Finding practical solutions to mycotoxins in commercial production: a nutritionist’s perspective

Introduction

Whether grain is produced in temperate, subtropical or tropical climates, if high rainfall and humidity are experienced in the harvest season, infection of the grain by mould is likely. The range of ingredients affected by mould includes grains, oilseeds, roughages and milling by-products. Where there is mould growth, the likelihood of mycotoxins being present is significant.

Moulds are tremendously adaptable organisms, able to metabolise a large variety of substrates over a wide range of environmental conditions of temperature, moisture and pH. Once one or more of the growing conditions become limiting, sporulation occurs and toxins are produced. Toxin level varies; and although a mould known to produce toxin may be present, little toxin may be produced. Conditions known to favour mould growth may not result in high rates of toxin production. Because the mycotoxins are relatively stable chemicals, they are not easily removed from finished feeds by processes such as pelleting or expanding.

Mycotoxins not only affect animals fed infected grains but may be transmitted to animal products such as milk and meat, thereby potentially harming human health as well. Aflatoxins and the trichothecenes have been shown to affect human health. The public are very aware of food safety issues and are pro-active in demanding the right to a safe food supply. It is the responsibility of the producers of food to ensure that these standards are met.


Mycotoxins important in animal feeds

Compared to the number of known mould species, the number of mouldproducing toxins is not large and includes the genera Fusarium, Alternaria, Penicillium, Claviceps and Aspergillus. Some species can produce more than one type of mycotoxin (Table 1). The Fusarium moulds produce deoxynivalenol, fumonisins, moniliformin, T-2, HT-2, diacetoxyscirpenol, fusaric acid and zearalenone (Newman, 2000). The penicillia produce cyclopiazonic acid (Suksupath et al., 1989) and ochratoxin (Hurburgh, 1995). Many reports have shown that more than one toxin can appear in the same sample (Jelinek et al., 1989).


Table 1. Moulds and mycotoxins important in intensive animal production.

It is common practice to reduce the cost of animal feeds by mixing feed grade material with screenings or damaged grain not suitable for human consumption. It has been shown many times that grain screenings, cracked or broken grain and grain damaged by frost or water has a much greater chance of being contaminated by mycotoxin.

Coping with mycotoxin-contaminated feed

The employment of the principles of basic hygiene and good management of grain are the first steps in combating mycotoxin contamination. Moisture reduction by drying of grain; storage facilities free of residual contamination and disinfected to minimise infection and sound physical condition of grain silos will reduce the potential for mould attack. However, this will not reduce mycotoxin levels in ingredients infected in the field.

The practical aspects of dealing with mycotoxins already present in ingredients involve a number of factors. In an ideal world we would be able to quickly identify when a problem is being caused by a mycotoxin. There are laboratories specializing in mycotoxin testing in most feed-producing countries and there are test kits available for many toxins. In areas where mycotoxin infected grains are common, feed compounders typically have a regular testing program in place. In regions where mycotoxins are not necessarily expected, unexplained production problems prompt all sorts of remedies before mycotoxins are suspected as a last resort.

This is the case in Australia, which regards itself as a dry country where mould contamination of grain is comparatively rare. Clients observing a problem are more likely to hope that it goes away than to take any specific action because testing is costly and not guaranteed to identify the cause. Producers are always looking for the most cost effective solution but are not always prepared to admit there is a problem. It is only when a problem becomes chronic or is very obvious that they can be convinced to take action.

Having suspected or identified that mycotoxin is causing a production problem, the adviser is faced with recommending a procedure to reduce or eliminate its effects. Traditionally, if one was forced to use raw materials suspected of being contaminated with mycotoxins, they were managed by diluting the affected ingredients to reduce levels in the finished feed. This practice is still recommended, is valid and still has a place in mycotoxin management. However, it may not be possible to eliminate the toxic effects by dilution, especially if no uncontaminated material is available to include in the diet. For many years the feed industry has used inhibitors of mould growth such as the organic acids, but these compounds do not remove toxin already present in the feed. A process is required whereby the mycotoxin level in the feed is reduced. One process tried in the past and found to be uneconomic was ammonia treatment of aflatoxin contaminated grain (Doerr, 1988).


