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T-2 Toxin

T-2 is a type A trichothecene produced by strains of Fusarium sporotrichioides, Fusarium poae and Fusarium acuinatum.3, 5 These fungal strains are known to also produce HT-2 toxin and DAS. These fungi infect a great variety of cereal grains and grow well in cold climate regions or during wet storage conditions (ideal parameters are 6-24°C and humidity above 14%.3 The Fusarium mold normally appears at the tip of the ear, it normally has a white color, but pink or reddish forms have also been reported.3, 6 T-2 toxin is a non-volatile, water soluble mycotoxin and it exhibits a great tolerance to light and temperature.4 This mycotoxins produces metabolites such as HT-2, (hydrolysis), T-2 tetraol and neosolaniol (NEO). Several hydroxylated and de-epoxidated metabolites have also been reported.4

Toxicity

T-2 toxin has a broad array of toxic effects on animals. The mechanism of toxicity is common to other trichothecenes: inhibition of protein synthesis followed by disruption of the synthesis of DNA and RNA which interferes with the metabolism of membrane phospholipids.1, 4 This condition specifically affects rapidly dividing cells like the ones of the gastrointestinal tract, skin and lymphoid cells.1, 4, 5 Common symptoms include feed refusal, weight loss, vomiting and inhibition of immunity. Other symptoms are diarrhea, gastritis, emaciation, necrosis of cartilaginous tissues, apoptosis and death.1, 4, 5, 6 Furthermore, alteration of hematic values like reduction of serum proteins and cholesterol levels have also been observed.4 Poultry is particularly sensitive to type A trichothecenes compared to other species and exhibit peculiar symptoms like mouth and tongue lesions.1, 3, 4

Regulation

Currently there is no regulation for T-2 toxin in EU and USA.2, 7 At point number 3 of the official dossier of the EU about the presence of relevant mycotoxins in products intended for animal use, it is mentioned that contamination of material with T-2 and HT-2 could be a reason of concern and collection of further data is necessary.7 The FDA states that although no great information is available on this mycotoxin, they consider the critical level to be 500 ppb, based upon some North Dakota work.2

REFERENCES
  1. Grenier B., Applegate T.J., (2013). Modulation of Intestinal Function Following Mycotoxin Ingestion: Meta-Analysis of Published Experiments in Animals. Toxins (5) 396-430.
  2. http://www.isco.purdue.edu/feed/mycotoxins.htmhttp://www.fao.org/docrep/X5036E/x5036E1e.htm
  3. Krska R., Nährer K., Richard J. L., Rodrigues I., Schuhmacher R., Slate A. B., Whitaker T. B., (2012). Guide to Mycotoxins featuring Mycotoxin Risk Management in Animal Production. BIOMIN edition 2012.
  4. Li Y., Wang Z., Beier R.C., Shen J., De Smet D., De Saeger S., Zhang S. (2011). T-2 Toxin, a Trichothecene Mycotoxin: Review of Toxicity, Metabolism, and Analytical Methods. J. Agric. Food Chem. (59) 3441–3453.
  5. Marin S., Ramos A.J., Cano-Sancho G., Sanchis V., (2013). Mycotoxins: Occurrence, toxicology, and exposure assessment. Food and Chemical Toxicology (60) 218-237.
  6. Richard J.L., (2007). Some major mycotoxins and their mycotoxicoses - an overview. International Journal of Food Microbiology (119) 3-10.
  7. Commission regulation (EC) No 1881/2006. Communities, The commission of the European (2006).