"In Froim The Cold: CIA Secrecy and Operations"

[Ed Jewett]

I seem to remember that a mycotoxin that was used by the US in the first Gulf War?

Testing, testing, testing... anyone suffering horribly?

Right you are, chap.

Here's a smattering from among the top 12 or so in the Google search for "mycotoxins biowarfare".


TRICHOTHECENE MYCOTOXINS
INTRODUCTION |Top|
Trichothecene Mycotoxins are produced by fungi of the genera Fusarium, Myrotecium, Trichoderma, Stachybotrys and others. They inhibit protein synthesis, impair DNA synthesis, alter cell membrane structure and function, and inhibit mitochondrial respiration. The toxins, protein in nature, have a low molecular weight. They also contain food refusal and emetic factors. Trichothecene mycotoxins are highly persistent and stable for long periods of time.
0.5mg of the poison is enough to kill half the exposed humans. The skin of the victims can be irritated if the skin is exposed to the toxins. They can also cause radiomimetic injury of intestines, bone marrow, lymph nodes, spleen and thymus, leading to leukopenia and bone marrow atrophy. Effects are also found on central nervous, circulatory and reproductive systems.
After about 8 weeks from exposure to Normocyclic Trichothecenes, one will suffer from Alimentary Toxic Aleukia; burning sensation in the alimentary tract, vomiting, tachycardia, leukopenia, petechial hemorrhages with necrosis in skin and internal hemorrhages.
After about 8 weeks from exposure to Macrocyclic Trichothecenes, one will suffer from Stachybotryotoxicosis, conjunctivitis, rhinitis, leukopenia, dematis and pulmonary fibrosis.
PRECAUTIONS |Top|
An attack with Trichothecene Mycotoxins should be suspected if an aerosol attack happens in the form of yellow rain', with droplets of yellow fluid falling from the sky. Confirmation requires a blood test. Either that or someone is pissing on you.
Mycotoxins are not infectious or contagious so isolation is unnecessary. Improperly stored grain, especially under wet and cold conditions, may be badly infected by trichothecene-producing molds. Macrocyclic trichothecene mycotoxins may be liberated upon burning so contaminated clothing and hospital dressings should be steam sterilized and not burnt. Mixtures of macrocyclic trichothecenes are very potent and can cause death within 24 hours. Consumption of contaminated food and water should be avoided.
For protection, a gas mask and protective clothing is required. No vaccine has been developed yet. If exposed, wash contaminated skin with soap and water and irrigate eye with copius saline. Super-activated charcoal should be taken orally if the toxin was swallowed, to reduce absorption from the gut. Supportive therapy should also be provided when required to improve cardiovascular functions.
BIOLOGICAL WARFARE
AND TRICHOTHECENE MYCOTOXINS |Top|
Shortly after WWII, Russian military added species of Fusarium to flour and the flour was baked into bread and ingested by civilians. Some of them developed a lethal illness, Ailementary Toxic Aleukia, which is characterized by initial symptoms of abdominal pain, diarrhea, vomiting, prostration and with days, fever, chills, myalgias, and bone marrow depression with granulocytopenia and secondary sepsis. If the victim still lives, the victim will develop painful pharyngeal/laryngeal ulceration and diffuse bleeding into the skin, melena, bloody diarrhea, hematuria, hemalemesis, epistaxsis, and vaginal bleeding.
The United States and Britain had used Trichothecene Mycotoxins against Iraq in the 1991 war.
http://library.thinkquest.org/27393/tqtranslate.htm

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Trichothecenes are relatively easy to produce and aerosolize. They are very hearty compounds that can survive autoclaving, and they do not degrade when exposed to light. They can be ingested, inhaled, or absorbed through skin or mucous membranes. They can irritate or incapacitate at low doses and can kill in minutes at higher doses. As an aerosol, trichothecenes are roughly equipotent to mustard gases, although they are much more readily absorbed through the skin (5,11).

http://www.mold-survivor.com/when_biotox..._terr.html

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... it is the only potential biological weapon agent that can be absorbed through intact skin causing systemic toxicity.5 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.6 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.7 ... 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.10

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.11 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.12 Moreover, the same experts contend that yellow discoloration described on the foliage was merely the residue from fecal matter of honey bees.10

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.12 According to UNSCOM, Iraq researched trichothecene mycotoxins, including T-2 mycotoxin, and was capable of its possession.9 However, these matters remain unresolved, and much of the key information and data from these incidents remain classified.

