Clinical Features

In a bioterrorism attack with trichothecenes, the toxin(s) can adhere to and penetrate the skin, be inhaled, and can be ingested. In the alleged yellow rain incidents, symptoms of exposure from all 3 routes coexisted.

Contaminated clothing can serve as a reservoir for further toxin exposure. Early symptoms, beginning within minutes of exposure, include burning skin, redness, tenderness, blistering, and progression to skin necrosis with leathery blackening and sloughing of large areas of skin. Upper respiratory exposure may result in sneezing, nose bleed, shortness of breath, wheezing, and cough. Mouth and throat exposure causes pain and blood tinged saliva and sputum. Anorexia, nausea, vomiting and watery or bloody diarrhea with crampy abdominal pain occurs with gastrointestinal toxicity. Eye pain, tearing, redness, foreign body sensation and blurred vision may follow ocular exposure. Skin symptoms occur in minutes to hours and eye symptoms in minutes.

Systemic toxicity can occur via any route of exposure, and results in weakness, prostration, dizziness, and loss of coordination. Rapid heart rate, a drop in body temperature, and low blood pressure follow in fatal cases. Death may occur in minutes, hours or days. The most common symptoms are vomiting, diarrhea, burning skin, redness and severe itching, rash or blisters, bleeding, and shortness of breath.

Diagnosis

Clinical and epidemiological fi ndings provide clues to the diagnosis. Dead animals of multiple species, and physical evidence such as yellow, red, green, or other pigmented oily liquid are suggestive of mycotoxins.

Rapid onset of symptoms in minutes to hours supports a diagnosis of a chemical or toxin attack. Mustard and other blister agents must also be considered, but they have an odor, are visible, and can be rapidly detected. Symptoms from mustard toxicity are also delayed for several hours. Inhalation of staphylococcal enterotoxin B (SEB) or ricin aerosols can cause fever, cough, shortness of breath, and wheezing but does not affect the skin. Specifi c diagnosis of T-2 mycotoxins in the form of a rapid diagnostic test is not presently available in the fi eld. Serum and urine should be collected and sent to a reference lab for antigen detection.

The mycotoxins and metabolites are eliminated in the urine and feces; 50- 75% is eliminated within 24 hours, however, metabolites can be detected as late as 28 days after exposure. Pathologic specimens include blood, urine, lung, liver, and stomach contents.

Toxin Charateristics

The trichothecene mycotoxins are nonvolatile compounds produced by fi lamentous fungi (molds) of the genera Fusarium, Myrotecium, Trichoderma, Stachybotrys and others. There are approximately 150 trichothecene derivatives. 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 (sun light). They retain their bioactivity even when autoclaved; heating to 1500o F for 30 minutes is required for inactivation.

Decontamination can be achieved using a solution of hypochlorite (household bleach) combined with sodium chloride (salt) or caustic lime, with 1 hour contact time is required. Soap and water effectively remove this oily toxin from exposed skin or other surfaces.

Mechanism of Toxicity

The mycotoxins have multiple mechanisms of action, many of which are poorly understood. Their most notable effect stems from their ability to rapidly inhibit protein and nucleic acid synthesis. Mycotoxins are toxic to bone marrow, gastrointestinal tract and skin cells. Since this imitates the hematopoietic and lymphoid effects of radiation sickness, the mycotoxins are referred to as "radiomimetic agents." The mycotoxins also alter cell membrane structure and function.

Medical Management

No specific antidote or therapeutic regimen is currently available. All therapy is supportive. If a person is unprotected during an attack, the outer clothing should be removed and decontaminated by exposure to 5% hypochlorite (household bleach) for 6-10 hours.

The skin should be thoroughly washed with soap and uncontaminated water if available. This can reduce dermal toxicity, even if delayed 4-6 hours after exposure. Standard burn care is indicated for skin injuries. Standard therapy for poison ingestion, including the use of superactivated charcoal to absorb swallowed T-2, should be administered to casualties of an unprotected aerosol attack. Respiratory support may be necessary. The eyes should be irrigated with normal saline or water to remove toxin.

Preventative Measures

Physical protection of the skin, mucous membranes, and airway (use of chemical protective mask and clothing) are the only proven effective methods of protection during an attack. Washing with soap and water, up to 1 hour after dermal exposure to T-2, effectively prevents absorption through the skin.