Several lesser-known effects of mycotoxins in poultry related to disrupting gut integrity reinforce the importance of mycotoxin risk management to protect the health and profitability of flocks.
The discovery that mycotoxins affect animal health was surprisingly recent. It was in the 1960’s and it explained the sudden death of 100,000 turkeys in the United Kingdom. It turned out that Aspergillus growing on peanut meal produced small amounts of a compound called aflatoxin. The problem had been in the detection of such secondary metabolites of fungi that are often highly toxic but usually present in tiny quantities. Tiny but lethal in the case of those turkeys.
Mycotoxins and poultry disease susceptibility
Now there is growing awareness of the variety of mycotoxins, how frequently they are present in animal feed and, importantly, how much of their effect can simply be impaired performance and increased susceptibility to disease (Table 1).
|Area Affected||Mycotoxin Effect||Example References|
|Intestinal Tract||Direct lesions formed opening pathway to infection (e.g. T-2 toxin)||Sokolović et al., 2008|
|Reduced mucus protection, including reduced production of mucus producing goblet cells||Antonissen et al., 2011; Bracarense et al., 2012|
|Decreased production of tight junction (TJ) proteins, weakened TJ’s allow pathogen entry||Antonissen et al., 2014; Basso et al., 2013|
|Faster rate of epithelial cell death (apoptosis can reduce intestinal barrier integrity)||Antonissen et al., 2014; Gitter et al., 2000|
|Slower rate of cell replacement in epithelium||Antonissen et al., 2014|
|Mucosal damage leading to nutrient availability for pathogen proliferation||Antonissen et al., 2014|
|Intestinal inflammatory response impairing animal growth and health and interfering with appropriate immune response to pathogens||Przybylska-Gornowicz et al., 2015|
|Immune Cells||Protein synthesis inhibition reducing rate of immune cell production and activity||Maresca, 2013|
|DNA fragmentation in immune cells reducing immune response. Also exacerbates DNA damage caused by pathogens.||Payros et al., 2017|
|Faster rate of immune cell death||Pestka et al., 2008|
|Cytokines and Antibodies/ Immunoglobulins||Cytokine production leading to inflammation||Pestka et al., 2010|
|Reduced response of antibodies when required||Grenier et al., 2011|
|Also wasteful increased production of antibodies as part of inflammatory response||Grenier et al., 2011; Obremski, 2014|
|Reduced vaccine response||Grenier et al., 2011 (Figure 2)|
A growing trend of pathogenic diseases such as salmonellosis, necrotic enteritis, etc., are putting a pressure on poultry production, reducing productivity and increasing the cost of therapeutic treatment. While we historically link mycotoxins in poultry to classic symptoms such as reduced feed intake, oral lesions, reduced productivity, etc., producers are often unaware of the link between mycotoxins and health.
Lesser known effects in poultry
Some of the common mycotoxins are actually quite poorly absorbed in a normal poultry gut. Trichothecenes (Deoxynivalenol or DON, T-2, etc.) and fumonisins (FUM) are very poorly absorbed in poultry, approximately 10% and 1%, respectively (Grenier et al., 2016).
There is now clear evidence that even if these mycotoxins are not in the bloodstream, they can still affect the gut wall. This in turn can increase the colonization of the epithelium by pathogens, the entry of pathogens into the animal and reduce the ability of an animal to fight infection.
The inflammatory response to these mycotoxins is an energy cost to the animal that can result in significant loss in productivity. This overresponse of the immune system to mycotoxins also interferes with the appropriate response to disease.
Gut barrier erosion
The gut wall is the first barrier that pathogens must overcome to infect a bird. Mycotoxins compromise the integrity of this barrier in many ways. Reduced barrier integrity increases the potential for colonization and uptake of pathogens e.g. Salmonella spp. (Vandenbroucke et al., 2011, increased uptake of bacteria), Clostridia (Antonissen et al., 2014, increased necrotic enteritis lesions as seen in Figure 1) and Eimeria (Grenier, 2016, increased lesions and shedding of oocysts).