For related information, see Medscape's Disaster Preparedness and Aftermath Resource Center.....


http://emedicine.medscape.com/article/830892-overview

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Mass casualties occurred in the Soviet Union in the 1930s and 1940s when Fusarium-contaminated wheat flour was baked into bread, causing alimentary toxic aleukia with a 60% mortality rate. Symptoms began with abdominal pain, diarrhea, vomiting, and prostration, and within days, fever, chills, myalgias and bone marrow depression with granulocytopenia and secondary sepsis occurred. Further symptoms included pharyngeal or laryngeal ulceration and diffuse bleeding into the skin (petechiae and ecchymoses), melena, bloody diarrhea, hematuria, hematemesis, epistaxis, vaginal bleeding, pancytopenia and gastrointestinal ulceration. Fusarium sporotrichoides contamination was found in affected grain in 1932, spurring research for medical purposes and for use in biological warfare. The active ingredient was found to be trichothecene T-2 mycotoxin, and it was produced in quantity and weaponized prior to the passage of the Biological Weapons Convention in 1972. The Soviets were accused of using the agent, dubbed "yellow rain", to cause 6,300 deaths in Laos, Kampuchea, and Afghanistan between 1975 and 1981.[4][5] The supposed biological warfare agent was later shown to be bee feces.[6][7]
Following an outbreak of Fusarium oxysporum that affected coca plantations in Peru, and other crops planted in the area, the United States has proposed the use of the agent as a mycoherbicide in drug eradication. In 2000, a proposal was passed to use the agent as part of Plan Colombia. In response to concerns use of the fungus could be perceived as biological warfare, the Clinton Administration "waived" this use of Fusarium. A subsequent law passed in 2006 has mandated the testing of mycoherbicide agents - either Fusarium oxysporum or Crivellia papaveracea - in field trials in U.S. territory.[8] Use of Fusarium oxysporum for these tests has raised concerns because resistant coca from the previous outbreak has been widely cultivated, and the fungus has been implicated in the birth of 31 anencephalic children in the Rio Grande region of Texas in 1991[citation needed], the loss of palm trees in Los Angeles, and eye infections from contact lens solutions.[9] The alternative Crivellia papaveracea is less well known; despite decades of study in the Soviet biowarfare lab in Tashkent, Uzbekistan, the relevant mycotoxins reportedly have not yet been isolated, named, or studied.[8]

http://en.wikipedia.org/wiki/Fusarium

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Tricothecene mycotoxins, Biological warfare - Toxins



Tricothecene mycotoxins are low-molecular-weight, non-volatile compounds produced by filamentous fungi (moulds) of the genera including Fusarium, Myrotecium, Trichoderma and Stachbotrys. The structures of almost 150 tricothecene derivatives have been identified.

Unlike most biological agents, tricothecence mycotoxins pose a threat not only to wounds and respiration but through access to the skin. The virus in non-contagious, but poses a threat as a military or terrorist agent if aerosolised or disseminated via contaminated foodstuffs. Toxins most likely to be weaponised include diacetoxyscirpenol (DAS), Nivalenol, 4-Deoxynivalenol (DON) and T-2. As the most stable, T-2 is the most likely to be utilised as a chemical threat.
The complete article appears in the following publication: Publication Title Jane's Nuclear, Biological and Chemical Defence Publication date Jan 21, 2010 Section Biological warfare - Toxins Publication synopsis Jane's Nuclear, Biological and Chemical Defence offers both expert analysis of the NBC threat and comprehensive details on the manufacturers and their products involved in meeting that threat. It is ideal for providing guidance for threat assessment and for the procurement of defensive equipment identified as a requirement. Equipment entries include detailed descriptions, including specifications, together with availability status, manufacturer details and pictures or diagrams to enable comparison and appraisal. Key Contents relating to the threat include: Know your enemy: A global, country-by-country review of NBC capabilities Know their arsenal: NBC agents and their effects Know your own response options: Technical developments in the NBC field The depth and breadth of information covers

• Manufacturers and products associated with detection, including sensor systems, C3I and reconnaissance systems
  
• Individual and collective protection
  
• Decontamination
  
• Demilitarisation
  
• Training and simulation
  
• A comprehensive list of contractors
  

Different sections provide in-depth detail covering

• Analysis
  
• Biological Warfare
  
• Biological Warfare - Bacteria
  
• Biological Warfare - Fungi
  
• Biological Warfare - Rickettsiae
  
• Biological Warfare - Toxins
  
• Biological Warfare - Viruses
  
• Chemical Warfare
  
• Chemical Warfare - Blister Agents Vesicants
  
• Chemical Warfare - Blood Agents
  
• Chemical Warfare - Choking Agents
  
• Chemical Warfare - Incapacitating Agents
  
• Chemical Warfare - Nerve Agents
  
• Chemical Warfare - Precursors
  
• Chemical Warfare - Tear Agents
  
• Chemical Warfare - Vomiting Agents
  
• Contractors
  
• Decontamination
  
• Demilitarisation
  
• Detection (C3i Systems)
  
