Mycotoxins (T2)Signs and Symptoms:
Exposure causes skin pain, pruritus, redness, vesicles, necrosis and sloughing of epidermis. Effects on the airway include nose and throat pain, nasal discharge, itching and sneezing, cough, dyspnea, wheezing, chest pain and hemoptysis. Toxin also produces effects after ingestion or eye contact. Severe poisoning can result in prostration, weakness, ataxia, collapse, shock and death.
Poisoning should be suspected if an aerosol attack occurs in the form of "yellow rain" with droplets of yellow fluid contaminating clothes and the environment. Confirmation requires testing of blood, tissue and environmental samples.
There is no specific antidote. Super activated charcoal should be given orally if the toxin is swallowed.
The only defense is to wear a protective mask and clothing during an attack. No specific immunotherapy or chemotherapy is available for use in the field.
Isolation and Decontamination:
Standard Precautions for healthcare workers
Outer clothing should be removed and exposed skin should be decontaminated with soap and water. Eye exposure should be treated with copious saline irrigation. Once decontamination is complete, isolation is not required. Environmental decontamination requires the use of a hypochlorite solution under alkaline conditions such as 1 percent sodium hypochlorite and 0.1M NAOH with one hour contact time.
The trichothecene mycotoxins are low molecular weight (250-500 daltons) nonvolatile compounds produced by filamentous fungi (molds) of the genera Fusarium, Myrotecium, Trichoderma, Stachybotrys and others. The structures of approximately 150 trichothecene derivatives have been described. These substances are relatively insoluble in water but are highly soluble in ethanol, methanol and propylene glycol. The trichothecenes are extremely stable to heat and ultraviolet light inactivation. Heating to 1500 degrees Fahrenheit for 30 minutes is required for inactivation, while brief exposure to NaOCl destroys toxic activity. The potential for use as a BW toxin was demonstrated to the Russian military shortly after World War II when flour contaminated with species of Fusarium was unknowingly baked into bread that was ingested by civilians. Some developed a protracted lethal illness called alimentary toxic aleukia characterized by initial symptoms of abdominal pain, diarrhea, vomiting, prostration, and within days, fever, chills, myalgias and bone marrow depression with granulocytopenia and secondary sepsis. Survival beyond this point allowed the development of painful pharyngeal/laryngeal ulceration as well as diffuse bleeding into the skin (petechiae and ecchymoses), melena, bloody diarrhea, hematuria, hematemesis, epistaxis and vaginal bleeding. Pancytopenia, and gastrointestinal ulceration and erosion were secondary to the ability of these toxins to profoundly arrest bone marrow and mucosal protein synthesis and cell cycle progression through DNA replication.
History and significance
Mycotoxins allegedly have been used in aerosol form ("yellow rain") to produce lethal and non-lethal casualties in Laos in the late 1970s, Kampuchea between 1979 and 1981, and Afghanistan around the same time. It has been estimated that there were more than 6,300 deaths in Laos, 1,000 in Kampuchea and 3,042 in Afghanistan. The alleged victims were usually unarmed civilians or guerrilla forces. These groups were not reportedly protected with masks or chemically protective clothing and had little or no capability of destroying the attacking enemy aircraft. These attacks were alleged to have occurred in remote jungle areas which made confirmation of attacks and recovery of agent extremely difficult. Some investigators have claimed that the "yellow clouds" were, in fact, bee feces produced by swarms of migrating insects. Much controversy has centered upon the veracity of eyewitness and victim accounts, but there is evidence to make these allegations of BW agent use in these areas possible.
T-2 and other mycotoxins may enter the body through the skin and digestive or respiratory epithelium. They are fast acting potent inhibitors of protein and nucleic acid synthesis. Their main effects are on rapidly proliferating tissues such as the bone marrow, skin, mucosal epithelia and germ cells. In a successful BW attack with trichothecene toxin (T-2), the toxins can adhere to and penetrate the skin, be inhaled, or ingested. Clothing would be contaminated and serve as a reservoir for further toxin exposure. Early symptoms appear within minutes of exposure and include burning skin pain, redness, tenderness, blistering and progression to skin necrosis with leathery blackening and sloughing of large areas of skin in lethal cases. Nasal contact is manifested by nasal itching and pain, sneezing, epistaxis and rhinorrhea; pulmonary and tracheobronchial toxicity by dyspnea, wheezing and cough; and mouth and throat exposure by pain and blood tinged saliva and sputum. Anorexia, nausea, vomiting and watery or bloody diarrhea with abdominal pain occurs with gastrointestinal toxicity. Eye pain, tearing, redness, foreign body sensation and blurred vision may follow entry of toxin into the eyes. Skin symptoms occur in minutes to hours and eye symptoms in minutes. Systemic toxicity is manifested by weakness, prostration, dizziness, ataxia and loss of coordination. Tachycardia, hypothermia and hypotension follow in fatal cases. Death may occur in minutes, hours or days. The most common symptoms are vomiting, diarrhea, skin involvement with burning pain, redness and pruritus, rash or blisters, bleeding and dyspnea.
Rapid onset of symptoms in minutes to hours supports a diagnosis of a chemical or toxin attack. Mustard agents must be considered but they have odor and visibility and can be rapidly detected by a field available chemical test. Symptoms from mustard toxicity are also delayed for several hours after which mustard can cause skin, eye and respiratory symptoms. Staphylococcal enterotoxin B delivered by an aerosol attack can cause fever, cough, dyspnea and wheezing but does not involve the skin and eyes. Nausea, vomiting and diarrhea may follow swallowing of inhaled toxin. Ricin inhalation can cause severe respiratory distress, cough, nausea and arthralgias. Swallowed agent can cause vomiting, diarrhea and gastrointestinal bleeding, but it spares the skin, nose and eyes. Specific diagnosis of T-2 mycotoxins in the form of a rapid diagnostic test is not presently available in the field. Removal of blood and tissue from fatal cases and environmental samples for testing using a gas liquid chromatography-mass spectrometry technique will confirm the toxic exposure. This system can detect as little as 0.1 to 1.0 ppb of T-2. This degree of sensitivity is capable of measuring T-2 levels in the plasma of toxin victims.
Use of a chemical protective mask and clothing prior to and during a mycotoxin aerosol attack will prevent illness. If a soldier is unprotected during an attack the outer uniform should be removed within four hours and decontaminated by exposure to 5 percent hypochlorite for up to 10 hours. The skin should be thoroughly washed with soap and uncontaminated water if available. The M291 skin decontamination kit should also be used to remove skin adherent T-2. Superactivated charcoal can absorb swallowed T-2 and should be administered to victims of an unprotected aerosol attack. The eyes should be irrigated with normal saline or water to remove toxin. No specific antidote or therapeutic regimen is currently available. All therapy is supportive.
Physical protection of the skin and airway are the only proven effective methods of protection during an attack. Immunological (vaccines) and chemo-protective pretreatments are being studied in animal models, but are not available for field use by those in a war.