AFLATOXICOSIS
Aflatoxicosis occurs following the ingestion of aflatoxins, a group of difuranocoumarins produced by toxigenic strains of Aspergillus flavus or Aspergillus parasiticus. The major aflatoxins are B1, B2, G1 and G2 and aflatoxin M1, an hydroxylated metabolite found primarily in animal tissues and fluids (milk and urine) as a metabolic product of aflatoxin B1.
Aspergillus spp. are saprophytic organisms, which are disseminated via their conidia and carried by wind or insects to the growing crop. Initially fungi can grow in grains and can form sufficient moisture from metabolism to allow further growth and the production of mycotoxins. Grain stored under high moisture/humidity (>14%) at warm temperatures (>20°C) and/or inadequately dried can potentially become contaminated.
Aflatoxicosis has been documented worldwide and in many animal species, with a considerable variation in susceptibility between species and within age groups. Among domestic animals, calves, pigs and dogs are highly sensitive to toxic effects; among avian species, ducklings and turkey poults are the most sensitive, whereas chickens are the most resistant(2). In general, birds are more susceptible than mammals, and young birds are more susceptible than adult birds. Mortality caused by the exposure to aflatoxins has been reported in free-ranging birds, mainly from North America, including a variety of duck species (mallard (Anas platyrhynchos), lesser scaup (Aythya affinis), gadwall (Anas strepera) and blue- and green-winged teal (Anas carolinensis)), snow geese (Chen caerulescens) and sandhill cranes ( Grus canadensis). Aflatoxin concentrations of 800mg∕kg have been found to produce subclinical hepatic injury in young white-tailed deer (Odocoileus virginianus)(3).
The aflatoxins are primarily hepatotoxic, immunosuppressive, carcinogenic, teratogenic and mutagenic. Afla- toxicosis can occur in two forms (acute and subacute) depending upon the concentration of toxins in food and length of exposure.
The subacute form is usually associated with prolonged exposure to low concentration of toxin and is generally characterized by a slowly developing illness and reduced growth rate. Chronic exposure can also result in a shrunken, fibrous liver with regenerative nodules, or it may result in tumours in birds. Immunosuppression can also occur in affected groups of animals. Acute aflatoxicosis is associated with a high concentration of toxin, and clinical signs are characterized by ataxia, opisthotonos and death. Hepatopathy and cutaneous haemorrhages have been documented in young birds older than 3 weeks of age. Liver haemorrhages can occur as multiple focal areas, or as diffuse areas. Haemorrhages in many organs and excessive fluid in the thorax and abdomen may be observed.The diagnosis is difficult because clinical signs are not specific. Tissues can be examined for gross lesions and typical microscopic lesions (e.g. liver necrosis and/or proliferation of lesions in the bile ducts). Measurement of aflatoxin levels in ingesta and tissues collected from affected animals and from grain are important for confirming the diagnosis. Aflatoxin intoxications can be prevented by appropriate measures, particularly the careful handling of grains and feed, especially following harvesting and during storage. Treatment with ammonia gas at high temperature and pressure has been used to detoxify contaminated batches of feed, whereas addition of hydrate sodium calcium aluminosilicate to feed has been reported to reduce aflatoxin toxicity.