Can low levels of mycotoxins harm the poultry industry?


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Symptoms of poultry diseases, arising due to lapses in their diets or the farm environment, allow veterinarians and nutritionists to take action and treat the problem accordingly. Often, disease manifestations can be attributed to several causes and thus, understanding the root of the problem can be hard. In this article, we explore how mycotoxins, toxic metabolites produced by molds, can harm the gastrointestinal tract (GIT), open the gate to infectious agents and/or predispose animals to a number of factors that will reduce performance and cause disease outbreaks.

The gut barrier

The GIT is probably one of the most amazing organs in the body, including that of chickens. It can digest food but it does not digest itself. It is the most extensively exposed surface in the body and therefore the most important barrier between the internal and external environments.

In poultry, the GIT harbors more than 650 different species of bacteria, contains over 20 different hormones, digests and absorbs the vast majority of nutrients, and accounts for 20% of the body’s total energy expenditure while being the largest organ of the immune system.

GIT exposure to mycotoxins

Whenever mycotoxins are discussed at a feed mill or farm, the first question raised usually concerns the mycotoxin level that triggers a symptom of disease. With the (high) limits imposed by regulatory bodies (European Commission in the European Union, and Food and Drug Administration in the USA) for the presence of mycotoxins in animal feed, levels below those thresholds may be dismissed as benign.

The general understanding is that in many cases, mycotoxins occur without any symptoms at levels below the regulatory limits and therefore their amounts are not high enough to be absorbed, attack target organs and cause mycotoxicoses. This understanding overlooks the fact that even subclinical levels of mycotoxins can and do cause harm to animals.

Indeed, it can be argued that not all mycotoxins cross the intestinal barrier; thus, not all mycotoxins will result in mycotoxicoses. Nonetheless, intestinal cells are the first cells to be exposed to mycotoxins and often at higher concentrations than in other tissues. Therefore, the intestinal epithelium and its entire extension can be compromised by non-absorbed toxins before absorption can even begin.

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Effects of mycotoxin exposure

There are many studies focusing on the different levels of impact of mycotoxins in the GIT. A meta-analysis published by Grenier and Applegate (2013) thoroughly reviews how mycotoxins can modulate intestinal functions. In terms of morphology of the intestinal villi, studies show that feeding poultry low or moderate levels of deoxynivalenol (DON) alone or combined with other fusariotoxins leads to a reduction in villi height in both the duodenum and jejunum.

Figure 1. The effect of Fusarium mycotoxins on the intestinal epithelium.

The practical consequence of this is that there is a smaller absorptive area available for nutrient uptake, with obvious impacts on animal performance. Interestingly, it seems that mycotoxins such as DON and T-2 have a direct effect on glucose transporters in the jejunum. This leads to an anti-nutritional effect (decreased glucose absorption) and may potentially limit water reabsorption resulting in diarrhea.

Several studies have explored the effects of mycotoxins on the intestinal defense against parasitic and bacterial infections. Chicks fed with the mycotoxin Ochratoxin A (OTA) presented more severe lesions and mucosal damage and more E. acervulina and E. adenoeides oocysts than those not exposed to the toxin.

Studies with a more commonly occurring mycotoxin showed that even at dosages below those regarded safe for poultry, DON modulated the intestinal response and intestinal recovery following a coccidial infection. In particular, the recruitment and stimulation of lymphocytes was inhibited at the site of infection, which delays the clearance of the parasitic infection.

Other factors that might explain coccidial outbreaks in the field despite the use of coccidiostats were explored in experiments in which the efficacy of lasalocid was reduced in broiler diets contaminated with T-2.

Experiments dealing with Afla and T-2 contamination of poultry feeds and birds’ increased susceptibility to diseases were so far unable to establish a correlation between Salmonella typhimurium colonization and mycotoxin levels. For other mycotoxins, such as OTA, this interaction has been proven and the number of colony forming units (CFU) found in the duodenal and cecal contents increased when animals ingested OTA-contami­nated feed.

More studies are available showing that DON in particular increases the intestinal inflammatory response to S. typhimurium and leads to a significant increase in both the invasion and epithelial translocation of Salmonella in swine. Similar observations were obtained when FUM were present concomitantly with E. coli in swine diets—prolonged intestinal infection, increased intestinal colonization and translocation of bacteria and dissemination into the lungs, liver and spleen were observed.

As research in this field develops, the subclinical effects of mycotoxins can be more confidently addressed. Gunther Antonissen, a researcher from Ghent University, presented his research findings at the 2014 European Poultry Conference, adding to the above-mentioned effects the negative impact of subclinical concentrations of mycotoxins on the uptake and efficiency of vaccines and other medication. His review published in 2014 summarizes decades of mycotoxin research on the susceptibility to infectious diseases.

Table 1 provides a summary of the literature on the effects of mycotoxins on poulty.

Table 1. Summary of the literature on the effect of mycotoxins in poultry.

Intestinal inflamation

Since the intestinal mucosal surface is heavily exposed to foreign materials, it is widely recognized that this surface usually presents itself in a normal state of reactivity and mild inflammation. Controlling this inflammation is of utmost importance, not only to reduce the energy and protein required to overcome inflammation, which could otherwise by directed towards performance, but also to avoid any escalation into disease outbreaks.

Antibiotic growth promoters (AGPs) seem to improve animal performance through their action and efficacy towards reducing inflammation, amongst other effects. With increasing pressure to reduce AGPs in animals exported to markets that have banned their usage, such as the EU, birds may now be more exposed to the risks of mycotoxins and other inflammatory agents.

Several studies on different animal species, including humans, clearly show that the fusariotoxin DON leads to an up-regulation of pro-inflammatory cytokines in the gut epithelium, promoting a rapid mucosal inflammatory response, especially when present at low concentrations in feed. It is important to keep in mind that tight junction proteins are regulated by such cytokines.

Similarly, FUM seem to alter the barrier function of the gut epithelium due to their well-known effect on sphingolipids, which play a crucial role in the maintenance of the tight junction barrier. From a practical standpoint, these events can lead to intestinal disorders and disease outbreaks among farmed animals as increased intestinal permeability allows the entry of antigens which would otherwise be restricted to the gut lumen.

Conclusion

Mycotoxins’ general effects include impaired nutrient uptake, immune suppression and decreased performance. They can compromise several key functions of the GIT including decreased surface area available for nutrient absorption, modulation of nutrient transporters, and/or loss of barrier function. Several mycotoxins act as inhibitors of protein synthesis; many specifically target rapidly dividing and activated cells which are predominant in the gut epithelium. Others increase the persistence of intestinal pathogens and potentiate intestinal inflammation.

Yes, even low levels of mycotoxins can harm the poultry industry. This is especially so when several mycotoxins co-occur in feeds, when exposure to several different pathogens are often not adequately­ controlled by biosecurity measures and when the usage of by-products in feeds further contributes to the total load of inflammatory agents to which animals are exposed.

Mycotoxin risk management tools are available to mitigate the negative impacts of mycotoxins in animal health and performance. Due to its long-standing R&D commitment, BIOMIN is the first, and so far, only feed additive company to have successfully registered in the EU a technological feed additive that is capable of reducing the negative impacts of mycotoxins in animals.

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