Aflatoxicosis (brooder pneumonia)

Occurrence: Worldwide
Species affected: All species
Age affected: All, young most susceptible
Causes: Consumption of high moisture grains containing aflatoxins produced by Aspergillus flavus, A. parasiticus, Penicillium puberulum.
Effects: Sleepiness, depression, paleness, reduced egg production, fertility and hatchability. Depressed growth, feed conversion, increased bruising and downgrading can occur.

Detailed cause:
Muycotoxins are toxin metabolic byproducts of fungal growth on grains. High moisture content of grains can lead to fungal growth and toxin production. Fungi can produce toxins before or after grain harvest. Drought and insect damage to grain increase susceptibility of grain to fungal growth. All species and ages can be affected. The disease course can be acute to chronic dependent upon doses, duration of exposure and age of the bird. Acute disease seen if young are given high amounts (1,000 ppb of Aflatoxin B1). Chronic disease seen in birds older than 5 weeks, given low levels (ppb) for several weeks.
Consumption of feed containing grains (usually corn) which contain toxins causes the disease. Aflatoxins are a group of related poisons produced by several fungi: Aspergillus flavus, A. parasiticus and Penicillium puberulum. (Afla comes from Aspergillus flavus "A" for Aspergillus and "fla" for flavus). The most common and toxic aflatoxin is aflatoxin B1 followed by B2, G1 and G2. Aflatoxicol, flatoxitrem and cyclopiazonic acid are other toxic metabolites produced by these fungi on mouldy corn. The longer grain is stored, especially under warm, moist conditions, the more fungi grow and can produce toxins. It is a feed storage problem. Aflatoxins are immunodepressive and carceinogenic. 1.0 ppm or greater of AF B1 can produce morbidity and mortality; 500-1,000 ppb can reduce weight grain and feed efficiency; and 200-500 ppb can produce immune depression.

Clinical signs:
Signs include sleepiness, depression, paleness. Reduced egg production, fertility and hatchability. Depressed growth, feed conversion and increased bruising and downgrading can occur.

Postmortem lesions:
Lesions include scattered haemorrhage in the muscles, skin and intestinal tract, fluid around the heart, enlarged pale kidneys, and pale enlarged fatty livers with haemorrhage and anaemia.

The clinical history, and gross and microscopic lesions are important. Microscopically, the liver shows fatty change, swollen hepatocytes and bile duct hyperplasia.
An ultra violet (UV)(black) light can be used to test corn for the presence of cogic acid (blue green fluorescence) producing fungi.
Feed analysis using column chromatography is the only method for a definite diagnosis. Test kits are available for aflatoxin B1 using ELISA methodology or minicolumns.
It simulates infectious bursal disease (IBD), fatty liver syndrome, and malabsorption syndrome.

Detailed treatment:
Feed can be prevented from growing mould by incorporating a mould inhibitor. Aluminosilicates in the feed such as zeolites will bind the inactive aflatoxin. Quality control of feeds is important. Check grains for greater than 16% moisture.
Contaminated feed should be diluted with noncontaminated grain or treated with ammonia, which inactivates aflatoxin. Heat-treatment will kill the fungi. Gentian Violet kills fungi and binds aflatoxin. In general low moisture corn (below 14%) should be fed. Mouldy corn should not be added to the finished feed. Contaminated feed may be given to older pullets, which are less susceptible.
Two feed bins at farm will reduce grain and feed storage time, which reduces fungal growth and toxin formation.
Increasing the protein content of feed by 1%, increasing vitamin and mineral content of feed and adding Gentian violet to feed have a sparing effect on aflatoxin-induced disease.

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