*Dr. Radka Borutova is a business development manager for NutriAd International.

POULTRY producers in several U.S. states are bracing for more losses as a strain of highly pathogenic avian influenza (HPAI) has been forcing them to destroy millions of chickens and turkeys.

HPAI H5 infections have been reported in U.S. poultry (backyard and commercial flocks), captive wild birds and wild birds. HPAI H5 detections began in December 2014 and have continued into June. The U.S. Department of Agriculture is reporting H5 bird flu virus detections in 19 U.S. states — 14 states with outbreaks in poultry and five states with detections in wild birds only.

On the other hand, low-pathogenic avian influenza (LPAI) occurs naturally in wild birds and can spread to domesticated birds. In most cases, LPAI causes no signs of infection or only minor symptoms in birds. These strains of the disease pose little significant threat to human health. LPAI strains are common in the U.S. and around the world.

USDA plays both an international and a domestic role in controlling the spread of avian influenza and reducing its effects on agriculture and public health. It is aware of and prepared for the emergence of new types of influenza virus.

USDA's plans that are currently in place — which include surveillance, reporting, biosecurity, movement control, vaccination and depopulation — can be adjusted and applied to effectively control any new virus outbreak.

Virus control, mycotoxins

Extensive research over the last couple of decades has confirmed that mycotoxins are commonly prevalent in the majority of feed ingredients. Acute cases caused by ingestion of high levels of mycotoxins may result in mortality and a marked decline in the productivity of poultry characterized by obvious clinical signs and postmortem lesions.

However, in most cases, mycotoxicosis is chronic and caused by low-level ingestion of fungal metabolites. This results in a measurable decline in performance and the occurrence of non-specific changes, including subcutaneous hemorrhage and immunosuppression (D'Mello et al., 1999).

The question is: Can mycotoxins significantly affect the normal immune system functions of birds, which can cause them to become much more susceptible to different viral, bacterial or parasitic diseases? The answer is yes, they can and they do.

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.

Several reports show that mycotoxins such as aflatoxins, ochratoxins, patulin or fumonisins are able to affect the inflammatory response. They can act at different levels, for instance, by directly affecting the viability of phagocytes (macrophages and neutrophils). Alternatively, they can impair the activity or the secretory functions of these cells.

The broad immunosuppressive effect of mycotoxins on cellular and humoral-mediated immune responses has been demonstrated to decrease host resistance to infectious diseases. For example, T-2 toxin increases the susceptibility of chickens to infection by salmonella species (Kubena et al., 2001) and Cryptosporidium baileyi (Bekesi et al., 1997).

Similarly, the ingestion of aflatoxins increases the severity of infection of coccidiosis and salmonellosis in chickens and Japanese quail (Kubena et al., 2001).

Ochratoxin A has also been found to increase the susceptibility of chickens to coccidiosis (Stoev et al. 2002), salmonellosis (Fukata et al., 1996) and colibacillosis (Kumar et al., 2003).

Vaccination response

It is well known that immunity birds acquire through vaccination can be impaired by ingestion of mycotoxins. A study by Hegazy el al. (2011) in Egypt 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 the efficacy of vaccines (Oswald et al., 2005). The presence of mycotoxins in poultry rations could lead to a breakdown in vaccinal immunity and to the occurrence of diseases such as infectious bursal disease virus (Somvanshi and Mohanty, 1991), adenovirus (Shivachandra et al., 2003) or Marek's disease (Batra et al., 1991).

Low levels of toxins — below observable overt toxicity — in rations are also likely to alter normal immune functions.

Mycotoxin deactivation

Effective mycotoxin management is a very complex topic and consists of many different strategies. Without proper mycotoxin management, birds, as well as other animal species, will be constantly exposed to different concentrations and combinations of mycotoxins. The bird's immune system will be weakened and will not be able to defend against infectious diseases like, for example, avian influenza.

The most well-known approach for detoxification of mycotoxins involves the use of nutritionally inert feed additives with the capacity to bind and immobilize mycotoxins in the gastrointestinal tract of animals, thus reducing their bioavailability (Magnoli et al., 2011).

Although this approach successfully eliminates the risk of certain mycotoxins such as aflatoxins, it does not work comprehensively on all of the mycotoxins relevant to the poultry industry.

In general, the negative effects of a mycotoxin on the body of an animal depends upon the extent and rate of its absorption from the gastrointestinal tract, its distribution, its binding or localization in tissues, its biodegradation and its excretion processes. Natural bio-inactivation is a complex mix of different processes that can occur simultaneously to provide a defense against a variety of mycotoxins.

