AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Overview
 
Trichothecene mycotoxins are low molecular weight (250-500 Daltons) nonvolatile compounds produced by more than 350 species of fungi. While the toxin confers survival advantage to the fungi, it is pathogenic to animals and humans. All trichothecenes share a common 12,13-epoxytrichothene skeleton and are subdivided into 4 chemical groups (A, B, C, D). T-2 mycotoxin is the most extensively studied of the trichothecenes, and, according to current declassified literature, it is the only mycotoxin known to have been used as a biological weapon. 
 
Unlike most biological toxins that do not affect the skin, T-2 mycotoxin is a potent active dermal irritant. Moreover, it is the only potential biological weapon agent that can be absorbed through intact skin causing systemic toxicity. Clinical symptoms may be present within seconds of exposure. While larger amounts of T-2 toxin is required for a lethal dose than for other chemical warfare agents such as VX, soman, or sarin, its potent effect as a blistering agent is well noted. T-2 mycotoxins can be delivered via food or water sources, as well as, via droplets, aerosols, or smoke from various dispersal systems and exploding munitions. These properties make T-2 mycotoxin a potentially viable biological warfare agent. The reported LD 50 of T-2 toxin is approximately 1 mg/kg.
 
Trichothecene mycotoxins are extremely stable proteins that are resistant to heat and ultraviolet light inactivation. These substances are relatively insoluble in water but highly soluble in ethanol, methanol, and propylene glycol. Heating to 500ºF for 30 minutes can inactivate the toxin, and exposure to sodium hypochlorite can destroy the toxic activity of the toxin. 
 
Historical significance
 
In 1931, several Ukrainian veterinarians reported a unique disease in horses that was characterized by lip edema, stomatitis, oral necrosis, rhinitis, and conjunctivitis. This clinical effect progressed through well-defined stages including pancytopenia, coagulopathy, neurologic compromise, superinfections, and death. On autopsy, the afflicted animals were found to have diffuse hemorrhage and necrosis of the entire alimentary tract giving rise to the name alimentary toxic aleukia (ATA). 

The potential use for T-2 mycotoxin as a biological weapon was later realized in Orenburg, Russia, during World War II when civilians consumed wheat that was unintentionally contaminated with the Fusarium fungi. The victims developed protracted lethal illness with a disease pattern similar to ATA. In 1940, Soviet scientists coined the term stachybotryotoxicosis to describe the acute syndrome (sore throat, bloody nasal discharge, dyspnea, cough, and fever) resulting from the inhalation of Stachybotrys mycotoxin. Twenty years later, the trichothecene mycotoxin was discovered, and the T-2 toxin was isolated.
 
The allegations surrounding the use of T-2 mycotoxin as a biological warfare agent remains a controversy to this day. Based on extensive eyewitness and victim accounts, the aerosolized form of T-2 mycotoxin called "yellow rain" was delivered by low-flying aircraft that dropped the yellow oily liquid on the victims. T-2 mycotoxin has been allegedly used during the military conflicts in Laos (1975-81), Kampuchea (1979-81), and Afghanistan (1979-81) to produce lethal and nonlethal casualties. More than 6300 deaths in Laos, 1000 in Kampuchea, and 3000 in Afghanistan have been attributed to yellow rain exposure. Although several United States chemical weapons experts have matched samples from the Laos conflict to trichothecene signature, these charges have been disputed by other weapons experts who contend T-2 mycotoxins may have occurred naturally in Laos and that exposure was due to the ingestion of contaminated foods. Moreover, the same experts contend that yellow discoloration described on the foliage was merely the residue from fecal matter of honey bees.

Victim reports from the 1991 Desert Storm campaign have also alleged the possibility of a T-2 mycotoxin exposure from a detonated Iraqi missile over a US military camp in Saudi Arabia. According to UNSCOM, Iraq researched trichothecene mycotoxins, including T-2 mycotoxin, and was capable of its possession. However, these matters remain unresolved, and much of the key information and data from these incidents remain classified.  

Pathophysiology

Trichothecene mycotoxins are markedly cytotoxic and potentially immunosuppressive. They are potent fast-acting inhibitors of protein and nucleic acid synthesis. T-2 toxin is thought to bind and inactivate the peptidyl-transferase activity at the transcription site. This results in the inhibition of protein synthesis, the effect of which is most pronounced in actively proliferating cells such as those found in the skin, gastrointestinal tract, and bone marrow. Additionally, T-2 toxin is thought to disrupt DNA polymerases, terminal deoxynucleotidyl transferase, monoamine oxidase, and several proteins involved in the coagulation pathway.  

