Mycotoxins are now virtually ubiquitous in poultry diets, and with ever increasing sophistication of testing sensitivity, they are routinely isolated as contaminants of most grains and some vegetable protein ingredients. We still do not know the cause of high levels of mold growth occurring in pre-harvest grains. Certainly such aerobic molds are more prevalent in hot humid conditions, and insect damage to the standing crop seems to provide a route of entry for the mold. Unfortunately, visual inspection of harvested grains can be misleading in regard to mycotoxin content. Likewise, merely because grains appear moldy, does not mean to say that they are contaminated with harmful toxins. In storage, the major factors affecting mold growth are again temperature and humidity. The higher the temperature, the greater the chance of mold growth. However such mold growth rarely occurs in grains containing less than 14 - 15% moisture. Unfortunately, many grain silos are not waterproof, or grains are not aerated, and so pockets of moisture can cause microclimates ideal for mold growth. The following is a review of the major mycotoxins affecting meat birds and egg layers.
Aflatoxin - Produced by the Aspergillus flavus mold, aflatoxin is one of the most potent carcinogens known. Usually present in cereals in ppb levels, acute toxicity will occur at 1.2 ppm. Aflatoxin B1 is the most common form of the toxin, the B designation relating to the fact that the toxin fluoresces a blue color when exposed to ultraviolet light, and so this can be used in the screening of ingredients. Blue fluorescence occurs with other components, and so this simple test screens out negative samples, but needs subsequent chemical analysis for confirmation. Aflatoxin is found in most cereals, although corn and milo are the most common hosts. As with any mold, Aspergillus growth is greatly reduced when corn or milo moisture levels are less than 15%.
Aflatoxin is a potent hepatotoxin, and so varying degrees of liver breakdown occur. As toxicity develops, normal liver function declines, and reduced growth rate is quickly followed by death. Toxicity is enhanced by the presence of other toxins such as ochratoxin and T2 toxin. The effects of aflatoxin are also much worse if birds are infected with aspergillosis. There also seems to be a nutrient interaction, because toxicity is more severe when diets are low in either crude protein or methionine or when the diet contains marginal levels of riboflavin, folic acid or vitamin D3. There is no treatment for acute aflatoxicosis, although because of the liver disruption, giving higher levels of antioxidants and/or selenium seems to slow the onset of symptoms and speed up recovery if aflatoxin is removed from the diet.
There are a number of effective preventative measures, although not all of these are economical. Treating infected grains with ammonia, hexane or hydrogen peroxide have all been shown to reduce aflatoxin levels. Under commercial conditions adding binding agents to the feed seems to reduce the adverse effects of aflatoxin. To date, aluminosilicates, bentonite clays and yeast cell walls have proven effective. For example adding 10 - 15 kg/tonne of hydrated sodium-calcium aluminosilicate has been shown to drastically reduce mortality in broilers and turkeys fed diets containing 0.5 - 1.0 ppm aflatoxin. Such aluminosilicates have limited effects on other mycotoxins.
Tricothecenes - Three mycotoxins, namely T2, DAS (diacetoxyscirpenol) and DON (Deoxynivalenol or vomitoxin) are included in this group. All of these mycotoxins are produced by Fusarium species molds such as Fusarium graminearum and Fusarium roseum. The tricothecenes affect protein metabolism and have the characteristic feature of causing mouth lesions in most animals. However DON does not seem to be particularly harmful to poultry. Unlike the situation in pigs and other mammals, birds can tolerate up to 20 ppm of this mycotoxin. T2 and DAS however are more toxic, causing problems at 2 - 4 ppm. The adverse effect of tricothecenes is made even worse by the presence of aflatoxin or ochratoxin, and seems to be worse in young broilers fed ionophore vs non-ionophore anticoccidials. There are no really effective treatments, and while the addition of relatively high levels of antioxidants may slow the disruption of protein synthesis, they are not effective long-term. Adsorbents and binding agents are being developed that specifically bind these toxins.
Ochratoxin - As with other mycotoxins, there are a number of forms of ochratoxin, although ochra toxin A (OA) is by far the most significant for poultry. OA is produced by a number of molds, with Aspergillus and Penicillium species being most commonly involved. OA is toxic at 2 ppm and as with tricothecenes, it has an adverse effect on protein synthesis. However, OA also affects kidney function and so the classical signs are swollen kidneys and associated increased water intake with wet excreta. Secondary visceral gout, which appears as urate deposits over the viscera, is common with OA toxicity, due essentially to failure of uric acid clearance by the kidney tubules. OA toxicity is compounded by the presence of aflatoxin, DON and T2 toxicosis, and also made worse by feeding diets high in vanadium (usually as a contaminant of phosphates or limestone). There are no effective preventative measures, although birds sometimes respond to diet manipulation in the form of increasing crude protein levels. There are also reports of beneficial response to increasing diet vitamin C levels, especially in egg layers.
Other mycotoxins - There are a diverse group of other mycotoxins that periodically cause problems for poultry. Their occurrence is less frequent than the major mycotoxins already discussed, and in some instances exact toxicity levels have not been clearly established.Table 2.25 summarizes these mycotoxins in terms of effect on poultry and their probable threshold for toxicity.
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