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Includes "Yellow Rain"

This discussion is one of the  best I have found with regard to toxins and bio-toxins.  It also shows how easy it would be for terrorists inside the USA to make some toxins from scratch.


Toxins are defined as any toxic substance of natural origin produced by an animal, plant, or microbe. They are different from chemical agents such as VX, cyanide, or mustard in that they are not man-made. They are non-volatile, are usually not dermally active (mycotoxins are an exception), and tend to be more toxic per weight than many chemical agents. Their lack of volatility also distinguishes them from many of the chemical threat agents, and is very important in that they would not be either a persistent battlefield threat or be likely to produce secondary or person to person exposures.

Many of the toxins, such as low molecular weight toxins and some peptides, are quite stable, where as the stability of the larger protein bacterial toxins is more variable. The bacterial toxins, such as botulinum toxins or shiga toxin, tend to be the most toxic in terms of dose required for lethality (see Table 1, Appendix A), whereas the mycotoxins tend to be among the least toxic compounds, thousands of times less toxic than the botulinum toxins. Some toxins are more toxic by the aerosol route than when delivered orally or parenterally (ricin, saxitoxin, and T2 mycotoxins are examples), whereas botulinum toxins have lower toxicity when delivered by the aerosol route than when ingested. Botulinum is so toxic inherently, however, that this characteristic does not limit its potential as a biological warfare agent.

The utility of many toxins as military weapons is potentially limited by their inherent low toxicity (too much toxin would be required), or by the fact that some which are very toxic, such as saxitoxin, can only feasibly be produced in minute quantities. The relationship between aerosol toxicity and the quantity of toxin required to provide an effective open-air exposure is shown in Figure 1, Appendix A. The lower the lethal dose for fifty percent of those exposed (LD50), in micrograms per kilogram, the less agent would be required to cover a large battlefield sized area. The converse is also true, and means that for some agents such as ricin, very large quantities (tons) would be needed for an effective open-air attack.

Where toxins are concerned, incapacitation as well as lethality must be considered. Several toxins cause significant illness at levels much lower than the level required for lethality, and are thus militarily significant in their ability to incapacitate soldiers.

This manual will cover four toxins considered to be among the most likely toxins which could be used against U.S. forces: botulinum toxins, staphylococcal enterotoxin B (SEB), ricin, and T-2 mycotoxins.




Signs and Symptoms: Ptosis, generalized weakness, dizziness, dry mouth and throat, blurred vision and diplopia, dysarthria, dysphonia, and dysphagia followed by symmetrical descending flaccid paralysis and development of respiratory failure. Symptoms begin as early as 24-36 hours but may take several days after inhalation of toxin.

Diagnosis: Clinical diagnosis. No routine laboratory findings. Biowarfare attack should be suspected if numerous collocated casualties have progressive descending bulbar, muscular, and respiratory weakness.

Treatment: Intubation and ventilatory assistance for respiratory failure. Tracheostomy may be required. Administration of botulinum antitoxin (IND product) may prevent or decrease progression to respiratory failure and hasten recovery.

Prophylaxis: Pentavalent toxoid vaccine (types A, B, C, D, and E) is available as an IND product for those at high risk of exposure.

Decontamination: Hypochlorite (0.5% for 10-15 minutes) and/or soap and water. Toxin is not dermally active and secondary aerosols are not a hazard from patients.


The botulinum toxins are a group of seven related neurotoxins produced by the bacillus Clostridium botulinum. These toxins, types A through G, could be delivered by aerosol over concentrations of troops. When inhaled, these toxins produce a clinical picture very similar to foodborne intoxication, although the time to onset of paralytic symptoms may actually be longer than for foodborne cases, and may vary by type and dose of toxin. The clinical syndrome produced by one or more of these toxins is known as "botulism".


Botulinum toxins have caused numerous cases of botulism when ingested in improperly prepared or canned foods.  Many deaths have occurred secondary to such incidents. It is feasible to deliver botulinum toxins as a biological weapon, and other countries have weaponized or are suspected to have weaponized one or more of this group of toxins. Iraq admitted to a United Nations inspection team in August of 1991 that it had done research on the offensive use of botulinum toxins prior to the Persian Gulf War, which occurred in January and February of that year. Further information given in 1995 revealed that Iraq had not only researched, but had filled and deployed over 100 munitions with botulinum toxin.


