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Trichothecene Poisoning

Bowel movements, stool - blood or black (hematochezia) (melena) [Pg.423]

Bowel movements - diarrhea Breathing - diff, acute (acute dyspnea) [Pg.423]

Breath sounds, gen - wheezes Cough - acute NS Dizziness (lightheaded) [Pg.423]

conjunctivae - injected Eyes, vision - blurred Eyes - pain [Pg.423]

Variable with exposure route and intensity Death may occur in minutes-days %. [Pg.424]


Staphylococcus food poisoning, 215-217 Sulfur mustard poisoning, 403-406 Tetrodotoxin poisoning, 414-417 Thallium poisoning, 418-421 Trichinellosis, 222-226 Trichothecene poisoning, 422-425 Typhoid fever, 232-236 Typhus - epidemic, 237-241 Typhus - murine, 242-245 Typhus - scrub, 246-249 Viral gastroenteritis, 254-256 West Nile fever, 261-265 Yellow fever, 270-273 Yersiniosis, 274-277... [Pg.487]

Sulfuryl fluoride poisoning, 399-402 Sulfur mustard poisoning, 403-406 Trichothecene poisoning, 422-425... [Pg.493]

Group 2 includes some 80 sesquiterpene trichothecenes, which are particularly associated with fungi belonging to the group Fusarium. Fusarium species are widely known both as plant pathogens and contaminants of stored foods snch as maize. Trichothecenes are strong inhibitors of protein synthesis in mammalian cells. There have been many incidents of poisoning of farm animals cansed by contamination of their food by these componnds. [Pg.13]

Trichothecenes are composed of 40 or more structurally related compounds produced by a variety of molds, including Cephalosporium, Fusarium, Myrothecium, and Trichoderma, which grow predominantly on grains. Much of the available information on human toxicity of trichothecenes was obtained from an outbreak of poisoning in Siberia in 1944, mentioned above. [Pg.401]

M. K. Matossian, Poisons of the Past Molds, Epidemics and History, New Haven, Conn., Yale University Press, 1989 Selected mycotoxins, ochratoxins, trichothecenes, ergot . [Pg.318]

Matossian, Poisons of the Past Selected mycotoxins, ochratoxins, trichothecenes, ergot . [Pg.318]

Both no vaccine and no specific therapy are currently available for protection against any of the trichothecene mycotoxins and for poisoning by them. [Pg.80]

Several studies investigated the in vivo toxicity of macrocyclic trichothecenes [135], It is assumed that their toxic effects are based on the inhibition of protein synthesis, with a slowly progressing respiratory depression and paralysis of skeletal muscles. The epidermal remains of these plant species that produce acute intoxication in rumiants were also quantified by microhistological analysis in the gastrointestinal content of sheep which had been experimentally poisoned [136]. [Pg.751]

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. [Pg.670]

The so-called stachybotryotoxicosis occurs mainly in Ukraine, Hungary, and other East European countries. The symptoms in horses, pigs, cattle, and poultry are skin necrosis, inner hemorrhages, states of shock, irritations of stomach mucous membranes, reduced leukocyte count, nervousness. In severe cases the animals die within 1 - 3 d. Farm-workers who handle infected hay and straw may also show signs of poisoning such as skin and mucous irritations, cough, nosebleeds, fever, etc. Like all trichothecenes the S. inhibit eukaryotic protein biosynthesis. [Pg.573]

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. [Pg.156]

Jarvis BB, Wang S, Cox C, Rao MM, Philip V, Varashin MS, Barros CS (1996) Brazilian Baccharis Toxins Livestock Poisoning and the Isolation of Macrocyclic Trichothecene Glucosides. Nat Toxins 4 58... [Pg.120]

Habermehl GG, Busam L, Heydel P, Mebs D, Tokamia CH, Dobereiner J, S nxml M (1985) Macrocyclic Trichothecenes Cause of Livestock Poisoning by the Brazilian Plant Baccharis coridifolia. Toxicon 23 731... [Pg.124]

Toxins are natural substances that are poisonous. Animals (snake venom), plants (ricin from castor beans), bacteria (botulism toxin), and fungi (trichothecene mycotoxin T2) produce toxins. A man-made chemical substance that is poisonous is called a poison, not a toxin. To be useful as a weapon, a toxin has to be stable enough to be stored and must be producible in sufficient quantities. Some very potent toxins do not lend themselves to weapons use because they cannot be produced in more than minute quantities. [Pg.65]

While some biological toxins can be synthesized artificially, the practical method for producing these poisonous substances is to extract them from living organisms. For example, botulinum toxin is the active poison in the bacterium Clostridium botulinum. Trichothecene or T2 toxin is derived from species of Fusarium mold, and is unique among BW agents for its ability to cause pain and injury on contact with unprotected skin. [Pg.197]

Toxins produced by fungi, i.e., mycotoxins, are considered possible BW agent candidates and have been controversial for decades, including the putative agent in Yellow Rain. Trichothecene (T2) toxin is among the most poisonous of the known mycotoxins. Because the Fusarium toxin s effects in animals... [Pg.213]

Ueno, Y., K. Ishii, K. Sakai, S. Kanaeda, H. Tsunoda, T. Toshitsugu, and M. Enomoto Microbial survey on bean hulls poisoning of horses with the isolation of toxic trichothecenes, neosolaniol, and T-2 toxin of Fusarium solani. Jpn. J. Exp. Med. 42,187 (1972). [Pg.218]


See other pages where Trichothecene Poisoning is mentioned: [Pg.422]    [Pg.423]    [Pg.425]    [Pg.474]    [Pg.477]    [Pg.486]    [Pg.494]    [Pg.94]    [Pg.102]    [Pg.422]    [Pg.423]    [Pg.425]    [Pg.474]    [Pg.477]    [Pg.486]    [Pg.494]    [Pg.94]    [Pg.102]    [Pg.100]    [Pg.177]    [Pg.509]    [Pg.27]    [Pg.2]    [Pg.144]    [Pg.278]    [Pg.239]    [Pg.168]    [Pg.146]    [Pg.417]    [Pg.164]    [Pg.7]    [Pg.106]    [Pg.108]    [Pg.110]    [Pg.111]    [Pg.115]    [Pg.229]   


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