Mycotoxins: Unpredictable Contributors to Development of Infectious Diseases01 March 2015
Radka Borutova, Business development manager with Nutriad International (Belgium), presents a study demonstrating that effective mycotoxin control offers the opportunity to modify the response by broilers to vaccination and improve bird health and performance.
The rapidly expanding US ethanol industry is generating a growing supply of co-products, mostly in the form of dried distillers' grain and solubles (DDGS). In the United States, 90 per cent of the co-products of maize-based ethanol are fed to livestock. An unintended consequence is that animals are likely to be fed higher levels of mycotoxins.
During the production of ethanol from maize, mainly the endosperm (82 per cent of the grain) undergoes fermentation and distillation processes. For dry-milled products, the most highly mycotoxin-contaminated fractions are those that contain the whole or the outer portions of the grain (Hazel and Patel, 2004). Based on this knowledge, it is widely accepted that the co-products of ethanol production will concentrate by up to three times the previously existing mycotoxins in maize (Wu and Munkvold, 2008).
The use of DDGS in poultry diets has increased as the availability of this reasonably priced feed ingredient has risen over the past several years. The US Poultry & Egg Association published preliminary results of research where certain levels of DDGS (15 per cent in poultry diets) may lead to decreased bird performance. When the birds have a mild to moderate Clostridium perfringens challenge, this can lead to more severe cases of necrotic enteritis as well as a decrease in technical performance.
Mycotoxins as facilitators of necrotic enteritis development
The disease necrotic enteritis was first described in chickens in England in 1961 and since that time has been reported in the majority of countries around the world. Necrotic enteritis has been identified in broilers, laying hens, turkeys and quail. Necrotic enteritis has been estimated to affect up to 40 per cent of US commercial broiler flocks and is believed to cost the industry about five cents per broiler in the United States (McDevitt et al., 2006).
Necrotic enteritis is caused by toxins produced by Clostridium perfringens. While anything that causes intestinal irritation can lead to necrotic enteritis, stress, intestinal disease (particularly coccidiosis), intestinal parasites (especially round worms), and immune suppression by mold toxins (mycotoxins), chicken anaemia virus, Gumboro disease or Marek’s disease have all been specifically linked to the disease.
Avian mycotoxicosis is considered to be one of the most important problems in the poultry industry. It causes severe losses not only in terms of lost performance, but also as an immunosuppressive agent increasing the bird’s susceptibility to diseases and mortality.
The gastrointestinal tract represents the first barrier against ingested chemicals, feed contaminants and natural toxins. Following ingestion of mycotoxin-contaminated feed, intestinal epithelial cells can be exposed to toxins. Direct intestinal damage can be exerted by the biological action of mycotoxins. Trichothecenes like deoxynivalenol (DON) or T-2 toxin affect actively dividing cells such as those lining the gastrointestinal tract. It should be noted that the gastrointestinal tract is also sensitive to trichothecene-induced apoptosis affecting mainly the gastric mucosa, gastric granular epithelium and intestinal crypt cell epithelium (Bondy and Pestka, 2000).
The toxic action of trichothecenes results in extensive necrosis of oral mucosa and gizzard lesions (Leeson et al., 1995). The T-2 toxin inhibits DNA, RNA and protein synthesis in eukaryotic cells, affecting the cell cycle and inducing apoptosis programmed death of cells (Rocha et al., 2005). Antonissen et al (2012) found that feeding deoxynivalenol (DON) contaminated feed in concentrations lower than the maximum EU guidance contamination level of 5ppm to broilers is a predisposing factor for the development of necrotic enteritis.
Mycotoxins strengthen impact of coccidia
DON was able to replace the most well-known predisposing factor of necrotic enteritis, which is coccidiosis. According to Girgis et al. (2010) the combination of DON, zearalenone (ZEN) and fumonisins alters the Eimeria-induced immune response. Moreover, mycotoxin contamination of broiler feed may reduce the efficacy of anti-coccidial treatment with lasalocid (Varga and Vanyi, 1992).
What is the role of mycotoxins in vaccination failure?
It is well known that immunity acquired through vaccination can be impaired by ingestion of mycotoxins. The Egyptian study of Hegazy el al. (2011) revealed that mycotoxicosis might be the cause of vaccination failure against avian influenza virus. Mycotoxin-induced immunosuppression may be manifested as depressed T- or B-lymphocyte activity and suppressed production and impaired macrophage/neutrophil-effector functions (Hatori et al., 1991). Mycotoxins reduce the level of antibodies following infection or vaccination and reduce the activity of phagocytic cells.
