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.
• Aflatoxin G1 & G2 : produced by Aspergillus parasiticus.

• Aflatoxin M1 : metabolite of aflatoxin B1 in humans and animals

(exposure in ng can come from mother's milk).
• 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
important clue to a mycotoxin problem, as can improvement due to ntio
correction of feed management deficiencies. n:
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