Mycotoxicoses in Poultry

Mycotoxins are predominantly naturally produced secondary metabolites produced by strains of certain species of fungi under some environmental conditions. A single species of fungi can produce multiple mycotoxins.

Poultry are susceptible to hundreds of mycotoxins. Pathogenicity in poultry is dependent on life stage and species of poultry affected as well as level of mycotoxin exposure and individual susceptibility.

Mycotoxins can have additive, synergistic, and antagonistic effects with other toxins, infectious agents, and nutritional requirements. Mycotoxins can also interact with drugs used as therapeutic agents and diminish the effects of vaccines administered to poultry.

Common mycotoxins associated with mycotoxicoses in poultry include aflatoxins Aflatoxicosis in Poultry The aflatoxins are toxic and carcinogenic metabolites of Aspergillus spp (Aspergillus flavus, A parasiticus, and others) that affect poultry as well as other animals. See... read more , ochratoxins Ochratoxicosis Ochratoxins are quite toxic to poultry, as nephrotoxins produced chiefly by Penicillium viridicatum and Aspergillus ochraceus in grains and feed. Ochratoxicosis primarily causes... read more , fumonisins, zearalenone, and trichothecenes Fusariotoxicosis in Poultry The genus Fusarium produces many mycotoxins injurious to poultry. The trichothecene mycotoxins produce caustic and radiomimetic patterns of disease exemplified by T-2 toxin and diacetoxyscirpenol... read more such as deoxynivalenol (DON) and T-2 toxins.

Exposure to mycotoxins can occur via ingestion of contaminated feed or bedding material. Mycotoxins can affect cereal grains and other agricultural commodities before harvest or after harvest during transport or storage. Once formed, they are chemically stable and persist in the contaminated ingredient even through becoming a finished feed.

Chronic or intermittent exposure can occur in regions where grain and feed ingredients are of poor quality and when feed storage is substandard or prolonged. Impaired production efficiency can be a clue to a mycotoxin problem, as can improvement due to correction of feed management deficiencies.

Clinical signs of mycotoxin exposure in poultry may include the following:

Toxin exposure associated with consumption of a new batch of feed may result in subclinical or transient disease. Initially, refusal of new feed may be the only clinical sign.

Oral ulcers and crusts occurring on the palate or tip of the tongue and esophagus can occur with exposure to mycotoxins, including aflatoxin and mycotoxins produced by Fusarium toxins, such as the trichothecenes T-2 toxin (T-2), deoxynivalenol (DON), and scirpenol. (See and photographs.)

On necropsy, gizzard ulcerations, proventriculitis, and enteritis can be indicators of exposure to mycotoxins such as trichothecenes, including T-2, HT-2 toxin, DON, and nivalenol, among others (see and photographs).

Flushing, a diuresis response, and pasting with urates around the vent could also indicate exposure to mycotoxins, particularly nephrotoxic mycotoxins such as ochratoxin, oosporein, citrinin, and aflatoxins.

Mycotoxicosis in poultry can be suspected when the history, clinical signs, and lesions are suggestive of feed intoxication and when moldy ingredients or feed is evident.

Definitive diagnosis of mycotoxicosis involves detection and quantitation of the specific toxins. This can be difficult because of the rapid and high-volume use of feed and ingredients in commercial flocks.

Diagnostic laboratories differ in their respective capability to test for mycotoxins and should be contacted before sending samples. Poultry that are sick or recently dead, along with a representative feed sample, should be submitted for testing.

A necropsy and related diagnostic tests should accompany feed analysis if mycotoxicosis is suspected. Concurrent infectious or parasitic disease may occur. Sometimes mycotoxicosis is suspected but not confirmed by feed analysis. In these situations, a complete laboratory evaluation can exclude other diseases.

Feed and ingredient samples should be properly collected and promptly submitted for analysis. Mycotoxin hotspots may occur in a batch of toxic feed or grain. Multiple samples taken from different sites increase the likelihood of confirming mycotoxin presence.

Samples should be collected at sites of ingredient storage, feed manufacture and transport, and feed bins and feeders. Fungal activity increases as feed moves from the feed mill to the feeder pans.

Representative feed samples (500 g of the feed being used when birds became sick) should be transported in clean paper bags that are properly labeled. Sealed plastic or glass containers should only be used for short-term storage and transport because feed and grain rapidly deteriorate in airtight containers, and plastic bags can entrap moisture content.

For treatment of mycotoxicosis in poultry, contaminated feed or bedding should be replaced. Concurrent diseases should be treated to alleviate disease interactions, and substandard management practices must be corrected.

Some mycotoxins increase requirements for vitamins, electrolytes, trace minerals (especially selenium and zinc), protein, and lipids and can be compensated for by feed supplementation and water-based treatment.

Nonspecific treatments using activated charcoal (digestive tract adsorption) in the feed have a sparing effect but are not practical for larger production units. In larger scale production, the use of clays and derivatives from yeast, bacteria, and plants has more practical applications.

Certain enzymes have potential to biodegrade specific mycotoxins, such as fumonisins, into nontoxic metabolites (enzymatic biotransformation). However, availability of detoxifying enzymes is limited.

Extra-label treatment with antifungal drugs labeled for use in other species (eg, nystatin and triazole antifungal agents) may not be permitted in certain jurisdictions.

Prevention of mycotoxicoses in poultry should focus on using feed and ingredients free of mycotoxins and on management practices that prevent mold growth and mycotoxin formation during feed transport and storage.

Preharvest agricultural measures such as crop rotation, tilling, proper fertilization, and pest control can decrease some of the stressors that influence mycotoxin occurrence.

Postharvest techniques such as regular inspection of feed storage and feeding systems can identify flow problems that allow residual feed and enhance fungal activity and mycotoxin formation.

Mycotoxins can form in decayed, crusted feed in feeders, feed mills, and storage bins; thorough cleaning and correcting the problem can have immediate benefits. Temperature extremes cause moisture condensation and migration in bins and promote mycotoxin formation.

Ventilation of poultry houses to avoid high relative humidity also decreases the moisture available for fungal growth and toxin formation in the feed.

Antifungal agents added to feeds to prevent fungal growth have no effect on toxin already formed but may be cost-effective in conjunction with other feed management practices.

Organic acids (0.5–1.5 g of propionic acid/kg of feed) are effective inhibitors; however, the effectiveness may be decreased by the particle size of feed ingredients and the buffering effect of certain ingredients.

Sorbent compounds such as hydrated sodium calcium aluminosilicate (HSCAS) effectively bind and prevent absorption of aflatoxin.

Esterified glucomannan, derived from the cell wall of the yeast Saccharomyces cerevisiae, is protective against aflatoxin B₁ and ochratoxins. It decreases toxicity through the binding and decreased bioavailability of fumonisins, zearalenone, and T-2 toxin.

Various other fermentation products, algae and plant extracts, and microbial feed additives have demonstrated ability to bind or degrade mycotoxins and may be applicable and appropriate for the situation.