Suppressed immune function by mycotoxins can eventually decrease resistance to infectious diseases, reactivate chronic infections and/or decrease vaccines efficacy (Oswald et al., 2005).
The presence of mycotoxins in poultry rations could therefore lead to a breakdown in vaccinal immunity and to a consequent increase in the occurrence of diseases such as infectious bursal disease virus (IBDV) (Somvanshi and Mohanty, 1991) or adenovirus (Shivachandra et al., 2003). Low levels of toxins in rations, below observable overt toxicity, are also likely to alter normal immune functions.
Deoxynivalenol (DON) can modulate immunological parameters. Determination of serum titres of antibodies against Newcastle Disease (NCD) after regular vaccination is a method which can be used to evaluate immuno-modulating effects of certain mycotoxins in vivo.
Table 1 records the results of a study designed to quantify the impact of mycotoxin ingestion by broilers on response to NCD vaccination and to determine the efficacy of a mycotoxin deactivation product to mitigate those effects.
From the results, it can be concluded that the addition of the Fusarium mycotoxins (deoxynivalenol and zearalenone) significantly decreased anti-NCD titre compared with the control group.
The supplementation of a mycotoxin deactivation product without mycotoxins did not result in a change of NCD-antibodies versus the level in the control group.
The reduction in anti-NCD titre with mycotoxins was counteracted completely by the addition of an effective mycotoxin deactivation product to the contaminated feed.
Mycotoxins may alter animals’ susceptibility to infectious diseases by affecting intestinal health and the innate and adaptive immune systems.
Further research will be necessary to investigate the effects of mycotoxins on infectious diseases and to develop practical, economically justified solutions to counteract mycotoxin contamination of feed and its effects on animal health.
The results of this study indicate that the use of effective mycotoxin control which is currently available offers an opportunity to significantly modify animal response to vaccination and help to improve animal health and performance.
- Bondy, G.S. and Pestka J.J. 2000. Immunomodulation by fungal toxins. J Toxicol. Environ. Health Part B Crit. Rev. 3: 109-143.
- Girgis, G., Barta, J., Brash, M., Smith, T. 2010. Morphologic changes in the intestine of broiler breeder pullets fed diets naturally contaminated with fusarium mycotoxins with or without coccidial challenge. Avian Dis., 54, 67–73.
- Hatori, Y., Sharma, R.P. and Warren, R.P. 1991. Resistance of C57B1/6 mice to immunosuppressive effects of aflatoxin B1 and relationship with neuroendocrine mechanisms. Immunopharmacology 22:127-136.
- Hazel, C.M. and Patel, S., 2004. Influence of processing on trichothecene levels. Toxicology Letters 153: 51-59.
- Hegazy, A.M., Abdallah, F.M., Abd-El Samie, L.K., and Nazim, A.A. 2011.The relation between some immunosuppressive agents and widespread nature of highly pathogenic avian influenza (HPAI) post vaccination. Journal of American Science, 7 (9).
- Leeson S., G.J. Diaz, and J.D. Summers. 1995. Poultry metabolic disorders and mycotoxins pp. 190-216. University Books. Guelph, Ont., Canada.
- McDevitt, R.M., Brooker, J.D., Acamovic, T., Sparks, N.H.C., 2006. Necrotic enteritis; a continuing challenge for the poultry industry. World's Poultry Science Journal 62: 221-247.
- Oswald, I.P., Marin, D.E., Bouhet, S., Pinton, P., Taranu, I., and Accensi, F. 2005. Immunotoxicological risk of mycotoxins for domestic animals, Food Additives & Contaminants: Part A, 22:4, 354-360.
- Rocha O., K. Ansari, and F.M. Doohan. 2005. Effects of trichothecene mycotoxins on eukaryotic cells: a review. Food Addit. Contam. 22:369-78.
- Shivachandra, S.B., Sah, R.L., Singh, S.D., Kataria, J.M., and Manimaran, K. 2003. Immunosuppression in broiler chicks fed aflatoxin and inoculated with fowl adenovirus serotype-4 (FAV-4) associated with hydropericardium syndrome. Vet. Res. 27:39-51.
- Somvanshi, R. and Mohanty, G.C. 1991. Pathological studies on aflatoxicosis, infectious bursal disease and their interactions in chickens. Indian J. Vet. Pathol. 15:10-16.
- Varga, I. and Ványi, A. 1992. Interaction of T-2 fusariotoxin with anticoccidial efficacy of lasalocid in chickens. Int. J. Parasitol. 22:523–525.
- Wu, F. and Munkvold, G.P., 2008. Mycotoxins in ethanol co-products: modeling economic impacts on the livestock industry and management strategies. Journal of Agricultural and Food Chemistry 56: 3900-3911.