Routes of exposure
 
The trichothecene mycotoxins are well absorbed by topical, oral, and inhalational routes. As a dermal irritant and blistering agent, it is thought to be 400 times more potent than sulfur mustard. As an inhalational agent, its activity is considered comparable to that of mustard or lewisite. Mycotoxin is unique in that the systemic toxicity can result from any route of exposure (dermal, oral, or inhalational). 

Frequency

United States

Trichothecene mycotoxin exposures in the United States have largely been due to accidental ingestion of contaminated foodstuff. In 1993, however, an unusually high number of fatal pulmonary hemorrhages in infants originating from a small region of Ohio raised suspicion that the cause may have been due to trichothecene mycotoxin exposure in the homes secondary to mold overgrowth. Moreover, several cases of sudden infant death syndrome (SIDS) were thought to be related to Stachybotrys mycotoxin exposure in the homes secondary to mold overgrowth resulting from a flood. No well-documented epidemiologic information is available for exposure to T-2 mycotoxin as a result of bioweapon deployment other than the alleged uses in the previously mentioned military conflicts.

International

Several cases of "sick building syndrome" have been reported in Montreal, Canada. Dust samples collected and analyzed from the ventilation systems of suspected office buildings revealed trace amounts of at least 4 trichothecenes including T2 toxin. This was dismissed as mold overgrowth in the ventilation system.

Mortality/Morbidity

No human mortality or morbidity data are reported for T-2 mycotoxin use as a bioweapon. Information regarding mortality from ingestion of contaminated food is quite varied, with 10-60% mortality rate reported in Russia's Orenburg district. Mortality figures from the Kampuchea and Afghanistan uses of mycotoxin as a bioweapon do not report mortality rates, only total number of deaths. Not knowing the number of exposed individuals as related to the number of fatalities makes the calculation of mortality rates impossible.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

• Patients with cutaneous symptoms may report seeing clouds of a yellow-colored smoke or aerosol, but blue and green aerosols have also been reported.
• Patients may report yellow droplets on clothing.
• Immediate skin pain and burning on exposed surfaces is described. Eye pain and burning also should be reported.
• Suspicion of the toxin being placed in an ingested food source may exist. Ingested toxin probably has no taste, since no documentation supports a foul odor or taste in previous epidemics of toxin ingestion. This is further supported by the historical experience that many individuals become ill when exposed to contaminated food without any suspicion of having ingested tainted food.
• The most common symptoms occurring with most exposures include skin (or oral) pain (burning) and redness or rash, vomiting, diarrhea, dyspnea, and bleeding.

Physical

The early signs and symptoms of T-2 toxin poisoning does reflect the route of exposure. However, irrespective to the route of entry, the systemic toxicity follows a protracted course of illness that is well characterized. Early symptoms can manifest within seconds of exposure depending on the dose of exposure. Symptoms become prominent after minutes to hours upon exposure. They are described by the respective organ system.  

• Neurologic: No specific neurologic signs or symptoms are related to the toxin except for mild ataxia, which reflects systemic toxicity.
• Head, eyes, ears, nose, throat (HEENT)
• • Ocular exposure causes tearing, pain, conjunctivitis, and blurred vision.
  • Nasal mucosa results in sinus irritation, pain, rhinorrhea, sneezing, and potentially epistaxis.
  • Oral and oropharyngeal exposure results in pain and blood-tinged saliva and sputum.
• Respiratory
• • Cough, dyspnea and wheezing
  • Delayed signs can include hemoptysis. 
• Cardiovascular
• • Tachycardia
  • Vascular collapse in severe toxin exposure
• Gastrointestinal
• • Nausea and vomiting
  • Anorexia
  • Watery diarrhea with abdominal cramping
• Dermal
• • Painful erythema and tenderness
  • Blistering and bullous lesions, leading to desquamation
  • Necrosis and sloughing of dermal layer
• Systemic
• • Severe toxin exposure can result in early systemic toxicity. 
  • Severe dizziness, ataxia, and prostration
  • Tachycardia
  • Hypothermia
  • Vascular collapse
• Hematologic
• • Upon chronic exposure to T-2 toxin, the clinical syndrome of alimentary toxic aleukia (ATA) ensues. This presentation mirrors the stages of radiation sickness. The 4 stages are as follows:
  • • Stage 1: This stage may be seen in the emergency department. This stage results from the acute injury to the exposed cells and tissue. The symptoms reflect the route of toxin exposure.
    • Stage 2: This stage occurs weeks after the exposure. Insult to the bone marrow initially produces a transient lymphocytosis. This is soon followed by bone marrow suppression due to the antimitotic effects of T-2 toxin. The result is significant leukopenia, granulocytopenia, and thrombocytopenia.
    • Stage 3: This stage also occurs weeks after the exposure and is considered the hemorrhagic stage. The patient exhibits petechial hemorrhages, especially of the mucosal areas of the nasopharynx and oropharynx. These lesions develop to form ulcerated and necrotic lesions, which can result in significant bleeding from the esophagus and the gastrointestinal tract. Moreover, the edema that accompanies the mucosal injury may threaten the airway. Also, severe coagulopathy may occur. During this stage, the patient is at a higher risk for sepsis because the immune system is significantly compromised.  
    • Stage 4: During the recovery phase, the necrotic lesions heal and the bone marrow recovers.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Vesicant (mustard and lewisite) exposure

Onset of pain may mimic T-2 mycotoxin exposure.