• Detection (Reconnaissance Systems)
  
• Detection (Sensor Systems) - Biological
  
• Detection (Sensor Systems) - Chemical
  
• Detection (Sensor Systems) - Nuclear
  
• Glossary
  
• Nbc Capabilities
  
• Nuclear Weapons And Their Effects
  
• Protection (Collective)
  
• Protection (Individual) - Body Protection
  
• Protection (Individual) - Filters
  
• Protection (Individual) - Masks (Aircrew)
  
• Protection (Individual) - Masks (General Issue)
  
• Protection (Individual) - Medical Countermeasures
  
• Radiological Weapons And Their Effects
  
• Technical Developments
  
• Training And Simulation
  

You may purchase a full subscription to this service through the Jane's Online Catalogue.


http://www.janes.com/articles/Janes-Nucl...oxins.html

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BIOLOGICAL WARFARE AND ITS CUTANEOUS MANIFESTATIONS
Thomas W. McGovern, MD, MAJ, MC
George W. Christopher, LTC, USAF, MC


Clinical Features
Human intoxication is rare. An entity known as alimentary toxic aleukia, reported in Russia since the 19th century, is thought to result from ingestion of mycotoxins while eating foods prepared from moldy grain. Signs and symptoms include vomiting, diarrhea, skin inflammation,' leukopenia, hemorrhage, and sepsis.[8,52]
More recently, and closer to home, trichothecene mycotoxins are thought to have caused fatal pulmonary hemorrhage in Cleveland area infants. In one area of Cleveland, it may have accounted for 5% of cases of sudden infant death syndrome between 1993-95. In all cases, the fungus Stachybotrys atra was found growing in water-saturated cellulose in the walls of poorly maintained homes.[7,29,31]

Cutaneous Manifestations
At low doses (nanograms), severe skin irritation with erythema, edema, and necrosis is observed. Vesication often occurred with Yellow Rain' attacks; T-2 (one of the trichothecenes) mycotoxin is estimated to be 400 times more potent than alkylating agents (mustards) in producing skin injury.[99]
Figure 14: Vesicles and erosions on the back of hairless guinea pigs at 1,2,7 and 14 days after application of ( bottom to top) 25, 50, 100 or 200 ng of T-2 mycotoxin in 2ul of methanol. (Reprinted from McGovern TW, Friedlander AM. Plague. In: Sidell FR, Takafuji ET, Franz DR, eds. Medical Aspects of Chemical and Biological Warfare. Chapter 23 In: Zajtchuk R, Bellamy RF, eds. Textbook of Military Medicine. Washington, DC: US Department of the Army, Office of the Surgeon General, and Borden Institute; 1997:493.
T-2 mycotoxins can be absorbed through the skin and cause death with an LD50 of 2-12 mg/kg compared to that for mustards (4500 mg/kg) and lewisite (37 mg/kg).[100,101] In Southeast Asia, the skin was thought to be the major site of deposition of aerosol spray or coarse mists.[8]

BW considerations
Epidemiologic, intelligence, and trichothecene assay evidence suggest that trichothecene mycotoxins were used in Southeast Asia between 1974 and 1981.[8,91] Nearly 400 alleged attacks reportedly resulted in approximately 10,000 deaths. In Laos, the attacks were described as yellow rain,' a sticky yellow liquid that fell and sounded like rain or looked like a yellow cloud of dust, powder, mist, smoke, or insect spray. The liquid dried rapidly to form a powder. Most attacks used yellow pigment, but some attacks used red, green, white, or brown smoke or vapor. More than 80% of attacks were by air to surface rockets.[98]
Microgram exposure caused eye irritation, corneal damage, and impaired vision. At 0.1-0.2 LD50, emesis and diarrhea occurred. Aerosols caused death within minutes to hours by destroying alveoli. The toxins affect rapidly proliferating tissues and are cytotoxic to most eukaryotic cells by inhibiting protein and RNA synthesis. After entering the circulation, regardless of portal of entry, they affect all rapidly proliferating tissues.
A protective mask and full-body clothing should be donned at the first sign of a yellow rain' attack. Afterwards, battle dress uniforms (BDUs) and contaminated areas of skin should be washed with soap and water followed by a water rinse. Washing within 4-6 hours of exposure removes 80-98% of the toxin and prevented death and dermal lesions in experimental animals. No known specific therapy exists, although high doses of systemic steroids decreases primary and secondary toxin injury.[8]


http://www.telemedicine.org/biowar/biologic.htm



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U.S. Army Biowarfare Research and How it Impacts Mold Illness

http://www.esgtesting.com/Portal/Documen...arfare.pdf

A One-Page pdf





Each of the links has far more than was excerpted.