CBRNE - T-2 Mycotoxins Clinical Presentation
- Author: Chan W Park, MD; Chief Editor: Robert G Darling, MD, FACEP more...
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.[12]
- 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.[3]
- 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.[18]
- The most common symptoms occurring with most exposures include skin (or oral) pain (burning) and redness or rash, vomiting, diarrhea, dyspnea, and bleeding.[2]
Physical
The early signs and symptoms of T-2 toxin poisoning do 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.[2] 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.
Joffee A. Fusarium Species: Their Biology and Toxicology. NY: John Wiley & Sons; 1986:225-292.
Darling, Woods, et al. USAMRIID's Medical Management of Biological Casualties Handbook. 5th. Fort Detrick, Frederick, MD: USAMRIID; 2004. [Full Text].
McGovern TW, Christopher GW. Biological warfare and its cutaneous manifestations. The Electronic Textbook of Dermatology [serial online]. 1995-2001;Available from: The Internet Dermatology Society, Inc. Accessed 2010. Available at http://www.telemedicine.org/biowar/biologic.htm.
Ueno Y. Trichothecene mycotoxins: Mycology, chemistry, and toxicology. Advances in food and nutrition research. 1989;3:301-353.
Franz DR, Jahrling PB, Friedlander AM, McClain DJ, Hoover DL, Bryne WR, et al. Clinical recognition and management of patients exposed to biological warfare agents. JAMA. Aug 6 1997;278(5):399-411. [Medline].
Marrs TC, Edginton JA, Price PN, Upshall DG. Acute toxicity of T2 mycotoxin to the guinea-pig by inhalation and subcutaneous routes. Br J Exp Pathol. Apr 1986;67(2):259-68. [Medline].
Wannemacher RW Jr, Wiener SL. Trichothecene mycotoxins. In: Sidell FR, Takafuji ET, Franz DR. Medical Aspects of Chemical and Biological Warfare. Falls Church, Va: Office of the Surgeon General, US Dept of the Army; 1997:655-676.
Blazes DL, Lawler JV, Lazarus AA. When biotoxins are tools of terror. Early recognition of intentional poisoning can attenuate effects. Postgrad Med. Aug 2002;112(2):89-92, 95-6, 98. [Medline].
Zilinskas RA. Iraq's biological weapons. The past as future?. JAMA. Aug 6 1997;278(5):418-24. [Medline].
Holstege CP, Bechtel LK, Reilly TH, Wispelwey BP, Dobmeier SG. Unusual but potential agents of terrorists. Emerg Med Clin North Am. May 2007;25(2):549-66; abstract xi. [Medline].
Haig AM. Chemical Warfare in Southeast Asia and Afghanistan: Report to the Congress From Secretary of State Alexander M. Haig. Special Report No. 98. Washington, DC: US Department of State; March 22, 1982.
Schieffer HB. Facts, not Rhetoric, on Yellow Rain. Nature. July 1983;304:10.
Henghold WB 2nd. Other biologic toxin bioweapons: ricin, staphylococcal enterotoxin B, and trichothecene mycotoxins. Dermatol Clin. Jul 2004;22(3):257-62, v. [Medline].
Johnsen H, Odden E, Johnsen BA, Bøyum A, Amundsen E. Cytotoxicity and effects of T2-toxin on plasma proteins involved in coagulation, fibrinolysis and kallikrein-kinin system. Arch Toxicol. Jan 1988;61(3):237-40. [Medline].
Dearborn DG, Smith PG, Brooks LJ, Carroll-Pankhurst C, Kosick R, Dahms BB. Update: pulmonary hemorrhage/hemosiderosis among infants-Cleveland, Ohio 1993-1996. MMWR Morbidity Mortality Weekly Report. 1997;46:33-35.
Richards CA. Stachybotrys atra suspected in three infant deaths: 18 others sickened. Journal of Pediatric Infectious Disease. 1997;10:1-8.
Pestka JJ, Yike I, Dearborn DG, Ward MD, Harkema JR. Stachybotrys chartarum, trichothecene mycotoxins, and damp building-related illness: new insights into a public health enigma. Toxicol Sci. Jul 2008;104(1):4-26. [Medline].
Schoenthal. Mycotoxins in food and the plague of Athens. Journal of Nutritional Medicine. 1994;4:83-85.
Dohnal V, Jezkova A, Jun D, Kuca K. Metabolic pathways of T-2 toxin. Curr Drug Metab. Jan 2008;9(1):77-82. [Medline].
Zapor M, Fishbain JT. Aerosolized biologic toxins as agents of warfare and terrorism. Respir Care Clin N Am. Mar 2004;10(1):111-22. [Medline].
Wannemacher RW. Dermal toxicity of T-2 toxin in guinea pigs, rats and cynomolgus monkeys. Tricothecenes and Other Mycotoxins. 1985;423-432.
Fricke RF, Jorge J. Assessment of efficacy of activated charcoal for treatment of acute T-2 toxin poisoning. J Toxicol Clin Toxicol. 1990;28(4):421-31. [Medline].
Shohami E, Wisotsky B, Kempski O, Feuerstein G. Therapeutic effect of dexamethasone in T-2 toxicosis. Pharm Res. Dec 1987;4(6):527-30. [Medline].
Poppenga RH, Lundeen GR, Beasley VR, Buck WB. Assessment of a general therapeutic protocol for the treatment of acute T-2 toxicosis in swine. Vet Hum Toxicol. Jun 1987;29(3):237-9. [Medline].
Tucker JB. Mycotoxins and Gulf War Illness: A Possible Link [The National Gulf War Resource Center Web site]. The National Gulf War Resource Center. Available at http://www.ngwrc.org/. Accessed 2001.

