A mycotoxicosis is a disease caused by a toxin that is produced by a fungus. In poultry, this usually results when fungi grow in grains and feeds. Hundreds of mycotoxins have been identified and many are pathogenic. Mycotoxins may have additive or even synergistic effects with other mycotoxins, infectious agents, and nutritional deficiencies. Many are chemically stable and maintain toxicity over time. (Also see Mycotoxicoses.)
The significance of mycotoxin problems in poultry is probably considerable yet insidious. The impact on poultry production may be best measured indirectly by the improvements in weight gain, feed efficiency, pigmentation, egg production, and reproductive performance that accompany effective control programs for mycotoxins.
The aflatoxins are toxic and carcinogenic metabolites of Aspergillus flavus, A parasiticus, and others. 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. Susceptibility to aflatoxins varies, but in general, ducklings, turkeys, and pheasants are susceptible, while chickens, Japanese quail, and guinea fowl are relatively resistant.
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.
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 (DAS). Deoxynivalenol (vomitoxin, DON) and zearalenone are common trichothecene mycotoxins that are relatively nontoxic for poultry, but may cause disease in pigs.
Fusariotoxicosis in poultry caused by the trichothecenes results in feed refusal, caustic injury of the oral mucosa and areas of the skin in contact with the mold, acute digestive disease, and injury to the bone marrow and immune system. Lesions include necrosis and ulceration of the oral mucosa, reddening of the GI mucosa, mottling of the liver, atrophy of the spleen and other lymphoid organs, and visceral hemorrhages. In laying hens, egg production decreases, accompanied by depression, recumbency, feed refusal, and cyanosis of the comb and wattles. Ducks and geese develop necrosis and pseudomembranous inflammation of the esophagus, proventriculus, and gizzard.
Other Fusarium mycotoxins cause defective growth of long bones. The fumonisin mycotoxins produced by F verticillioides (formerly F moniliforme) impair feed conversion without causing specific lesions. Moniliformin is also produced by F verticillioides and is cardiotoxic and nephrotoxic in poultry. F verticillioides causes ear rot, kernel rot, and stalk rot of unharvested corn and is found in stored high-moisture shelled corn, and on other grains that appear sound.
Ochratoxins are quite toxic to poultry. These nephrotoxins are produced chiefly by Penicillium viridicatum and Aspergillus ochraceus in grains and feed. Ochratoxicosis causes primarily renal disease but also affects the liver, immune system, and bone marrow. Severe intoxication causes reduced spontaneous activity, huddling, hypothermia, diarrhea, rapid weight loss, and death. Moderate intoxication impairs weight gain, feed conversion, pigmentation, carcass yield, egg production, fertility, and hatchability.
Toxic ergot alkaloids are produced by Claviceps spp, which are fungi that attack cereal grains. Rye is especially affected, but also wheat and other leading cereal grains. The mycotoxins form in the sclerotium, a visible, hard, dark mass of mycelium that displaces the grain tissue. Within the sclerotium are the ergot alkaloids, which affect the nervous system, causing convulsive and sensory neurologic disorders; the vascular system, causing vasoconstriction and gangrene of the extremities; and the endocrine system, influencing the neuroendocrine control of the anterior pituitary.
In chicks, the toes become discolored due to vasoconstriction and ischemia. In older birds, vasoconstriction affects the comb, wattles, face, and eyelids, which become atrophied and disfigured. Vesicles and ulcers develop on the shanks of the legs and on the tops and sides of the toes. In laying hens, feed consumption and egg production are reduced.
Citrinin is produced by Penicillium and Aspergillus and is a natural contaminant of corn, rice, and other cereal grains. Citrinin causes a diuresis that results in watery fecal droppings and reductions in weight gain. At necropsy, lesions are generally mild and involve the kidney.
Oosporein is a mycotoxin produced by Chaetomium spp that causes gout and high mortality in poultry. Chaetomium spp are found on feeds and grains, including peanuts, rice, and corn. Oosporein mycotoxicosis is seen as visceral and articular gout related to impaired renal function and elevated plasma concentrations of uric acid. Chickens are more sensitive to oosporein than turkeys. Water consumption increases during intoxication, and fecal droppings become unformed and fluid.
This is a metabolite of Aspergillus flavus, which is the predominant producer of aflatoxin in feeds and grains. In chickens, cyclopiazonic acid causes impaired feed conversion, decreased weight gain, and mortality. Lesions develop in the proventriculus, gizzard, liver, and spleen. The proventriculus is dilated and the mucosa is thickened and sometimes ulcerated.
This biogenic precursor to aflatoxin is hepatotoxic and hepatocarcinogenic but is less common than aflatoxin.
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 transient disease. Chronic or intermittent exposure can occur in 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 correction of feed management deficiencies.
Definitive diagnosis involves detection and quantitation of the specific toxin(s). This can be difficult because of the rapid and voluminous use of feed and ingredients in poultry operations. Diagnostic laboratories differ in the capability to test for mycotoxins and should be contacted before sending samples. Feed and also birds that are sick or recently dead should be submitted. A necropsy and related diagnostic tests should accompany feed analysis if mycotoxicosis is suspected. Concurrent diseases can adversely affect production and should be considered. 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 formation can be localized in a batch of feed or grain. Multiple samples taken from different sites increase the likelihood of confirming a mycotoxin formation zone (hot spot).
Samples should be collected at sites of ingredient storage, feed manufacture and transport, feed bins, and feeders. Fungal activity increases as feed is moved from the feed mill to the feeder pans. Samples of 500 g (1 lb) should be collected and submitted in separate containers. Clean paper bags, properly labeled, are adequate. Sealed plastic or glass containers are appropriate only for short-term storage and transport, because feed and grain rapidly deteriorate in airtight containers.
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.
The focus of prevention 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 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) are effective in binding and preventing absorption of aflatoxin. Esterified-glucomannan, a yeast cell wall derivative of 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.
Last full review/revision March 2012 by Frederic J. Hoerr, DVM, PhD, DACVP, DACPV