Trichothecene mycotoxins are perhaps a more obscure cause of food-borne disease of some historical importance. Produced by fungus growing at low temperatures on grain, these toxins are extremely fastidious. Trichothecene mycotoxins may affect refugee populations or those involved in disasters that interrupt the normal harvesting and processing of cereal grains. They are thought to be responsible for the illness and death of thousands in Soviet Russia during and after World War II when wheat was unable to be harvested in a timely fashion. Their resistance to degradation makes them easy to weaponize. Refugees from Cambodia and Laos after the Vietnam War have reported "Yellow Rain," possibly dropped from low-flying aircraft, causing symptoms of trichothecene mycotoxin poisoning. It also has been suggested that these toxins have been used by both the Soviets in Afghanistan and by Iraq in its battles with Iran.
Trichothecene mycotoxins produce systemic toxicity and have irritant/vesicant properties. Research has found that trichothecenes inhibit DNA synthesis, protein synthesis, ribosome function, and mitochondrial protein synthesis. In addition, they produce single-strand DNA breaks and inhibit cellular thiol enzymes. The net result is multisystem toxicity, bone marrow suppression, and immune suppression, known as a "radiomimetic" syndrome. Trichothecenes are rapidly absorbed through abraded skin, inhalation, and the GI tract. The US Army has estimated the LD50 at 1.2 mg/kg by the oral route.
Dermal or ocular contact will cause irritation, blistering, and eye irritation, followed by systemic toxicity. Inhalation is accompanied by eye irritation, rhinorrhea, dysphagia, dyspnea, chest pain, and hemoptysis, followed by systemic symptoms that may lead to pulmonary edema and cardiovascular collapse. Oral ingestion causes mouth and throat irritation, vomiting and diarrhea, followed by GI bleeding and systemic toxicity. Chronic ingestion (e.g., in the case of contaminated grain) will cause alimentary toxic aleukia.
Poisoning with trichothecene mycotoxins is diagnosed based on environmental findings and the patient's clinical picture. It may be differentiated from mustard gas exposure by the presence of systemic symptoms and the absence of mustard gas agents on field testing. Exposure to ricin may be ruled out by the presence of skin irritation and blistering in the patient exposed to trichothecenes. Radiation levels will not be above background in environments contaminated with trichothecenes. Currently there is no field test for trichothecenes. Samples from grain or exposed surfaces may be sent to a reference lab for confirmatory testing (e.g., gas chromatography/mass spectroscopy).
Trichothecenes and their metabolites may be detected in the serum and urine for up to 28 days after exposure. Clinical specimens should be sent to a reference lab for either antigen detection or GC/MS techniques.
If the toxin has been ingested, activated charcoal should be administered. Treatment for those with trichothecene poisoning is supportive; there is no specific antidote. Attention should be given to maintaining a patent airway, adequate respiratory effort and oxygenation, and hemodynamic status. Standard burn and wound care applies to skin wounds. Hematology/oncology consultation should be obtained for those patients exhibiting signs of coagulopathy or bone marrow suppression. Antibiotic coverage should be considered for those patients with signs of sepsis or infection.
Rescuers should wear protective chemical suits as contact with contaminated skin or clothing leads to dermal irritation. Patients should be decontaminated with soap and water. Their clothing should be removed and confiscated. Surfaces and equipment need to be decontaminated in a solution of 1% sodium hypochlorite with 0.1 M sodium hydroxide for 1 hour of contact time. There are no special precautions for health care workers once decontamination is complete.
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