Aflatoxicosis (Mycotoxicosis)

Aflatoxicosis is the Mycotoxicosis produced by Aspergillus flavus, Aspergillus parasiticus or Penicillium puberulum.

Mycotoxicosis is the poisonous condition resulting from consumption of these toxic chemicals released by fungus that grows in food grains prior to harvest, during storage or after inclusion in finished feed stuff.

Fungus produces large number of chemical substances as by products. Many of these fungus products are toxic but some of them have medicinal effects.

Mycotoxins produced by fungus are stable in nature and their toxic effects are not eliminated following milling or storage.

Thousands of chemically varying mycotoxins have been identified but the toxin producing capacity and the amount produced may vary depends on the factors such as strain of fungus, temperature of the atmosphere where in the fungus growing, moisture, types of fungus, degree of stress on the host plant etc.

Aflatoxicosis, ochratoxicosis and trichothecene mycotoxicosis are the most common mycotoxicoses affects commercial poultry.

Aflatoxin is released in corn (maize), peanuts, cottonseed, millet, sorghum and other food grains while the plant grow in them.

Etiology

• Aspergillus flavus is produce majority of the toxins.
• A. parasiticus produce mainly alflatoxin.
• Aspergillus species are ubiquitous in the natural environment. Possess both toxigenic and non-toxigenic strains.
• Produce Aflatoxin in warm (30-35ºC) and high humidity (90-99%).
• Aflatoxicosis is caused by aflatoxins, produced by Aspergillus flavus and Aspergillus parasiticus.
• Aflatoxins are commonly found in corn, milo, cottonseed and peanuts.
• Aflatoxin concentrations in grains produced contain enough aflatoxin to cause acute aflatoxicosis.
• There are five important aflatoxins, called aflatoxin B1, B2, G1, G2, and M1.
• Aflatoxin M1 is a metabolite of aflatoxin.
• B1 found in milk and urine. It is not found in feed.
• Aflatoxin B1 is found most frequently and in the highest concentrations in naturally contaminated feed.

Epidemiology

Prevalence of infection

• Problems occur worldwide, but especially climates with high temperature and humidity and where grain is harvested with high water content

Predisposing factors

• High grain humidity, and damage due to insects, as well as poor storage conditions are major predisposing causes.

The following factors increases the release of Aflatoxin:

• Plant stress by insects damage
• Poor nutrition
• Harvest delay
• Post harvest storage in cold

Susceptiility

• B1, B2, G1, G2 but B1 are the toxins naturally produced Aflatoxins.
• B1 toxin present in highest concentration and is the most toxic not degraded by food processing and storage.
• Young birds are more susceptible to Aflatoxin than adults.
• Ducks are 10 times more susceptible than chickens.
• Turkeys are moderately affect than chicken and ducks.

Economic Impact

• Economic impact is considerable in some countries.

Transmission

• The route of infection is by ingestion of fungal spores, which are readily carried in the air.

Host Affected

• Generally, ruminants are most resistant and swine and avian species least resistant to adverse effects.

Pathogenesis

• Mycotoxins are ingested and then absorbed through the skin, mucous and airways. Once ingested, it compromise the immune system and damage body functions. Metabolites bind to DNA and RNA genetic materials thereby reduce the synthesis of protein and cause decrease cell mediated immunity & humoral immunity.
• Changes in these metabolites develops enlargement of liver, kidney and spleen.
• Atrophy of bursa, thymus and testes.
• Exposure to high concentration leads to accumulation of fat as clear vacuoles in the cytoplasm of hepatocytes produce enlarged friable yellow liver.
• The continued exposure cause intra hepatic biliary epithelial hyperplasia and extra medullary haemotopoiesis
• Toxin also induce anemia.
• Petechial haemorrhages or bruises increased due to decreased clotting factors and increased capillary fragility.
• Aflatoxin is excreted rapidly in bile and urine but not accumulated or stored in the body tissues.
• Hypersensitivity: an allergic reaction to moulds and spores.
• Aflatoxin is a liver poison (hepatotoxin) in all species.
• Ruminants tolerate the aflatoxin better than monogastrics or poultry.
• It causes liver damage at higher doses and liver cancer at lower doses.
• Aflatoxin exposure can depress the immune system.
• It may cause abortions in some instances, however the circumstances necessary for abortions to occur are not well defined.
• By ingestion of B1 Aflatoxin undergoes biotransformation to numerous highly reactive metabolities with diverse negative effects on metabolism.

Clinical Signs

• Acute exposure of all species it causes depression, anorexia, reduced gain or milk production, subnormal body temperature.
• Chronic exposure  in  poultry leads to decreased growth rate, reduced feed efficiency, steatorrhoea (fat in feces) and bruising.
• Chronic exposure in swine develops anorexia, unthriftiness, slow growth, icterus, mild anemia, ascites, increased susceptibility to infection.
• Chronic exposure in cattle causes  slow rumen motility for 24 to 48 hours.

Necropsy findings

Acute exposure

• Hemorrhages
• Ascites

Chronic exposure

• Pale, soft, clay-colored liver, mild anemia, icterus and ascites.

Histopathological changes like Hepatocyte degeneration and necrosis; centrilobular hemorrhagic hepatic necrosis, fatty changes and regeneration of hepatocytes; bile duct epithelial proliferation progressing to interlobular fibroplasia and extensive proliferation; Karyomegaly, atypical nuclei, hepatocytic vacuolization  and  bile retention.

Diagnosis

• Based on clinical signs and blood biochemical parameters such as anemia, elevated liver enzymes, serum bile acids, albumin:globulin ratio; prothrombin activity.
• Tissue or fluid analysis: Aflatoxin M1 present in milk or urine. Parent compound may be present in kidney or liver.

Grain or feed analysis

Aflatoxins are present in corn, peanuts or cotton seed.

• Decreased performance may occur at concentrations as low as 200 ppb in young, sensitive species.
• At 200 ppb immunity may be impaired.
• At 200 to 400 ppb hepatic lesions become evident.
• At 400 ppb clinical illness become obvious.
• Violative residues in milk can occur at concentrations at or near 50 ppb aflatoxin M1.

Differential Diagnosis

• Other mycotoxicoses
• Other fungal infections (like ergot)

Treatment

• Stop exposure to fungus.
• Stop feeding contaminated ration and replace with non-contaminated ration.
• Supportive treatment.
• Provide supportive treatment as clinical situation dictates

Prevention & Control

• Mycotoxicoses may be prevented by careful choice of raw materials, reduction in moisture  content of the raw materials and hygienic storage.
• Antimycotic feed additives may also be used but may not deal with toxins already formed.
• Feeds with high levels of fishmeals are particularly susceptible and should not be stored for more than 3 weeks.
• Pelletising feed may reduce fungal counts but does not affect toxins.
• Certain minerals additives have been shown to bind mycotoxins and reduce their effects.
• Good stock control, management of feeders and bins, and avoidance of feed spillage are all important.