Mycotoxins can severely affect feed quality. As a result, they will negatively influence the health and immune status of animals such as poultry. Effective mycotoxin control will keep these negative aspects within limits.
By Radka Borutova, Biomin, Austria
The gut and the immune system form a complex integrated structure that has evolved to provide effective digestion and defence against ingested toxins and pathogenic bacteria. Nowadays, animal health has major implications for the food supply, public health and international trade. There is increasing reluctance to rely upon therapeutic solutions in animal health using drugs and medicines. Consequently nutrition is being more widely used as a practical solution for maintaining animal health.
To develop a positive nutrition-based health strategy it is necessary to consider the basic interactions between health and nutrition and to challenge the current concepts of nutritional requirements based on avoidance of deficiency symptoms. Feed components and nutrients influence health in many different ways. By manipulating or selecting them, feed quality may be maintained and risk of mycotoxin contamination may be reduced.
Nutritional components have a positive effect in maintaining the gastrointestinal tract and alleviating the threat of enteric diseases. They influence many non-infectious diseases through control of oxidative stress. It is becoming evident in raising animals for food that nutrition is all there is and a nutrition-based health strategy must play a major role in the future development of animal production.
Effects on the GIT
Contamination of feed commodities by moulds and mycotoxins is considered to be one of the most important negative factors in crop production and animal feed quality. It is well documented that mycotoxin consumption causes a decrease in performance including decreased growth rate and poor feed efficiency. There has been extensive research addressing the different causes by which mycotoxins can alter animal productivity.
The gastrointestinal tract (GIT) 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 high concentrations of toxins. Direct intestinal damage can be exerted by the biological action of mycotoxins. There are direct effects of trichothecenes on protein synthesis in eukaryotic cells. This is due to interaction with the ribosomal units preventing either initiation of protein synthesis or elongation of the polypeptidic chains. Trichothecenes affect actively dividing cells such as those lining the gastrointestinal tract.
Another relevant effect of some mycotoxins (fumonisin B1 and ochratoxin A) is that they alter the barrier function of the intestinal epithelium measured as a decrease in the transepithelial electrical resistance. Poults fed grains naturally contaminated with Fusarium mycotoxins had decreased villus height in the duodenum, and decreased villus height and apparent villus surface in the jejunum, during the starter period. In addition to the morphological changes induced to the intestinal villi by DON it is suggested that this mycotoxin inhibits Na+ transport and Na+ -D-glucose co-transport in the jejunum of layers resulting in a reduction of glucose uptake when the intestine is exposed to DON. Aflatoxins fed to broiler chickens decreased the production of pancreatic secretions whereas aflatoxins fed to layers produced an increase in the production of pancreatic enzymes.
Increase in pathogenic bacteria
Even though some bacterial strains are affected by mycotoxins there is evidence that mycotoxins increase pathogenic bacteria colonisation of the intestinal tract in animal species. Layer chickens treated with ochratoxin A (3 mg/kg) had higher susceptibility to a Salmonella challenge compared to the control group. E. coli challenge in broilers receiving an experimental diet containing 2 ppm of ochratoxin more than doubled the mortality compared to birds that received the bacterial challenge and a diet without mycotoxins. No birds died in the treatment receiving the diet with mycotoxin alone demonstrating that it is the combination of mycotoxins and pathogenic bacteria what causes the most devastating effects.
Gross and histopathological lesions of birds inoculated with E. coli were also more severe in birds receiving a diet containing 2 ppm of ochratoxin than in birds receiving a diet with no significant levels of mycotoxins. Parasitic infections are more severe in combination with mycotoxins. It has been demonstrated that birds treated with lasalocid do develop clinical coccidiosis when the levels of T-toxin exceeded 0.5 ppm. Moreover, chronic ingestion of DON - comparable to concentrations occurring in contaminated food and feed - was reported to impair the intestinal transfer and uptake of nutrients.
Endotoxins also harmful
Endotoxins are lipopolysaccharides (LPS) derived from the cell membranes of Gram-negative bacteria and are responsible for its organisation and stability. In pharmaceutical industries it is possible to find endotoxins during production processes or in the final product. Although endotoxins are linked within the bacterial cell wall, they are continuously liberated into the environment. The release does not happen only with cell death but also during growth and division. A single Escherichia colicontains about two million LPS molecules per cell.
Since bacteria can grow in nutrient poor media, such as water, saline, and buffers, endotoxins are found almost everywhere. Endotoxins are present in dust, feed, drinking water as a part of a bacterial cell wall or as fragments of whole bacteria. The mucosal surface of the gastrointestinal tract is covered with a one cell layer, the mucosal epithelium. Intestinal epithelium is constantly exposed to gram negative bacteria, which are able to directly deposit their toxic and proinflammatory constituents such as LPS at the intestinal epithelial apical surface. LPS is a potent toxin that elicits several immediate proinflammatory responses in mammalian cells.
Despite the density of these bacteria and their toxins, the intestinal epithelium does not activate proinflammatory responses to these organisms. Both innate and acquired immune systems protect the GIT against microbial endotoxins. In conditions where the body is exposed to LPS excessively or systemically (as when small concentrations of LPS enter the blood stream), a systemic inflammatory reaction can occur, leading to multiple pathophysiological effects, such as endotoxin shock, tissue injury and death. However, endotoxin does not act directly against cells or organs but through activation of the immune system, especially through monocytes and macrophages, with the release of a range of proinflammatory mediators, such as tumor necrosis factor (TNF), interleukin (IL)-6 and IL-1.
Enhanced growth performance
Although ultimately beneficial in treating the infection, antibiotic therapy has been hypothesised to initially increase the circulating load of free endotoxin by killing or lysing the infecting bacteria.
Antimicrobials have been used for more than 50 years to enhance growth performance and to prevent disease in livestock feeding environments. There is growing concern about the potential of antimicrobials in livestock diets to contribute to the growing list of antibiotic-resistant human pathogens. Although the use of antimicrobials for growth promotion in livestock diets is still allowed in the United States, most countries in Europe are implementing strict guidelines and regulations for the use of dietaryantimicrobials (Regulation (EC), 2003).
Several drugs have been investigated to counteract endotoxins. Antibiotics differ in potential for endotoxin liberation according to their bacteriostatic or bactericidal effect. Antibiotics can also bind endotoxins, Polymyxin B or Colistin being the example, but were shown to be toxic themselves. The most remarkable adverse effects of these drugs are nephrotoxicity (chiefly acute renal failure) and neurotoxicity.
The use of antibiotics in farming operations (therapeutic use) clearly leads to the development of antibiotic-resistant pathogens. This causes problems when those antibiotic-resistant pathogens get into people. That is why a feed additive was developed for its positive effect on health and immune status of animals exposed to mycotoxins and endotoxins.
The Mycofix product line offers a complex-strategy solution for the counteraction of mycotoxin and endotoxin effects. Adsorption components enable the binding of both, adsorbable mycotoxins (aflatoxins, fumonisins, ergot alkaloids) and endotoxins. The biological constituent and inactivated bioprotein biotransform non-adsorbable mycotoxins into non-toxic metabolites. On one hand the biological constituent stimulates the production of the anti-inflammatory cytokine (IL-10) and the macrophage activity and on the other hand it inhibits the production of pro-inflammatory cytokines (IL-6 and TNF- ).
Moreover, the phytophytic substance incorporated in order to protect the liver, seems to be effective in inhibiting pro-inflammatory cytokines (IL-6 and TNF- ) production. The phytogenic substances inhibit pro-inflammatory cytokine (IL-6) production therefore support the immune system.