Botulinum toxins are proteins of approximately 150,000 kD molecular weight which can be produced from the anaerobic bacterium Clostridium botulinum. As noted above, there are seven distinct but related neurotoxins, A through G, produced by different strains of the clostridial bacillus. All seven types act by a similar mechanism. The toxins produce similar effects when inhaled or ingested, although the time course may vary depending on the route of exposure and the dose received. Although an aerosol attack is by far the most likely scenario for the use of botulinum toxins, theoretically the agent could be used to sabotage food supplies; enemy special forces or terrorists might use this method in certain scenarios to produce foodborne botulism in those so targeted.


The botulinum toxins as a group are among the most toxic compounds known to man. Table 1 in Appendix A shows the comparative lethality of selected toxins and chemical agents in laboratory mice. Botulinum toxin is the most toxic compound per weight of agent, requiring only 0.001 microgram per kilogram of body weight to kill 50 percent of the animals studied. As a group, bacterial toxins such as botulinum tend to be the most lethal of all toxins. Note that botulinum toxin is 15,000 times more toxic than VX and 100,000 times more toxic than Sarin, two of the well known organophosphate nerve agents.

Botulinum toxins act by binding to the presynaptic nerve terminal at the neuromuscular junction and at cholinergic autonomic sites. These toxins then act to prevent the release of acetylcholine presynaptically, and thus block neurotransmission. This interruption of neurotransmission causes both bulbar palsies and the skeletal muscle weakness seen in clinical botulism.

Unlike the situation with nerve agent intoxication, where there is in effect too much acetylcholine due to inhibition of acetylcholinesterase, the problem in botulism is lack of the neurotransmitter in the synapse. Thus, pharmacologic measures such as atropine are not helpful in botulism and could even exacerbate symptoms.


The onset of symptoms of inhalation botulism may vary from 24 to 36 hours, to several days following exposure. Recent primate studies indicate that the signs and symptoms may in fact not appear for several days when a low dose of the toxin is inhaled versus a shorter time period following ingestion of toxin or inhalation of higher doses. Bulbar palsies are prominent early, with eye symptoms such as blurred vision due to mydriasis, diplopia, ptosis, and photophobia, in addition to other bulbar signs such as dysarthria, dysphonia, and dysphagia. Skeletal muscle paralysis follows, with a symmetrical, descending, and progressive weakness which may culminate abruptly in respiratory failure. Progression from onset of symptoms to respiratory failure has occurred in as little as 24 hours in cases of foodborne botulism.

Physical examination usually reveals an alert and oriented patient without fever. Postural hypotension may be present. Mucous membranes may be dry and crusted and the patient may complain of dry mouth or even sore throat. There may be difficulty with speaking and with swallowing. Gag reflex may be absent. Pupils may be dilated and even fixed. Ptosis and extraocular muscle palsies may also be observed. Variable degrees of skeletal muscle weakness may be observed depending on the degree of progression in an individual patient. Deep tendon reflexes may be present or absent. With severe respiratory muscle paralysis, the patient may become cyanotic or exhibit narcosis from CO2 retention.


The occurrence of an epidemic of cases of a descending and progressive bulbar and skeletal paralysis in afebrile patients points to the diagnosis of botulinum intoxication. Foodborne outbreaks tend to occur in small clusters and do not generally occur in soldiers on military rations such as MRE's (Meals, Ready to Eat). Higher numbers of cases in a theater of operations should raise at least the possibility of a biological warfare attack with aerosolized botulinum toxin. Foodborne outbreaks are theoretically possible in troops on normal "A" rations.

Individual cases might be confused clinically with other neuromuscular disorders such as Guillain-Barre syndrome, myasthenia gravis, or tick paralysis. The edrophonium or Tensilon® test may be transiently positive in botulism, so it may not distinguish botulinum intoxication from myasthenia. The cerebrospinal fluid in botulism is normal and the paralysis is generally symmetrical, which distinguishes it from enteroviral myelitis. Mental status changes generally seen in viral encephalitis should not occur with botulinum intoxication.

It may become necessary to distinguish nerve agent and/or atropine poisoning from botulinum intoxication. Nerve agent poisoning produces copious respiratory secretions and miotic pupils, whereas there is if anything a decrease in secretions in botulinum intoxication. Atropine overdose is distinguished from botulism by its central nervous system excitation (hallucinations and delirium) even though the mucous membranes are dry and mydriasis is present. The clinical differences between botulinum intoxication and nerve agent poisoning are depicted in Table 3, Appendix A.