At the same time mycotoxins compromise the immune system causing wasteful inflammation and a reduced ability to combat mycotoxins.
Another more hidden link between mycotoxins and diseases has also been identified: that mycotoxins can impair the response to vaccines (Figure 2).
Mycotoxin risk management
Given all of the links between mycotoxins and disease, a mycotoxin risk management program is necessary to safeguard poultry health. This includes monitoring of mycotoxin levels in feed, good feed storage and hygiene as well as an effective mycotoxin deactivator product that can effectively address particularly the trichothecene mycotoxins such as DON and T-2.
DON is not able to be bound effectively by binder products. With proven biotransformation of trichothecenes, Mycofix® is the only mycotoxin deactivator to successfully obtain the worldwide benchmark of European registration for activity against trichothecenes.
Antonissen, G., Martel, A., Pasmans, F., Ducatelle, R., Verbrugghe, E., Vandenbroucke, V., Li, S., Haesebrouck, F., Van Immerseel, F. and Croubels, S., 2014. The impact of Fusarium mycotoxins on human and animal host susceptibility to infectious diseases. Toxins, 6(2), pp.430-452.
Basso, K., Gomes, F. and Bracarense, A.P.L., 2013. Deoxynivanelol and fumonisin, alone or in combination, induce changes on intestinal junction complexes and in E-cadherin expression. Toxins, 5(12), pp.2341-2352.
Bracarense, A.P.F., Lucioli, J., Grenier, B., Pacheco, G.D., Moll, W.D., Schatzmayr, G. and Oswald, I.P., 2012. Chronic ingestion of deoxynivalenol and fumonisin, alone or in interaction, induces morphological and immunological changes in the intestine of piglets. British Journal of Nutrition, 107(12), pp.1776-1786.
Gitter, A.H., Bendfeldt, K., Schulzke, J.D. and Fromm, M., 2000. Leaks in the epithelial barrier caused by spontaneous and TNF-α-induced single-cell apoptosis. The FASEB Journal, 14(12), pp.1749-1753.
Grenier, B., Loureiro‐Bracarense, A.P., Lucioli, J., Pacheco, G.D., Cossalter, A.M., Moll, W.D., Schatzmayr, G. and Oswald, I.P., 2011. Individual and combined effects of subclinical doses of deoxynivalenol and fumonisins in piglets. Molecular nutrition & food research, 55(5), pp.761-771.
Maresca, M., 2013. From the gut to the brain: Journey and pathophysiological effects of the food-associated trichothecene mycotoxin deoxynivalenol. Toxins, 5(4), pp.784-820.
Obremski, K., 2014. Changes in Th1 and Th2 cytokine concentrations in ileal Peyer’s patches in gilts exposed to zearalenone. Polish journal of veterinary sciences, 17(1), pp.53-59.
Payros, D., Dobrindt, U., Martin, P., Secher, T., Bracarense, A.P.F., Boury, M., Laffitte, J., Pinton, P., Oswald, E. and Oswald, I.P., 2017. The Food Contaminant Deoxynivalenol Exacerbates the Genotoxicity of Gut Microbiota. mBio, 8(2), pp.e00007-17.
Pestka, J.J., 2008. Mechanisms of deoxynivalenol-induced gene expression and apoptosis. Food additives and contaminants, 25(9), pp.1128-1140.
Pestka, J.J., 2010. Deoxynivalenol: mechanisms of action, human exposure, and toxicological relevance. Archives of toxicology, 84(9), pp.663-679.
Przybylska-Gornowicz, B., Tarasiuk, M., Lewczuk, B., Prusik, M., Ziółkowska, N., Zielonka, Ł., Gajęcki, M. and Gajęcka, M., 2015. The effects of low doses of two Fusarium toxins, zearalenone and deoxynivalenol, on the pig jejunum. A light and electron microscopic study. Toxins, 7(11), pp.4684-4705.
Sokolović, M., Garaj-Vrhovac, V. and Šimpraga, B., 2008. T-2 toxin: incidence and toxicity in poultry. Arhiv za higijenu rada i toksikologiju, 59(1), pp.43-52.