Natural mycotoxin bio-inactivation generally takes place in the gastrointestinal tract and liver and is a consequence of the action of gastrointestinal microflora and tissue enzymes. In the gastrointestinal tract, naturally occurring bacteria, yeast and protozoa have the ability to bio-inactivate mycotoxins from the trichothecenes family into nontoxic or less-toxic metabolites.

In poultry, T-2 toxin is usually metabolized and eliminated after ingestion. This process takes place in the crop, small intestine and liver, where hydrolysis, hydroxylation, de-epoxidation and conjugation yield more than 20 different metabolites.

Bio-inactivation has been one of the proven approaches for detoxifying the non-adsorbable mycotoxins (trichothecenes) by either altering their molecular structure into nontoxic metabolites or by binding onto the surface of probiotic bacteria (El Nezami et al., 2002).

Summary

In conclusion, mycotoxins may alter the bird's susceptibility to infectious diseases by affecting the intestinal health and innate and adaptive immune systems.

Further research will be necessary to investigate the impact of mycotoxins on infectious diseases and to develop practical and economically justified solutions to counteract mycotoxin contamination of feed and the effects on animal health.

References

Batra, P., A.K. Pruthi and J.R. Sadana. 1991. Effect of aflatoxin B1 on the efficacy of turkey herpes virus vaccine against Marek's disease. Research in Veterinary Science. 51:115-119.

Bekesi, L., S. Hornok, G. Szigeti, M. Dobos-Kovacs, Z. Szell and I. Varga. 1997. Effect of F-2 and T-2 fusariotoxins on experimental Cryptosporidium baileyi infection in chickens. Int. J. Parasitology. 27:1531-1536.

D'Mello, J., C. Placinta and A. Macdonald. 1999. Fusarium mycotoxins: A review of global implications for animal health, welfare and productivity. Animal Feed Sci. Tech. 80:183-205.

El-Nezami, H., N. Polychronaki, S. Salminen and H. Mykkanen. 2002. Binding rather than metabolism may explain the interaction of two food-grade lactobacillus strains with zearalenone and its derivative alpha-zearalenol. Appl. Env. Microbiol. 68:3545-3549.

Fukata, T., K. Sasai, E. Baba and A. Arakawa. 1996. Effect of ochratoxin A on Salmonella typhimurium-challenged layer chickens. Avian Diseases. 40:924-926.

Hatori, Y., R.P. Sharma and R.P. Warren. 1991. Resistance of C57B1/6 mice to immunosuppressive effects of aflatoxin B1 and relationship with neuroendocrine mechanisms. Immunopharmacology. 22:127-136.

Hegazy, A.M., F.M. Abdallah, L.K. Abd-El Samie and A.A. Nazim. 2011. The relation between some immunosuppressive agents and widespread nature of highly pathogenic avian influenza (HPAI) post vaccination. J. of American Sci. 7(9).

Kubena, L.F., R.H. Bailey, J.A. Byrd, C.R. Young, D.E. Corrier, L.H. Stanker and G.E. Rottinghaus. 2001. Cecal volatile fatty acids and broiler chick susceptibility to Salmonella typhimurium colonization as affected by aflatoxins and T-2 toxin. Poultry Sci. 80:411-417.

Kumar, A., N. Jindal, C.L. Shukla, Y. Pal, D.R. Ledoux and G.E. Rottinghaus. 2003. Effect of ochratoxin A on Escherichia coli-challenged broiler chicks. Avian Diseases. 47:415-424.

Magnoli, A., M. Monge, R. Miazzo, L. Cavaglieri, C. Magnoli, C. Merkis, A. Cristofolini, A. Dalcero and S. Chiacchiera. 2011. Effect of low levels of aflatoxin B1 on performance, biochemical parameters and aflatoxin B1 in broiler liver tissues in the presence of monensin and sodium bentonite. Poultry Sci. 90:48-58.

Oswald, I.P., D.E. Marin, S. Bouhet, P. Pinton, I. Taranu and F. Accensi. 2005. Immunotoxicological risk of mycotoxins for domestic animals. Food Additives & Contaminants. Part A. 22:4, 354-360.

Shivachandra, S.B., R.L. Sah, S.D. Singh, J.M. Kataria and K. Manimaran. 2003. Immunosuppression in broiler chicks fed aflatoxin and inoculated with fowl adenovirus serotype-4 (FAV-4) associated with hydropericardium syndrome. Veterinary Research. 27 p. 39-51.

Somvanshi, R., and G.C. Mohanty. 1991. Pathological studies on aflatoxicosis, infectious bursal disease and their interactions in chickens. Indian J. Veterinarian Pathology. 15:10-16.

Stoev, S.D., V. Koynarsky and P.G. Mantle. 2002. Clinicomorphological studies in chicks fed ochratoxin A while simultaneously developing coccidiosis. Veterinary Research Communications. 26:189-204.

Volume:87 Issue:25