Aflatoxicosis can affect all animals. The fungus Aspergillus flavus and possibly other species A. parasiticus and Penicillium verrucosum are able to produce highly toxic difuranocoumarin compounds known as aflatoxins. Intoxication with these compounds is known as aflatoxicosis. Aflatoxin B1 (B is for its blue fluorescence) is the most toxic of this group. Aflatoxicosis is not a significant problem in NZ, but it does occur in some species in Australia and it has very far reaching effects in humans and animals in many countries of the world.
Aspergillus flavus is a ubiquitous fungus and is found commonly in stored foods. It has been reported in stored peanuts, cereal grains, damaged nuts and grain and those which have not dried out sufficiently are also conducive to mould growth. The fungus will also grow readily in sorghum, meal and mouldy bread. In Queensland scavenging dogs frequently become affected from mouldy food obtained from rubbish tips and containers.
While the aflatoxins are poisonous to all domestic species, they are particularly toxic to ducks and least toxic for sheep. The toxic effects of aflatoxins are both dose and time dependent. The compounds are readily absorbed from the stomach and metabolised in the liver to a range of toxic and non toxic metabolites which are then excreted in the urine and milk. Aflatoxin inhibits RNA and protein synthesis and the pathological consequences of this in the liver are centrilobular necrosis in most species and marked fatty infiltration. This is often accompanied by biliary ductular hyperplasia and cirrhosis. Aflatoxins are highly carcinogenic and they may be implicated in neoplastic conditions of the liver in domestic animals.
In acute aflatoxicosis, animals may die suddenly without clinical signs. Less acutely affected animals show anorexia and depression accompanied by ataxia, dyspnoea and anaemia. There may be epistaxis, haemorrhagic gastroenteritis, jaundice, haematomata and severe hypoprothrombinaemia. In chronic aflatoxicosis, the efficiency of food conversion is reduced, animals become unthrifty, jaundiced, anaemic and depressed and there is an enhanced susceptibility to other infectious diseases. Pregnant animals may abort.
Liver lesions range from acute swelling with hepatocellular necrosis, fatty infiltration, biliary retention, biliary ductular hyperplasia, oedema of the gall bladder and ascites, to cirrhosis with regeneration nodules, fatty infiltration, hepatocellular pleomorphism and marked biliary duct hyperplasia. Haemorrhages under serous surfaces are common and free blood is often present in the alimentary tract. Subcutaneous haemorrhages and oedema of the mesentery are also present.
For a diagnosis of aflatoxicosis, analysis of feed for mycotoxins should be carried out. At necropsy, stomach contents should be assayed for aflatoxin, and the hydroxylated metabolites aflatoxin M1 and M2 may be isolated from the liver.
If a mycotoxicosis is confirmed, the only effective treatment is to remove contaminated feed. Recovery will depend on the nature and amount of toxin present and the duration of exposure to the contaminated feed.
Control of aflatoxicosis through preventing mycotoxin formation in stored feed is a major goal in controlling the toxic effects in livestock and poultry in particular. Good feed management practices (for example, systematic clean up of feedlines and augers; feed grain storage at proper moisture content, i.e. below 13%; inspection of grain regularly for temperature, insects and wet spots), will limit the possibility of fungal development in feeds and feedstuffs. In some areas of the world it is common practice to aerate and ventilate grain stores to prevent moisture spots forming.
Mycotoxins can be produced in crops prior to harvest so that harvesting at maturity and the avoidance of crop damage are important factors in preventing early mycotoxin development.
If, for economic reasons, it is necessary to use mouldy or suspect feed, the following principles may prevent toxicity developing:
Mildly affected animals may recover from the condition but usually after a long convalescence. It is considered that for all classes of food producing animals, chronic low grade aflatoxicosis may be a cause of depressed productivity.
Clarkson, J.R. (1980). Aflatoxicosis in swine: A Review. Vet Hum Toxicol. 22:20 22.
Vaid, J., Dawra, R.K. and Negi, S.S. (1981). Chronic Aflatoxicosis in Cattle. Veterinary and Human.Toxicology. 23:436 438.