out breaks occur mostly in pigs, sheep, and cattle; beef and dairy cattle are more susceptible than sheep or horses. Young animals of any species are more susceptible than adults, and nursing animals may be at increased risk because aflatoxins are excreted in the milk.

Human Risk Factors
Aflatoxins are an important consideration in the etiology of human hepatocellular carcinoma. Because the toxin is excreted in cows’ milk it has public health importance. High concentrations of aflatoxins in milk may continue to persist for 3 to 4 days after ingestion of the contaminated feed.


Pathogenesis

Aflatoxins are rapidly absorbed from the gastro intestinal tract, entering the portal blood system in a short period of time and concentrating in the liver.

In the liver aflatoxins undergo biotransformation, producing a range of metabolites. Cytochrome P450 is actively involved with the transformation of AFB1 to the toxic metabolite AFB1-8-9-epoxide, which forms adducts with DNA, RNA, and proteins.

AFB1-8-9-epoxide is detoxified by conjugation with glutathione. About 1% to 2% of ingested AFB1 is metabolized to AFM1 and secreted into the milk.

Excretion occurs primarily through the urine, bile and feces, but also to some extent in the milk, eggs and semen.

The toxic effects of aflatoxins are most pronounced in the liver where the metabolism of carbohydrates, lipids and proteins is impaired. The effects of AFB1-8-9-epoxide include inhibition of RNA and protein synthesis and resistance of DNA to repair. Hepatosis and hepatic insufficiency are the principal effects.


Clinical Findings

Cattle
Clinical signs include blindness, walking in circles, ear twitching, teeth grinding, frothing at the mouth, photosensitive dermatitis and keratoconjunctivitis, diarrhea, severe tenesmus, abortion, and anal prolapse. Recumbency is followed by terminal convulsions. The appetite is normal. Affected animals usually die within 48 hours, and calves in the 3 to 6month group are the most susceptible. Amounts of toxin insufficient to cause overt disease in cows may be sufficient to reduce food intake, weight gains, and milk production, and to be associated with diarrhea.

Pigs
In pigs, the period between when the toxin is ingested and when signs appear is thought to be quite long, at least 6 weeks, and varies with the toxicity of the batch of feed. The clinical syndrome includes a rough coat, depression, anorexia, weight loss, muscle tremors, staggering gait, walking in a daze, and recumbency. Some pigs have intermittent or hemorrhagic diarrhea and some have seizures just before death. The course of the disease may be as short as 6 to 12 hours. At necropsy there is icterus, ascites, swelling of the liver, and mesenteric edema.

Horses
Clinical signs are non specific but include depression, anorexia, fever, tremors, ataxia, icterus and hemorrhage. Necropsy lesions include encephalomalacia, hepatocyte necrosis and hepatic fibrosis, bile duct hyperplasia, hemorrhagic enteritis and myocardial degeneration.


Diagnosis confirmation depends on the detection of aflatoxins in the feed and blood serum, and the characteristic gross and histopathological findings in the liver.


Treatment

Symptomatic treatment of hepatic insufficiency is all that can be attempted.


Control

Contaminated feeds can be avoided by proper storage of feed and monitoring batches for aflatoxin content.