Annal

AFLATOXICOSIS INTRODUCTION: Aflatoxicosis in poultry primarily affects the liver, but can involve immunologic, digestive, and hematopoietic functions. It affects weight gain, feed intake, feed conversion efficiency, pigmentation, processing yield, egg production, male and female fertility, and hatchability. Some effects are directly attributable to toxins, while others are indirect, such as reduced feed intake. ETIOLOGY: Aspergillus flavus A.parasiticus

SPECIES AFFECTED: Susceptibility to aflatoxins varies, but in general, ducklings, turkeys, and pheasants are susceptible, while chickens, Japanese quail, and guinea fowl are relatively resistant.

TYPES OF TOXINS:

The most pronounced contamination has been encountered in tree nuts, peanuts, and other oilseeds, including corn and cottonseed. The major aflatoxins of concern are designated B1, B2, G1, and G2. These toxins are usually found together in various foods and feeds in various proportions; however, aflatoxin B1 is usually predominant and is the most toxic. When a commodity is analyzed by thin-layer chromatography, the aflatoxins separate into the individual components in the order given above; however, the first two fluoresce blue when viewed under ultraviolet light and the second two fluoresce green. Aflatoxin M a major metabolic product of aflatoxin B1 in animals and is usually excreted in the milk and urine of dairy cattle and other mammalian species that have consumed aflatoxin-contaminated food or feed.

Major types of aflatoxins and their metabolites At least 13 different types of aflatoxin are produced in nature. •

Aflatoxin B1 & B2 : produced by Aspergillus flavus and A. parasiticus.

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Aflatoxin G1 & G2 : produced by Aspergillus parasiticus.

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Aflatoxin M1 : metabolite of aflatoxin B1 in humans and animals (exposure in ng can come from mother's milk).

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Aflatoxin M2 : metabolite of aflatoxin B2 in milk of cattle fed on contaminated foods.

• Aflatoxicol.

PATHOLOGY: High-level aflatoxin exposure produces an acute necrosis, cirrhosis, and carcinoma of the liver exhibited by hemorrhage, acute liver damage, edema, alteration in digestion, and absorption and/or metabolism of nutrients.

Chronic, subclinical exposure does not lead to as dramatic of symptoms as acute aflatoxicosis. poultry, however, are particularly affected by aflatoxin exposure which leads to stunted growth and

delayed development. Chronic exposure also leads to a high risk of developing liver cancer, as the metabolite aflatoxin M1 can intercalate into DNA and alkylate the bases through its epoxide moiety. This is thought to cause mutations in the gene, an important gene in preventing cell cycle progression when there are DNA mutations.

CLINICAL SIGNS: * Clinical signs vary from general unthriftiness to high morbidity and mortality. At necropsy, the lesions are found mainly in the liver, which can be reddened due to necrosis and congestion or yellow due to lipid accumulation. * Hemorrhages may also occur. * In chronic aflatoxicosis, the liver becomes yellow to gray and atrophied. * The aflatoxins are carcinogenic, but tumor formation is rare with the natural disease, probably because the animals do not live long enough for this to occur.

LESIONS: Liver: Swollen and discolored initially but later becomes cirrhotic and nodular. May have necrotic foci. Ascites and hydropericardium are frequently present and may have generalized edema. Petechial hemorrhages at various sites and renal swelling may be present. Marked catarrhal enteritis is usually a feature. Histopath.: hyperplasia of biliary epithelium Aflatoxin is carcinogenic. Tumors usually develop in the liver.

Diagnosis: Mycotoxicosis should be suspected when the history, signs, and lesions are suggestive of feed intoxication. Toxin exposure associated with consumption of a new batch of feed may result in subclinical or P transient disease. Chronic or intermittent exposure can occur in reve

regions where grain and feed ingredients are of poor quality, and feed storage is substandard or prolonged. Impaired production can be an ntio important clue to a mycotoxin problem, as can improvement due to n: correction of feed management deficiencies. The focus should be on using feed and ingredients free of mycotoxins and on management practices that prevent mold growth and mycotoxin formation during feed transport and storage. Regular inspection of feed mills and feeding systems can identify flow problems, which allow residual feed and enhance fungal activity and mycotoxin formation. Mycotoxins can form in decayed, crusted feed in feeders, feed mills, and storage bins; appropriate cleaning can be immediately beneficial. Temperature extremes cause moisture condensation and migration in bins and promote mycotoxin formation.

Treatment: The toxic feed should be removed and replaced with unadulterated feed. Concurrent diseases should be treated to alleviate disease interactions, and substandard management practices must be corrected. Some mycotoxins increase requirements for vitamins, trace minerals (especially selenium), protein, and lipids, and can be compensated for by feed supplementation and water-based treatment. Nonspecific toxicologic therapies using activated charcoal (digestive tract adsorption) in the feed have a sparing effect but are not practical for larger production units.

REFERENCES: http://en.wikipedia.org/wiki/Aflatoxicosis#Pathology http://parrotdise.com/diseases.shtml