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 epithelium4. The toxic action of trichothecenes results in extensive necrosis of oral mucosa and gizzard lesions5. The T-2 toxin inhibits DNA, RNA and protein synthesis in eukaryotic cells, affecting the cell cycle and inducing apoptosis programmed death of cells6. Antonissen et al (2012) found that feeding deoxynivalenol (DON) contaminated feed in concentrations lower than the maximum EU guidance contamination level of 5 ppm to broilers is a predisposing factor for the development of necrotic enteritis. DON was able to replace the most well-known predisposing factor of necrotic enteritis which is coccidiosis. According to a study from 20107 the combination of DON, zearalenone (ZEN) and fumonisins alters the Eimeria-induced immune response (Girgis et al, 2010). Moreover, mycotoxin contamination of broiler feed may reduce the efficacy of anti-coccidial treatment with lasalocid8.