Toxicity of T-2 toxin in chickens

T-2 toxin and DON toxicity is variable in different poultry species. For instance, the order of sensivity for T-2 toxin is goose> duck> chicken (Mézes et al., 1998). The marked differences are related to severity and extent of changes. T-2 toxin is the most acutely toxic trichothecene and the exposure can occur through different routes (Sokolovic et al., 2008). In chronic exposure T-2 toxin and HT-2 toxin shows various toxic effects like diarrhea, lesions in oral cavity, gizzard and instestine (Wyatt et al., 1973), also liver damage, weight loss and emesis (Li et al., 2011). Sokolovic et al. (2008) investigated the effects of feeding T-2 toxin in concentrations around 1 to 5 mg/kg for one week, which resulted in lesions in the mouth. In laying hens common symptoms of chronic T-2 toxin exposure are the impaired feathering, reduced egg production and impaired hatchability (Diaz et al., 1994). T-2-toxin also has neurotoxic effects and it even destroys the blood-brain barrier resulting increase in indoleamin (e.g. serotonin) concentration of the brain (Wang et al., 1998), which causes feed refusal and abnormal behavior (MacDonald et al., 1988).

T-2 toxin has various adverse effects on farm animals. T-2 toxin and its main metabolite, HT-2 toxin are well-known inhibitors of protein, RNA and DNA synthesis (Murugesan et al., 2015). They bind to the 60S subunit of eukaryotic ribosomes and impair the function of peptidyl transferase (Feinberg and McLaughlin, 1989). Depending on the substituent, there are two types ('type-E' and 'type-I') of mechanisms of protein synthesis inhibition (Ehrlich and Daigle, 1987). 'Type-E' is responsible for inhibition of elongation as well as termination of protein synthesis, whereas 'type-I' is responsible for inhibition of initiation of protein synthesis. T-2 toxin and HT-2 toxin are 'type-I' inhibitors, while DON belongs to the 'type-E' inhibitors. T-2 toxin is also cytotoxic and genotoxic, and has pro-oxidant properties, therefore, it largely affects the performance of animals (Sokolovic et al., 2008). T-2 toxin is also responsible for inducing apoptosis (Yang et al., 2000) and it regulates cytokine production (Ouyang et al., 1995). Murugesan et al. (2015) described that it causes reduction in the weight of bursa of Fabricius, causes peroxidative changes in the liver, abnormal blood coagulation and hypoproteinaemia. In poultry species oral lesions, reduced growth, abnormal feathering, decreased egg production and lower egg shell quality are also documented. In geese, Ványi et al. (1994a) reported 50% reduction in the hatching rate at 0.2 mg/kg/day T-2 toxin exposure for 18 days and also decrease in the egg yield. As a result of T-2 toxin administration Ványi et al. (1994b) also reported involution of the oviduct, lymphocyte depletion, necrosis and amyloidosis in the spleen, catarrhal enteritis, signs of colloid stasis in the thyroid gland and large numbers of secretory granules in the cytoplasm of the adrenalineproducing cells of the adrenal gland in laying geese. In case of poultry the effects of T-2 toxin / HT-2 toxin are mostly dependent on time, on the applied dose and on the presence of other mycotoxins. T-2 toxin affects the immune system, which causes decrease in leukocyte counts (leukopenia) or reduced antibody formation after vaccination (Creppy, 2002). Sokolovic et al. (2008) described that in 7-day-old broiler chickens the LD50 of T-2 toxin was 4.97 mg/kg, while Chi et al. (1978) described a LD50 value in broiler chickens 6.3 mg/kg BW.