WHAT CRITERIA SHOULD WE LOOK FOR IN AN APPROACH TO REDUCING MYCOTOXIN CONTAMINATION PROBLEMS?

In deciding upon strategies to prevent mycotoxin-related problems, several criteria must be met. First, the product or practice must prevent transfer of mycotoxin to humans. Transfer to human food is the ultimate threat when animal feed is contaminated; and a primary goal must be protection of the consumer. Secondly, the strategy must be cost effective. This means it should restore animal performance to normal or near-normal levels and it must return a profit to the user. In addition, the product or practice must be effective against the widest possible spectrum of toxins. Frequently more than one mycotoxin is present in ingredients. Lastly, given that modern diets are closely formulated, anything added to feed to control mycotoxin problems should have a low enough inclusion rate to prevent reduction in the nutrient content of the diet. In animals such as broilers or young pigs, where feed intake limits economic performance, it is vital that non-nutritive feed additives take up as little space as possible.


CHOOSING A MYCOTOXIN BINDER

There are a number of products on the market that claim to reduce the levels of mycotoxin in animal feeds. It has been demonstrated that some inorganic minerals have the ability to reduce levels of aflatoxin in feed (Phillips et al., 1988; Hertrampf, 1994) and restore animal performance to more normal levels (Santurio et al., 1999). Mineral binders have been shown to be effective in vitro and in vivo (Doerr, 1988). These minerals include bentonite and other aluminosilicate clays. These inorganic clays are thought to act by ion exchange interactions between free radicals on the clays and potentially charged groups on the toxins. This is one reason the clay binders are most effective against the polar toxins such as the aflatoxins (Santurio et al., 1999).

Although the mineral clay binders satisfy some of the criteria for a successful mycotoxin reduction system, they have some serious shortcomings. First clays only bind a narrow spectrum of toxins. Clay binders offer little or no protection against toxins such as zearalenone or the trichothecenes because these toxins do not have functional polar groups (Devegowda et al., 1998). Further, it is necessary to add them to the diet at relatively high inclusion rates, generally more than 1% of the diet, which means that they take up valuable space in nutrient dense diets.

Another system available commercially combines the cross linked polymer, polyvinylpolypyrrolidone (PVPP) on a mineral base with epoxidase and esterase enzymes. Celik et al. (2000) have produced histochemical evidence of the efficacy of PVPP against the immunodepressive effects of aflatoxin. The supplier of this product claims efficacy against a number of toxins and cites as its mode of action binding and enzyme deactivation of mycotoxins. The proposed mechanism is essentially hydrogen binding with polar mycotoxins in a hydration layer that forms around the polymer. On the surface this concept satisfies a number of the above criteria; but trial work supporting the claims is not extensive at this stage. However, the concept is promising and may prove to be commercially viable.

One of the most recent and well-researched approaches to reducing the impact of mycotoxin contamination of feed is dietary inclusion of esterified glucomannans derived from yeast cell wall. It was found by Devegowda et al. (1995) that addition of yeast culture to broiler diets containing aflatoxin significantly improved weight gain and resulted in a heightened immune response. It was subsequently shown that binding of mycotoxins by yeast is due to a cell wall component; and that an esterified glucomannan fraction had significant binding activity for a number of mycotoxins (Devegowda et al., 1996). These authors went on to show that the modified glucomannan was able to bind several important mycotoxins at a higher level than inorganic binders and at a lower rate of inclusion in the diet (Devegowda et al., 1998; Table 2). The difference in strong versus total binding shown in this work indicated that the organic binder retained more of the toxin under changing pH conditions. This indicates that esterified glucomannan is more likely to retain bound toxin as the digesta moves through the digestive tract.

Raju and Devegowda (2000) fed broilers to 35 days of age experimental diets containing aflatoxin, ochratoxin A and T-2 toxin and found that although there was a trend toward better growth and feed conversion when esterified glucomannan (Mycosorb) was included in the diets, the positive effects were only statistically significant when the toxins were fed singly. However, body weight from 14 days on was significantly improved by Mycosorb addition when the diets contained more than one toxin. There were significant protective effects when blood chemistry and organ weights were considered. Smith et al. (2000) found that Mycosorb added to turkey feed containing deoxynivalenol and fusaric acid significantly improved growth and numerically improved gain:feed ratio.


