Mycotoxins and their interactions
The obstacles in the road to risk assessment
Typically mycotoxin risk assessment is very specific in terms of animal species and production stage as well as mycotoxin type; the first two approaches make much sense as mycotoxins affect, for example, poultry in a different way than cattle; and broilers in a different way than laying hens; but in the day to day of farming and feeding animals, having individual mycotoxin challenges is not a reality. In practical experience, mycotoxin multi-contamination is found very frequently. Since 2014, EW Nutrition has conducted more than 15,000 mycotoxin tests around the globe from both raw material and finished feeds samples. 80% of these samples were contaminated with more than one mycotoxin and almost one third was positive for four or more mycotoxins.
Synergies, additive effects and antagonisms
The toxicity of combinations of mycotoxins cannot be predicted based upon their individual toxicities; interactions can lead to toxic effects at concentrations at which no effects are expected and can be antagonistic, additive, or synergistic. Synergistic actions may occur when the single mycotoxins of a mixture act at different steps of the same mechanism; or when the presence of one mycotoxin increases absorption of another or decreases its metabolic degradation. Antagonism, on the other hand, may occur when mycotoxins compete with one another for the same target or receptor site. However the interactions are complex and their effects depend on the animal species, age, sex, nutritional status, dose and duration on exposure as well as on environmental factors. For example, the combined presence of DON and ZEA, very common, may give ground for additive effects. In a feeding trial the combined effects of DON and ZEA in poultry were studied, having a natural contamination of around 5000 ppb of DON and 300 ppb of ZEA. As it can be seen in figure 1, the mycotoxin challenged group (T2) had a lower average body weight than the control groups (Control: no challenge and no anti-mycotoxin additive and T1 a feed without mycotoxin challenge but having a mycotoxin binder); the challenge was counteracted by an anti-mycotoxin agent (Mastersorb® Gold, produced and commercialized by Ew-nutrition) (T3 and T4). Significant decreases in villi height in duodenum and jejunum of poultry have been found in several studies after ingestion of diets contaminated with DON, as well as apoptosis of intestinal and immune cells. ZEA has toxic effects on neutrophils, and decreases IGG, IGA, IGM and TNF-Υ synthesis, affecting immune function, which can explain the additive effect.
More interactions: the gastrointestinal tract
After ingestion of feed its components, including mycotoxins, first reach the gastro-intestinal epithelium. One of the functions of the intestinal mucosa is to act as a barrier to the external environment, preventing the passage of virus, microorganisms and toxins. The intestinal epithelium in its whole extension is in contact with mycotoxins often at higher concentrations than other tissues. Moreover mycotoxin exposure can increase the animals’ susceptibility to harmful agents present in the gastrointestinal tract. In that regard, the intake of DON, OTA and fumonisin (FUM) contaminated feed (separately or in combinations) is a predisposing factor for the development of necrotic enteritis (NE) due to their negative influence on the epithelial barrier. Furthermore, mycotoxins can influence the composition of the intestinal microbiota can potentially be mediated by mycotoxins.
Aflatoxins have immune-inhibitory activity in the intestinal barrier and can also damage the gut epithelium. An increase in populations of E. Coli, Salmonella, and total gram-negative bacteria has been found after the ingestion of aflatoxin contaminated feed in poultry and swine. In broilers challenged with AFB1 and AFB2 the E. Coli and coliform bacterial count in cecum content was significantly lower in a group of animals receiving the anti-mycotoxin agent Mastersorb® Gold than in a group challenged but not receiving the additive (figure 2), indicating a possible relationship between the bacterial count and the mycotoxin challenge. As shown in several examples and in the practice in animal production, mycotoxin risk assessment has to be used in thoughtful way, preventive measures, like limiting highly contaminated raw materials and using effective anti-mycotoxin additives, have to be taken seriously and will be reflected in better health, welfare and productivity of animals.
Figure 1: Body weight of broilers at 33 days of age fed a DON and ZEA contaminated diet with and without Mastersorb® Gold
Figure 2: E. coli and total coliform count of cecal content of broilers at 42 days of age fed an AFB1 and AFB2 contaminated diet with (green bars) and without (grey bars) Mastersorb® Gold