Mycotoxicoses in Poultry

Mycotoxicosis can be suspected when the history, signs, and lesions are suggestive of feed intoxication and when moldy ingredients or feed are evident. Toxin exposure associated with consumption of a new batch of feed may result in subclinical or transient disease. 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. Oral ulcers and crusts occurring on the palate or tip of the tongue occur with exposure to mycotoxins, including aflatoxin and mycotoxins produced by Fusarium.

Definitive diagnosis of mycotoxicosis involves detection and quantitation of the specific toxin(s). 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 should be submitted for testing with a representative feed sample. A necropsy and related diagnostic tests should accompany feed analysis if mycotoxicosis is suspected. Concurrent infectious or parasitic disease may occur. Sometimes, a mycotoxicosis is suspected but not confirmed by feed analysis. In these situations, a complete laboratory evaluation can exclude other significant 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. Test samples of 500 g (1 lb) 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.

For treatment of mycotoxicosis, 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.

Prevention of mycotoxicoses 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. Regular inspection of feed storage 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; 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 (propionic acid, 500–1,500 ppm [0.5–1.5 g/kg]) are effective inhibitors, but the effectiveness may be reduced 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 reduces toxicity through the binding and reduction in 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.