To differentiate lewisite from T-2 mycotoxin exposure, test the skin and clothing for the arsenic component of lewisite.

Onset of dermal symptoms (blistering, pain) from mustard exposure typically is delayed.

Staphylococcal enterotoxin B

Staphylococcal enterotoxin B may cause respiratory and GI symptoms, but  the burning dermal and mucocutaneous symptoms are absent.

Ricin intoxication

All symptoms for ricin intoxication are similar to T-2 mycotoxin with the exception of the painful dermal symptoms, which are not observed in ricin intoxication.

Other considerations

Symptoms of T-2 mycotoxin exposure are radiomimetic; thus, one must consider radiation sickness in the differential diagnosis. Nausea and vomiting have a large differential diagnosis. Examine patients with these symptoms without any suggestion of toxin exposure for other more common etiologies. The patient who may be more suggestive of a toxin exposure is a high-profile individual (ie, government official) who is vomiting with oral or cutaneous symptoms.

Patients presenting long after the initial exposure who now may be manifesting symptoms of the second stage of ATA may need to be investigated for a malignant process causing bone marrow replacement. Skin and mucosal erythema, blistering, ulceration, and necrosis can be the manifestation of many systemic diseases, which need to be considered.

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

With growing health concerns related to mold exposures and its related morbidity and mortality, devices have been developed to detect environmental mycotoxin exposure. To date, no data exist to differentiate the expected background levels of these substances from potential toxic and/or intentional contamination.  

T-2 toxin is rapidly metabolized to HT-2, T2-triol, and T-2 tetraol within hours after exposure. While these toxin metabolites may be detected in body fluids, tissue, and stomach contents for up to 28 days following exposure, these results are unlikely to be available to help the medical provider manage the patient. Newer urine assays detect T-2 metabolite for up to one week after exposure. Definitive diagnosis must be made in a reference laboratory using thin-layer or gas-liquid chromatography, mass or nuclear magnetic resonance spectrometry, radioimmunoassay, and enzyme-linked immunosorbent assay (ELISA) techniques.

• Perform immediate postexposure laboratory studies to assess for other disease conditions in the differential diagnosis.
• When considering T-2 mycotoxin exposure as the cause of the illness, collect nasal, throat, or respiratory secretions and send for mass spectrometric evaluation. 
• Collect serum, urine, and/or tissue samples for toxin detection from patients who are in the postexposure phase. ELISA screening tests and antibody assays that screen for mycotoxin exposure are available.
• Observing the absolute lymphocyte count over time may differentiate those individuals destined to develop bone marrow suppression.
• Coagulation panel may help identify patients who are at risk for developing severe coagulopathy.

Imaging Studies

• No specific imaging tests help diagnose T-2 toxin exposure. 

Procedures

• Warning: This is a potent dermally active toxin that is transmissible if not properly decontaminated. Do not approach the patient without observing universal precaution.  
• Decontamination procedure is as follows:
• • Remove all of the patient's clothing, and clean and scrub the entire skin surface with soap and water. Washing the contaminated area of the skin within 6 hours postexposure can remove 80-98% of the toxin and has been demonstrated to prevent skin lesions and death in experimental animals.
  • Contain clothing to avoid contamination of the health care environment.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Prehospital Care

• Warning: Mycotoxin is a potent dermally active toxin that is transmissible in the health care setting. Do not approach the patient without observing universal precaution.
• Use hazardous materials teams in patient rescue and decontamination.
• Decontamination is of paramount importance to avoid cross-contamination. Remove all clothing, and wash the patient in soap and water.
• For patients in extremis, attention to airway, breathing, and circulation per Advanced Trauma Life Support (ATLS) protocol needs to occur immediately as decontamination is being performed.  
• • While one team member is caring for issues involving the airway, breathing, and circulation, another member should be concerned primarily with patient decontamination.
  • Remove all clothing, and clean and scrub the patient's entire skin surface with soap and water. Washing the contaminated area of the skin within 6 hours postexposure can remove 80-98% of the toxin and has been demonstrated to prevent skin lesions and death in experimental animals.
  • Contain clothing to avoid contamination of the health care environment.
• Provide supportive measures addressing cardiovascular status as necessary.
• If the patient complains of eye pain or tearing, irrigate the eyes with copious amounts of water.
• No specific antidote exists for this toxin. General supportive measures are indicated.

