By Trevor K. Smith, Ph.D., P.Ag.
Mycotoxins are fungal metabolites that can reduce performance and alter metabolism of livestock and poultry. The pathological states arising in animals from the consumption of feeds contaminated with mycotoxins are referred to as mycotoxicoses.
Mycotoxins can be formed in the field preharvest and may continue to be formed under suboptimal storage conditions post harvest. High moisture content often predisposes feedstuffs to fungal growth and mycotoxin formation. Temperature is another key factor. Some fungi, such as Aspergillus flavus, are usually found in tropical and semi-tropical climates. This mold produces the carcinogenic hepatotoxin aflatoxin. Fusarium fungi, however, are more common in temperate climates.
The global frequency of mycotoxin-contamination of feedstuffs and the severity of mycotoxicoses in livestock and poultry appear to be increasing in recent years. This may be due, in part, to increased monitoring of suspect materials and an increased awareness of the symptoms of mycotoxicoses by veterinarians and producers. Global climate change has also contributed to an increased frequency of mycotoxin contamination of feed grains. Drought, excessive rainfall and flooding can all promote mold growth. Increased international trading of feedstuffs has also contributed to the problem as this increases the chance that a given compound feed will contain components of widely varying geographical origin. Such blends of ingredients increase the chance of the feed containing mixtures of different mycotoxins. This can result in toxicological synergies that increase the severity of mycotoxicoses.
Detecting Mycotoxins In Feed Grains
An important tool in managing the problems of mycotoxin contamination of feed grains is chemical analysis. When symptoms of mycotoxicoses are seen in livestock or when the grain supply in general is suspected of being contaminated, analysis should be undertaken. A major source of variation in mycotoxin analysis is the sampling protocol. Grain must be sampled thoroughly because fungal growth tends to be greatest in areas of high moisture and exposure to oxygen. This means that mycotoxins are often not distributed in a uniform manner and may be concentrated in certain areas.
The analytical methods used to determine mycotoxin concentrations vary but include thin-layer chromatography (TLC), gas-liquid chromatography (GLC), high-performance liquid chromatography (HPLC) and ELISA quick test kits. The application of ELISA technology to mycotoxin analysis has led to great advances in our understanding of mycotoxicoses. ELISA kits are rapid and inexpensive compared to more traditional techniques such as HPLC. They have the disadvantage, however, of being very specific (one toxin per assay) and they may be subject to interfering compounds that lead to falsely positive analyses.
The Concept Of Mycotoxin Synergy
Symptoms typical of mycotoxicoses are often seen in livestock and poultry despite analysis of the feed that indicates only very low concentrations of mycotoxins. In this situation it is not clear if a mycotoxin problem really exists, or if poor performance is due to management or nutritional factors.
It is now clear that unexpected toxicity may be due to toxicological interactions between different mycotoxins that exaggerate the toxicity. The likelihood of this occuring is greatest for the Fusarium mycotoxins. It has been shown that fusaric acid, the most common of the Fusarium mycotoxins, can increase the toxicity of the trichothecene deoxynivalenol (vomitoxin, DON). Fusaric acid, however, is seldom tested for, due to its low toxicity when consumed in the absence of other toxins.
An experiment was conducted to determine the potential for toxicological synergy when blends of grains naturally contaminated with Fuarium mycotoxins were fed to broiler chickens. Broiler chicks of a commercial strain were fed soybean meal, maize and wheat-based diets for eight weeks at the University of Guelph Arkell Poultry Research Station.
The four diets included: (1) a control, (2) a same diet formulated with a low level of contaminated corn and wheat, (3) a diet containing higher levels of contaminated corn and wheat, and (4) a highly contaminated diet + 0.2% polymeric glucomannan mycotoxin adsorbent. Three replicate pens of 30 birds were fed each diet. Weight gain and feed consumption were determined weekly.
Diets were adjusted for protein levels corresponding to starter (0-3 weeks), grower (4-6 weeks) and finisher (7-8 weeks) phases. Diets were analyzed for deoxynivalenol, fusaric acid, zearalenone and T-2 toxin. Blood samples were taken at the end of the starter and finisher phases and a clinical screen of serum metabolites was conducted. At the end of the experiment, samples of breast, thigh and leg tissue were tested for discoloration using a Minolta colorimeter.
Growth rate, feed consumption, feed efficiency and serum parameters were largely unaffected by diet with the exception of the finisher phase. In the finisher phase, the feeding of increasing levels of contaminated grains caused a significant depression in growth rates (Table1). This effect was overcome by the feeding of 0.2% glucomannan polymer. It was also observed that red blood cell counts and concentrations of hemoglobin (Table 2) and uric acid (Table 3) increased with the feeding of increasing amounts of contaminated grains. Changes in red blood cell count and hemoglobin are likely the result of fusaric acid lowering blood pressure and reducing blood flow to the lungs and other tissues. This stresses the birds, which try to compensate by increasing the oxygen trapping capacity of the blood. The increase in blood uric acid concentration reflects the inhibition of tissue protein synthesis by DON and other trichothecenes. The bird then uses dietary protein for energy purposes, and waste nitrogen is excreted as uric acid. This is a very expensive waste of dietary protein.
An increasing redness of breast meat was also observed (Table 3), as has been reported for turkey poults fed Fusarium culture material. This effect is likely due to peripheral pooling of blood caused by the reduced blood pressure resulting from consumption of fusaric acid. This, coupled with the increased red blood cell count and increased hemoglobin concentrations, would result in discoloration and increased frequency of condemnations at the processing plant. An increased frequency of bruising resulting from rough handling in transport is also possible.
There was also a significant depression in biliary immunoglobulin A in the finisher phase as increasing amounts of contaminated grains were fed (Table 4). Immunosuppression is characteristic of the effect of DON and other trichothecenes. This reduces the ability of the birds to combat secondary infection. It also compromises vaccination programs and this could represent one of the major economic costs of feed-borne mycotoxins.
It was concluded that Fusarium mycotoxicoses can be observed in broiler chickens with the feeding of naturally contaminated grains. Such toxicoses can be largely prevented by the feeding of an appropriate mycotoxin absorbent such as glucomannan polymer. Such polymers also improve the quality and safety of food products by minimizing tissue residues of mycotoxins.
Dr. Trevor Smith is Professor, Department of Animal and Poultry Science, University of Guelph, Guelph, Ontario, Canada. He may be contacted for references and further information by Emailing email@example.com.