Vomitoxin, also known as deoxynivalenol (DON), is a type B trichothecene, an epoxy-sesquiterpenoid. This mycotoxin occurs predominantly in grains such as wheat, barley, oats, rye, and corn, and less often in rice, sorghum, and triticale. The occurrence of deoxynivalenol is associated primarily with Fusarium graminearum (Gibberella zeae) and F. culmorum, both of which are important plant pathogens which cause fusarium head blight in wheat and gibberella or fusarium ear blight in corn. The incidence of fusarium head blight is strongly associated with moisture at the time of flowering (anthesis), and the timing of rainfall, rather than the amount, is the most critical factor. However, increased amount of moisture towards harvest time has been associated with lower amount of vomitoxin in wheat grain due to leaching of toxins.[1] Furthermore, deoxynivalenol contents are significantly affected by the susceptibility of cultivars towards Fusarium species, previous crop, tillage practices, and fungicide use.[2] It occurs abundantly in grains in Norway due to heavy rainfall.[3]
F. graminearum grows optimally at a temperature of 25 °C and at a water activity above 0.88. F. culmorum grows optimally at 21 °C and at a water activity above 0.87. The geographical distribution of the two species appears to be related to temperature, F. graminearum being the more common species occurring in warmer climates. Deoxynivalenol has been implicated in incidents of mycotoxicoses in both humans and farm animals.
Vomitoxin belongs to a class of mycotoxins (trichothecenes) which are strong inhibitors of protein synthesis;[4] exposure to vomitoxin causes the brain to decrease its uptake of the amino acid tryptophan and, in turn, its synthesis of serotonin. Reduced levels of serotonin are believed to be responsible for the anorexic effects of DON and other trichothecenes. Irritation of the gastrointestinal tract may also play a role in reducing food intake, and may also partially explain the high incidence of paraesophageal stomach ulcers observed in sows during food refusal. In humans DON is extensively glucuronidated and excreted via urine.[5]
When compared to other trichothecene mycotoxins which can form in grains and forages, vomitoxin is relatively mild. Reduced feed intake, with its accompanying decrease in performance, is the only symptom of vomitoxin toxicity livestock producers will likely encounter. This response to vomitoxin appears to occur through the central nervous system.