Emergency Department Care

• Warning: Mycotoxin is a potent dermally active toxin that is transmissible in the health care setting. Do not approach the patient without observing universal precaution.
• Never assume that a patient has been decontaminated in the prehospital setting. Reassess the patient's decontamination status. If the degree of prehospital decontamination is uncertain, rewash the patient to ensure the safety of staff and facility. 
• For patients in extremis, attention to airway, breathing, and circulation per ATLS protocol needs to occur immediately as decontamination is being performed.  
• • While one team member is caring for issues involving the airway, breathing, and circulation, another member should be concerned primarily with patient decontamination.
  • Remove all clothing, and clean and scrub the patient's entire skin surface with soap and water. Washing the contaminated area of the skin within 6 hours postexposure can remove 80-98% of the toxin and has been demonstrated to prevent skin lesions and death in experimental animals.
  • Contain clothing to avoid contamination of the health care environment.
• While no human studies have been conducted, survival benefits have been shown in animal models with the following treatment after T-2 toxin exposure.
• • Use of activated charcoal to absorb T2 toxin from the gut regardless of the portal of entry within 1 hour of exposure.
  • Dexamethasone administration (1 mg/kg at 12, 24, and 48 h) increased the survival rate in mice from zero to greater than 50%.  
• No specific antidote is available for T-2 mycotoxin exposure. Provide supportive measures, addressing respiratory and cardiovascular status as necessary.
• If the patient complains of eye pain or tearing, irrigate the eyes with copious amounts of water.

Consultations

• Required consultants are dictated by the disease course. Pulmonary consultation may be required for severe dyspnea of hemoptysis. A hematologist may be consulted for patients presenting with severe pancytopenia.
• Contact the local poison control center for additional clinical guidance. Some larger cities' poison control centers may have specific guidelines to follow concerning weapons of mass destruction.
• Consult the Federal Bureau of Investigation and Department of Homeland Security in any situation when nuclear, biological, or chemical weapon exposure is suspected.
• • Federal Bureau of Investigations
  • Department of Homeland Security

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The use of activated charcoal is advocated to patients who have orally ingested the toxin. Some sources advocate the use of activated charcoal even after inhalational exposure with the rationale being that the toxin that is adherent to the oral mucosa may be bound. While not clinically tested in human, theoretical use exists for administering colony-stimulating factors to patients presenting with bone marrow suppression.

Drug Category: Antidotes, adsorbent

These agents are used to neutralize toxins.

Drug Category: Granulocyte-stimulating factors

These agents are used to correct severe neutropenia.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

• In all suspected cases involving T-2 mycotoxin exposure, admission to the hospital is warranted. Supportive care should be instituted with particular attention to the prevention of superinfection. Depending on the time of exposure and the presenting symptoms, serial lymphocyte count may help identify patients who are immunocompromised.

In/Out Patient Meds

• Although not proven clinically, a theoretical use exists for administering colony-stimulating factors to patients presenting with bone marrow suppression.

Complications

• Airway compromise may be observed when the disease process includes significant airway edema or hemorrhage.

Prognosis

• Prognosis of mycotoxin exposure is difficult to assess, since the amount of toxin in previous human ingestions has not been documented. Death from actual toxin ingestion is much less of a concern than the sequelae of immune compromise and successive infection. This is supported by the documented history of the ingestion version of the disease (ATA). No current literature predicts the outcome of T-2 mycotoxin poisoning.

Patient Education

• For excellent patient education resources, visit eMedicine's Bioterrorism and Warfare Center. Also, see eMedicine's patient education articles Biological Warfare and Personal Protective Equipment.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Currently, discussion regarding the medicolegal issues involving physician reporting of biological, radiological, or chemical exposures to law enforcement agencies is ongoing. No legal guidance is available regarding this issue. Legal team consultation may be recommended prior to an actual incident.

Special Concerns

• If it is believed that a patient may have been exposed to any type of nuclear, biological, or chemical weapon of mass destruction, notify the local office of federal law enforcement authorities (eg, Federal Bureau of Investigation) immediately.
• • Federal Bureau of Investigations
  • Department of Homeland Security

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Donald A Locasto, MD, and Michael P Allswede, DO, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Chemical Terrorism Agents and Syndromes. Signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/chemical.html.
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REFERENCES

Section 12 of 12

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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Article Last Updated: Aug 19, 2008