Trichothecene mycotoxins treatment

In contrast to treatment for exposure to any of the other toxins, simply washing the skin with soap and water within 1 to 3 hours after exposure to the trichothecene mycotoxins will eliminate or greatly reduce the risk of illness or injury. 

In areas that have experienced a yellow rain attack, environmental assays have been in the range of 1 to 150 parts per million (ppm) and blood samples in the range of 1 to 296 parts per billion (ppb).8"1016 22 In the laboratory, at 10 and 50 minutes after an intramuscular exposure to 0.4 mg/kg of T-2 toxin in the dog, plasma concentrations of T-2 toxin were 150 and 25 ppb, and for HT-2 toxin were 50 and 75 ppb, respectively.60 Thus, any screening procedure for trichothecene mycotoxins in biomedical samples must have detection limits of 1 to 100 ppb. Most of the analytical procedures require extraction and cleanup treatment to remove interfering substances.73... 

No specific therapy for trichothecene-induced mycotoxicosis is known or is presently under experimental evaluation. Several therapeutic approaches have been evaluated in animal models. It is perhaps significant, however, that although experimental procedures for treatment of systemic exposure have been successful in reducing mortality in animal models, they have not been tested in primates. Thus, these treatments are not available for field use for humans exposed to trichothecene mycotoxins. 

Symptomatic measures for the treatment of exposure to trichothecene mycotoxins are modeled after the care of casualties of mustard poisoning.85 Irrigation of the eyes with large volumes of isotonic saline may assist in the mechanical removal of trichothecene mycotoxins, but would have limited useful therapeutic effects. After the skin has been decontaminated, some erythema may appear, accompanied by burning and itching. Most casualties whose skin has been treated with soap and water within 12 hours of exposure will have mild dermal effects these should be relieved by calamine and other lotion or cream, such as 0.25% camphor and methanol. 

Prophylactic induction of enzymes involved in the conjugation of xenobiotics reduced or prevented the acute toxic effects of T-2 toxin in the rat, while inhibition of these enzymes resulted in a higher toxicity for this trichothecene.96 Pretreatment with flavonoids,97 ascorbic acid,98 vitamin E," selenium,100 or chemoprotective compounds such as emetine101 that block trichothecene-cell association all reduce acute toxicity of these mycotoxins. However, none of these chemoprotective treatments have undergone extensive efficacy studies to evaluate their ability to protect against an aerosol or dermal exposure to trichothecene mycotoxins. 

No specific therapy for trichothecene mycotoxin poisoning is currently available. Skin decontamination with soap and water or the hypochlorite- (M258A1) or resin-based (M291) military decontamination kits can effectively remove toxin up to six hours after exposure, although none of them neutralize the toxin. Treatment of respiratory, dermal, and GI effects currently must be symptom based and supportive in nature. Superactive activated charcoal, for example, a common treatment for many orally taken poisons, has been shown to bind 0.48 mg T-2/gm charcoal in mice and improve survival rates significantly. 

Some microorganisms are also able to transform trichothecenes into less toxic compounds. For example, rumenal bacteria, bacteria from the large intestine of chickens, and bacterial populations from soil samples, were capable of transforming deoxynivalenol into 3-acetyldeoxynivalenol or 3-keto-4-deoxynivalenol (Binder et ah, 2000 Swanson et ah, 1987 He et ah, 1993 Shima et ah, 1997). Therefore, it seems likely that the development of wheat crops with the capability of eliminating this mycotoxin or bio-treatments could possibly be developed as a feasible strategy. 

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