Aflatoxicosis

AFLATOXICOSIS

  • Aflatoxins are highly toxic and carcinogenic metabolites produced by the fungi Aspergillus flavus and A.parasiticus
  • Aflatoxins are produced when environmental condition favour their growth on certain cereal grains, groundnuts and seeds
  • At least 17 different aflatoxins exist
  • All are structurally related to coumarins
  • The most important are B1, B2, G1, G2 and M1, and these are also the most widespread
  • The designations B and G refer to whether they fluoresce blue or green in ultraviolet light
  • Of these, aflatoxia B1 is the most prevalent and most toxic
  • Aflatoxin M1, a mammalian metabolite of B1, is excreted in milk
  • The most commonly contaminated foods, are groundnuts, maize and cottonseed
  • The first descriptions of aflatoxicosis appeared in 1952, when an epizootic toxic hepatitis (“Hepatitis X”) was described in dogs
  • Later in 1955, it was demonstrated to be the result of feeding commercial dog foods that contained contaminated groundnut meal
  • If was, however investigation in 1961 into a previously unrecognised disease of turkeys (“Turkey X disease”) in Great Britain, that killed over 1,00,000 turkeys, which first led to the identification of Brazilian groundnut meal as the common factor in the disorder and to the ultimate chemical isolation of aflatoxins.

Lesions

  • A number of factors influence the effects of aflatoxins
  • Young animals are more susceptible than adults and males are more susceptible than females
  • Poor nutritional status increases susceptibility
  • Considerable species variation also occurs
  • Young turkeys and ducklings are much more susceptible than chickens
  • Rats are more susceptible than mice, particularly to the carcinogenic effects of aflatoxins
  • Natural disease has been reported in dogs, cats, pigs and cattle but rarely in sheep and goats
  • Horses are relatively resistant
  • The dose of aflatoxin and the duration of exposure also influence the effects of its toxicity
  • Aflatoxins bind to nucleic acids and disrupt polyribosomes
  • This leads to interference with both nucleic acid and protein synthesis
  • They also result in impaired T cell function
  • More recently animal studies have revealed that afaltoxin can bind covalently with cellular DNA and cause mutations in proto-oncogenes or tumour suppressor genes, particularly p53
  • A particularly susceptible site for aflatoxin action is the guanosine base in codon 249 of the p53 gene, leading to G to T transversion at this site
  • This specific p53 mutation is found usually in hepatocellular carcinomas

Acute aflatoxicosis

  • This results from ingestion of large quantities of aflatoxins
  • This leads to severe hepatic necrosis within hours
  • Signs of liver damage develop rapidly and include jaundice, widespread haemorrhage and an increase in serum hepatic enzymes
  • Necrosis is mainly perioportal in turkeys
  • Ducklings, chickens, cats and adult rats midzonal in rabbits and centrilobular in pigs, cattle, dogs and guinea-pigs
  • Oedema and haemorrhage in gallbladder wall are consistent findings in pigs and dogs

Chronic aflatoxicosis

  • This is the more common form of the disease and results from exposure to a lower dosage of aflatoxins over a period of time
  • The effects develop over several days to months, but may be seen pathologically within one week
  • Signs include decreased growth rate, lowered productivity and eventually signs of liver disease
  • The most striking and consistent lesion in all species in marked proliferation of small bile ductules at the periphery of hepatic lobules
  • Changes in hepatocytes include fatty change, swelling and necrosis
  • Necrosis, however is not as extensive as in acute aflatoxicosis
  • As the lesion progresses, proliferation of connective tissue occurs
  • This leads to periportal fibrosis or cirrhosis
  • This is accompanied by nodular regeneration of hepatocytes with increase in nuclear size and megalocytic (big) hepathocytes
  • The carcinogenicity of aflatoxin is well established.
  • However, the precise conditions under which neoplasia develops are not completely understood
  • Hepatomas, hepatic cell carcinomas and cholangio-carcinomas have been produced experimentally by feeding aflatoxin to ducklings, turkey, rats, guinea-pigs, trouts (fish), sheep. Pigs and monkeys
  • Also in rats aflatoxins produce carcinoma of the oesophagus, glandular stomach, colon and kidneys
  • Among domestic animals, hepatic cell carcinomas have been observed only in pigs poisoned by aflatoxins

Diagnosis

  • Diagnosis depends on the detection of aflatoxin in the feed and blood serum and the characteristic gross and histopathological findings in the liver
  • Detection of aflatoxin can be done in two ways. (a) By biological testing (b) By chemical testing
  • Biological testing includes the detection of characteristic bile duct hyperplasia produced by aflatoxins in liver of ducklings and observation of death and abnormalities, in hatched chicks given aflatoxin through a hole in shell into the airsac
  • Chemical testing includes estimation of total aflatoxins by fluorotoxinometer
  • Aflatoxin B1 in mixed feeds can be detected by enzyme-linked immunosorbent screening methods
  • These include estimation of ELISA using method of AOAC for aflatoxin B1, dot ELISA for aflatoxin B1, B2, G1 in maize, cottonseed or groundnuts and dot immunobinding assay, column and thin layer chromatography for detection of aflatoxin in feed
Last modified: Thursday, 22 March 2012, 5:56 AM