Reports of ear rot in corn have generated questions regarding the effects of feeding this corn to poultry. The full extent of the possible contamination will not be known until the corn harvest is completed and analytical information becomes available. Depending on storage conditions, mold growth associated with storage may also increase in importance.
Presence of mold may or may not indicate the presence of mycotoxins of concern or that the mycotoxin(s) present should be of concern to feeding of poultry. Mold identification can assist with determining which potential mycotoxins that might be produced. Producers who grow their own corn can scout their fields prior to harvest and determine the different types of ear rot present which would indicate indirectly the types of mold present (See Steps to take when mold is present in corn [PDF]).
Mycotoxin production by the mold will vary as specific stress conditions are needed to produce the mycotoxins. Depending on the type of mycotoxin, level, poultry species and age, and duration of feeding, effects can range from not noticeable, or some depression in performance to acute conditions associated with clinical signs and toxicity. Certain combinations of mycotoxins often have more devastating effects at much lower levels in the feed.
In temperate climate regions, with cold, wet conditions pre-harvest, it is anticipated that Fusarium type molds will be the most prevalent. The main identified mycotoxins that can be produced by various Fusarium species include trichothecenes (T-2 toxin, diacetoxyscirpenol or DAS, vomitoxin or deoxynivalenol or DON), zearalenone (ZEA), and fumonisins. Grains contaminated with ZEA or fumonisins appear to be tolerated by poultry. A feed level as high as 800ppm ZEA was not detrimental. The FDA maximum recommended level (2001) for the total of all fumonisins is 30 ppm in corn and corn byproducts (used at not more than 50% of the diet) for breeding poultry and 100 ppm for poultry raised for slaughter.
The trichothecenes represent more of a risk. The clinical signs of trichothecenes include necrotic conditions in the gastrointestinal tract of the bird. A typical oral lesion associated with T-2 toxin ingestion is the formation of caseous plaques at the edges of the beak and mouth and on the tongue. Suppression of the immune system can occur as well. Abnormal feathering is observed along with declines in feed intake, growth and in egg layers, decreased egg production and shell quality.
Chickens and turkeys are considered to be less sensitive to DON as compared to T-2 toxin and DAS. DON however, can be a common contaminant of corn. The FDA advisory maximum level (2001) for DON is 10 ppm in corn and corn byproducts and 5 ppm in finished feed for chickens. Individual research studies showed no negative performance effects to 5 ppm, 20 ppm and 4.4 ppm of DON for broilers, layers, and turkey poults, respectively. In breeding chickens though, levels of DON to 5ppm resulted in a higher incidence of chick developmental abnormalities and unabsorbed yolk sac and delayed ossification. Recent studies where turkeys were fed diets naturally contaminated with Fusarium mold showed reduced body weight and impaired the immune system in growing turkeys. Levels of DON ranged from 2.2 to 3.3 ppm.
T-2 toxin and DAS are considered to be more toxic to poultry than aflatoxin. Studies with broilers indicated negative effects with levels of 1-4 ppm T-2 toxin with long term feeding of 0.4 ppm causing oral lesions. In laying hens, feeding levels of 1-4 ppm T-2 toxin resulted in decreased feed intake and egg production. In broiler breeders, 5 ppm decreased feed intake but no decrease in fertility or hatchability. DAS levels of .5 and 2 ppm decreased hatchability and egg production, respectively. When chicks and turkey poults were fed the same amount of T-2 toxin, turkey poults were more negatively affected than the chicks. Ducklings and pigeons are very sensitive. T-2 toxin has also been shown to interact with Salmonella spp resulting in increased mortality and lowered resistance to infection. T-2 toxin reduces the effectiveness of some anticoccidial ionophores. Presence in the feed of combinations of T-2 toxin and aflatoxin or T-2 toxin and DON can result in more severe effects than that experienced by the presence of the single mycotoxin in the feed.
Unfortunately, mycotoxins once present in the grain, are not decreased or destroyed by typical feed manufacturing processes. Ideally the feeding of Fusarium contaminated grains should be avoided especially for younger birds or egg producing poultry. Producers may want to consider a feed additive that binds or detoxifies the mycotoxins if levels are considered to be too high. Binding or sequestering the mycotoxin prevents its absorption in the gut. Some silicate minerals (bentonites and zeolites) have been shown to bind primarily aflatoxin but not other mycotoxins. Any such product should be thoroughly researched for its efficacy as there is wide variability in effectiveness. Another type of product is derived from yeast cell walls which has activity against Fusarium-produced mycotoxins and aflatoxin. Again any such product should be researched as to its efficacy in live animal models for the different types of mycotoxins and safety of use.
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