Trichothecenes vomiting

Yellow Rain A lethal yellow substance thought to have been dispersed aerially as a warfare agent in Southeast Asia and Afghanistan the lethal component is though to have been a trichothecene mycotoxin that was reported to produce severe nausea and vomiting, disturbances in the central nervous system. Fever, chills, and abnormally low blood pressure with a case mortality of approximately 50 percent. 

Contamination occurs primarily in wheat, barley, rye, and maize. Type A trichothecenes include mainly T-2 toxin, HT-2, and diacetoxyscirpenol (DAS) mycotoxins of the group B include mainly 4-deoxynivalenol (DON), commonly known as vomitoxin, and nivalenol (NIV). Toxic effects include nausea, vomiting, visual disorder, vertigo, throat irritation, and feed refusal in farm animals. The most toxic is T-2, followed by DAS and NIV, with DON being the least toxic in acute toxicity studies but the most widespread in grains worldwide and therefore the most studied. Issues related to chemical and physical data, occurrence, toxicity, absorption, distribution, and metabolism of trichothecenes are reviewed in WHO (89) and IARC (34). Physicochemical data for some selected Fusarium toxins is given by Sydenham et al. (90). The molecular structures of the main trichothecenes are shown in Fig. 9. 

Trichothecenes cause apoptosis and/or necrosis in the lymphoid, hematopoietic, and gastrointestinal systems resulting in leukopenia, vomiting, and diarrhea that can be lethal. In addition, trichothecenes are toxic to the skin and testes. Immune suppression and increased susceptibihty to infection may occur, especially in the late phase of the disease. The toxic effects from trichothecenes largely resemble those following radiation exposure (radiomimetic) due to effects on rapidly dividing cells in the intestine, bone marrow, and testis. 

Some trichothecene-induced effects may be due to neurotransmitter alteration in the central nervous system. Emesis or vomiting, which occurs with many of the trichothecenes when given at high doses, has been attributed to the stimulation of the chemoreceptor trigger zone in the area postrema of the medulla oblongata. However, studies with T-2 toxin in cats indicated that other mechanisms, such as the neural afferent pathways from the abdomen, implicated in radiation-induced emesis, may also be involved (Borison and Goodheart, 1989). DON alters serotonin activity in the central nervous system of swine which is important in... 

LD50 values, which may differ based on route of exposure and species exposed, can be used to compare the toxicity of trichothecenes (Table 26.1). For example, the LD50 values for i.p. exposure in the mouse are 5.2 mg/kg for T-2 toxin and 23 mg/kg for DAS, while for i.v. exposure in the pig they are 1.21 mg/kg for T-2 toxin and 0.37 mg/kg for DAS (Ueno, 1985). For T-2 toxin, oral LD50 values are not markedly different across species (Ueno, 1985) however, T-2 toxin was 10- to 50-fold more toxic when inhaled than when administered orally (Marrs et al, 1986). For DON, pigs are the most sensitive, followed by mice then rats. For DON in pigs, the main clinical effect at high levels is vomiting and at low levels reduced food intake or food refusal. Such responses apparently limit exposure and thus toxic manifestations. 

New bom animals are highly sensitive to the trichothecene mycotoxins. Diarrhea is one of characteristic responses of animals administered a sublethal dose of trichothecene my cotoxin, as well as loss of tension in skeletal muscle. Vomiting is often induced shortly after the administration of trichothecene mycotoxins and this vomiting occurs frequently with intervals. Trichothecene mycotoxins cause cellular damages to actively dividing cells, impairment of immunoresponses and inhibition of macromolecule syntheses. Also, toxicity of trichothecene mycotoxin to different animal species was demonstrated. 

The most common symptoms in both Southeast Asia and Afghanistan included vomiting (71%) diarrhea (53%) skin irritation, burning, and itching (44%) rash or blisters (33%) bleeding (52%) and dyspnea (48%).7 15 27 All of the symptoms listed could be attributed to trichothecene mycotoxin toxicity. 

Later signs and symptoms (8-24 h) would probably be similar (except for the degree of skin rash and blisters) for both large-particle and deep-respiratory aerosol exposure to trichothecene mycotoxins. They could include continued nausea and vomiting, diarrhea, burning erythema, skin rash and blisters, confusion, ataxia, chills, fever, hypotension, and bleeding. 

Trichothecene mycotoxins are noted for their marked stability under different environmental conditions. On a weight-for-weight basis, they are less toxic than other toxins such as ricin, botulinum, and staphylococcal enterotoxin B, but trichothecene mycotoxins are proven lethal agents in warfare. Symptoms include vomiting, pain, weakness, dizziness, ataxia, anorexia, diarrhea, bleeding, skin redness, blistering, and gangrene, as well as shock and rapid death. Sensitive immunoassays and chemical procedures are available for the identifi-... 

Ricin, staphylococcal enterotoxin B, and trichothecene mycotoxins T2 can also present with vomiting and diarrhea if ingested. See descriptions of these diseases under the respiratory and skin sections. 

Trichothecenes bind to eukaryotic ribosomes and inhibit protein synthesis (Pestka, Zhou, Moon, Chung, 2004). Different trichothecenes interfere with initiation, elongation and termination stages of protein synthesis. They are also immunosuppressive. Acute trichothecene mycotoxicosis are rare, but when ingested in high doses by farm animals they cause nausea, vomiting and diarrhea. DON is also called a vomitoxin or food refusal factor (Bennett Klich, 2003). Trichothecenes are not classifiable as to their carcinogenicity to humans (Class 3) (lARC). 

Trichothecenes Fusarium, Myrothecium Phomcrpsis, Stachybotrys, Trichoderma Trichothecium Hemorrhage, vomiting, dermatitis Central nervous system disorders GC HPLC-UV TLC Cereals... 

Approximately 180 trichothecenes are known. High moisture cereals are frequently contaminated with these toxins, considered as potent protein synthesis inhibitors and immune suppressors. Trichothecenes can produce the fatal syndrome named alimentary toxemia characterized by leucopenia (reduced white blood cell counts), multiple hemorrhages, loss of bone marrow, and esophageal cancer. In addition, the consumption of these toxins causes vomiting and reduces the efficiency of feed conversion in swine due to the considerably lower feed intake. In poultry, they cause hemorrhagic syndrome and other related problems that lower performance. 

TRICHOTHECENE MYCOTOXINS. A family of structurally related poisonous substances produced by various species of fungi, especially Acremorium (Cephalosporium), Fusarium, Myrothe-cium, Stachybotrys, Trichderme, and Verticumonosporium. Tri-chothecene mycotoxins are toxic to humans because they inhibit cellular protein synthesis. Prominent examples are deoxynivalenol (sometimes referred to as vomitoxin because it induces vomiting), diacetoxyscirpenol, HT-2, nivalenol, and T-2. These five toxins gained some notoriety in the so-caUed yellow rain events in Southeast Asia because of allegations that they were associated with Soviet-inspired use of chemical weapons (CW). 

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