Table 2. Total and strong binding percentages of certain mycotoxins by esterified glucomannan and other binding agents.

Work with sorghum ergot, a mycotoxin of emerging importance in countries where grain sorghums are grown, has demonstrated that Mycosorb is an effective binder of this toxin. When sorghum ergot alkaloid was added to the feed of broiler chickens, weight gain was significantly inhibited compared to a control containing no toxin. Adding modified glucomannan to the diet in the presence of toxin restored broiler growth and feed conversion to the same level as the negative control (Deo et al., 1999). Mycosorb was significantly superior to bentonite clay in binding sorghum ergot alkaloids and exhibited numerically superior binding to zeolite, even though the latter was included in the diet at a higher concentration. In practical situations in Australia, performance has been successfully maintained by adding the esterified glucomannan to the diets of layer breeder and commercial laying hens when sorghum contaminated with sorghum ergot was also present in the feed.


DOES ESTERIFIED GLUCOMANNAN MEET THE CRITERIA FOR SUCCESS IN MYCOTOXIN REDUCTION?

Mycosorb has been demonstrated to be a very effective binder of aflatoxins under physiological conditions (Devegowda et al., 1998), thereby satisfying the first criterion of promoting food safety. In feed trials in many countries Mycosorb has proved to be cost effective in terms of restoring performance reduced by the presence of mycotoxin (Manoj and Devegowda, 2000). Of the mycotoxin binders tested, esterified glucomannans are effective against the widest range of toxins. Mycosorb shows significant activity against mycotoxin when included in the diet at as little as 0.05%.

Although it is true that esterified glucomannan is not equally effective against all mycotoxins, it best meets the criteria of a successful mycotoxin reduction system and offers the nutritionist more opportunities for combating mycotoxin contamination than the other products on the market.


HOW LIKELY IS IT THAT A BINDER WILL BE COST EFFECTIVE?

Because costs of products, feeds and the prices received for end products vary across markets, economic evaluations must be done on a regional basis. However, it is possible to indicate the magnitude of performance improvements in each class of livestock likely to be economic when esterified glucomannan is used as a toxin binder.

In cost sensitive areas such as broilers and growing/finishing pigs, improvements in feed conversion are the biggest determinants of economics. In broilers, although research findings indicate that statistically significant gains in feed conversion are harder to demonstrate, it only requires a 0.02–0.03 unit improvement in feed conversion for addition of a mycotoxin binder to be profitable. A simple spreadsheet calculation will readily verify that, given the inputs and outputs are known. Liveweight gains in broilers and ducks have been demonstrated when mycotoxin contaminated feed is treated with toxin binders, but improvements in weight gain without improvements in feed conversion are not as profitable. Having said that, however, it would be unusual, in commercial situations, to have improvements in liveweight without improved feed conversion.
In laying hens, depending on the egg price, an improvement in egg yield of approximately 1% is about breakeven, so improvements over 1-2% in rate of lay or a similar reduction in cracked eggs are sufficient to be profitable.

In breeder hens, where the value of a day old chick comes into play, increases in hatchability of the order of 1% are generally profitable. In starting pigs, where feed intake is small and feed costs high, the cost of a toxin binder represents a small percentage of the overall feed cost. Further, any gains in piglet weight are magnified at the end of the growing period by reducing days to finish and improved feed conversion. In growing/finishing pigs, although feed is cheaper than broiler feed, feed conver sion is still vital and improvements in conversion of 0.03-0.04 are likely to be profitable. Where sows are affected and litter size is an issue, improvements in that parameter are highly profitable.


Conclusion

Although a number of systems are available to reduce the negative effects of mycotoxin contamination of animal feed, it is likely the highest success rate will be achieved by good mill hygiene and management combined with an effective toxin binder. The evidence currently indicates that the esterified glucomannans fulfill the necessary criteria for a safe and cost-effective solution to mycotoxin contamination.


References

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