Mycotoxins are a hardly avoidable risk in feed formulation with a huge impact on animal health and biological performance. Compared to other life stock species, ruminants have a much higher resistance to mycotoxins and their impacts due to an intensive ruminal degradation. Nevertheless, considering the fed raw materials, ruminants are exposed to a broader range of mycotoxins at higher concentra- tions. Regarding the type of utilization, dairy cows are more susceptible than beef cattle because of higher feed consumption and an increased metabolic stress.
Clinical impacts & resulting objectives
The clinical consequences of mycotoxin contamination depend strongly on the type of mycotoxin. For example, the presence of aflatoxins is of particular concern to humans, because one metabolite of Aflatoxin B1, known as AFM1, can be transferred through the milk into the human food chain. AFM1 can have severe impacts on human health being strongly hepatotoxic and carcinogenic. That is why we commonly find official limit values concerning AFB1 contamination in finished feed as well as AFM1 concentration in milk. Looking at health and biological performance of the animals themselves, the impacts of the fusarium toxins in particular, depend on the contamination rate and on the intensity of ruminal degradation. The inten- sity of ruminal degradation depends on the quality of protozoa population, rumen pH and passage time. For example, in vitro rumen simulations show a reduced disappearance of Deoxynivalenol, Niva- lenol and Enniatin B at conditions of rumen acidosis and lower microbial activity (Debevere, S. et al 2020). At high quantities and in case of decreased ruminal degradation, fusarium toxins may cause similar damages as in monogastric animals:
- Disruption of the gastrointestinal barrier, leaky gut
- Oxidative stress
- Immune suppression
- Liver stress
Consequently, efficient toxin binders have to target two essential points in ruminants:
Safe neutralization of aflatoxins through irreversible binding in or- der to prevent the excretion of AFM1 into the milk.
Neutralization of a broad spectrum of different mycotoxins in or- der to preserve animal health and biological performance.
Challenges of toxin binding
It’s like looking for the needle in a haystack. A toxin binder today should be…
- Effective against all kinds of mycotoxins
- As inexpensive as possible
- Not binding any nutrition
- Well documented
- Given at a very low dosage
The vast amount of toxin binder products on the market is confronted with a long list of requirements. And just a brief look at the quality and price diversity of the products indicates that there has to be huge differences between promises and reality. One of the most important differentiation character- istics is the covered range of mycotoxins. During the product development of B.I.O.Tox®, a focus was placed on multi-toxin binding. B.I.O.Tox® is a premix consisting of specially processed inorganic and organic compounds for mycotoxin adsorption.
Multi-toxin binding is an essential characteristic since there is hardly ever just one mycotoxin present in the feed. Moreover, raw material analysis is expensive and not always conclusive, as mycotoxins are not equally distributed in the feed. Therefore, it is more or less impossible to know the exact combi- nation of mycotoxins in the final feed. To be on the safe side, the use of a product that is able to bind several mycotoxins at the same time, is the best option. To test the power of B.I.O.Tox® for multi-toxin binding, a trial at the University Ghent (Faculty of Pharmaceutical Sciences) was conducted. The results are presented in figure 1.
Despite high quality standards, molds and their mycotoxins are a problem in animal feed. These toxic metabolic products can lead to performance loss in animals. They can also pass from the animal food chain into the human food chain.
B.I.O.Tox® enters the digestive tract of animals through feed intake, where it irreversibly binds the various mycotoxins and reduces or prevents resorption. Polar and nonpolar mycotoxins, such as afla- toxin B1, zearalenone, T-2 toxin and ochratoxin A, accumulate on the surface of the toxin binder (ad- sorption) and are eliminated as a complex (adsorbate) in the excreta.