Laboratory testing is generally not helpful in the diagnosis of botulism. Survivors do not usually develop an antibody response due to the very small amount of toxin necessary to produce clinical symptoms. Detection of toxin in serum or gastric contents is possible, however, with a mouse neutralization assay, the only test available, but only in specialized laboratories. Serum specimens should be drawn from suspected cases and held for testing at such a facility.


Respiratory failure secondary to paralysis of respiratory muscles is the most serious complication and, generally, the cause of death. Reported cases of botulism prior to 1950 had a mortality of 60%. With tracheostomy or endotracheal intubation and ventilatory assistance, fatalities should be less than five percent. Intensive and prolonged nursing care may be required for recovery (which may take several weeks or even months).

ANTITOXIN: In isolated cases of food-borne botulism, circulating toxin is present, perhaps due to continued absorption through the gut wall. Botulinum antitoxin (equine origin) has been used as an investigational new drug (IND) in those circumstances, and is thought to be helpful. Animal experiments show that after aerosol exposure, botulinum antitoxin can be very effective if given before the onset of clinical signs. Administration of antitoxin is reasonable if disease has not progressed to a stable state.

A trivalent equine antitoxin has been available from the Centers for Disease Control for cases of foodborne botulism. This product has all the disadvantages of a horse serum product, including the risks of anaphylaxis and serum sickness. A "despeciated" equine heptavalent antitoxin (against types A, B, C, D, E, F, and G) has been prepared by cleaving the Fc fragments from horse IgG molecules, leaving F(ab)2 fragments. This product is under advanced development, and is currently available under IND status. Its efficacy is inferred from its performance in animal studies. Disadvantages include rapid clearance by immune elimination, as well as a theoretical risk of serum sickness.

Use of the antitoxin requires skin testing for horse serum sensitivity prior to administration. Skin testing is performed by injecting 0.1 ml of a 1 to 10 dilution of antitoxin intradermally and monitoring the patient for 20 minutes. If the injection site becomes hyperemic (>0.5 cm diameter), or the patient develops fever, chills, hypotension, skin rash, respiratory difficulty, nausea, vomiting and/or generalized itching, the skin test is considered positive. If no allergic symptoms are observed, the antitoxin is administered intravenously, 10 mls over 20 minutes. This dose is repeated until there is no more improvement. With a positive skin test, desensitization is carried out by administering 0.01 - 0.1 ml of antitoxin subcutaneously, gradually increasing the dose every 20 minutes until 2.0 ml can be sustained without a marked reaction.


A pentavalent toxoid of Clostridium botulinum toxin types A, B, C, D, and E is available under an IND status. This product has been administered to several thousand volunteers and occupationally at-risk workers, and induces serum antitoxin levels that correspond to protective levels in experimental animal systems. The currently recommended schedule (0, 2, and 12 weeks, then a 1 year booster) induces protective antibody levels in greater than 90 percent of vaccines after one year. Adequate antibody levels are transiently induced after three injections, but decline prior to the one year booster.

Contraindications to the vaccine include sensitivities to alum, formaldehyde, and thimerosal, or hypersensitivity to a previous dose. Reactogenicity is mild, with two to four percent of vaccines reporting erythema, edema, or induration at the local site of injection which peaks at 24 to 48 hours, then dissipates. The frequency of such local reactions increases with each subsequent inoculation; after the second and third doses, seven to ten percent will have local reactions, with higher incidence (up to twenty percent or so) after boosters. Severe local reactions are rare, consisting of more extensive edema or induration. Systemic reactions are reported in up to three percent, consisting of fever, malaise, headache, and myalgia. Incapacitating reactions (local or systemic) are uncommon. The vaccine should be stored at refrigerator temperatures (not frozen).

Three or more vaccine doses (0, 2, and 12 weeks, then at 1 year if possible, all by deep subcutaneous injection) are recommended only to selected individuals or groups judged at high risk for exposure to botulinum toxin aerosols.  There is no indication at present for use of botulinum antitoxin as a prophylactic modality except under extremely specialized circumstances.




Signs and Symptoms: From 3-12 hours after aerosol exposure, sudden onset of fever, chills, headache, myalgia, and nonproductive cough. Some patients may develop shortness of breath and retrosternal chest pain. Fever may last 2 to 5 days, and cough may persist for up to 4 weeks. Patients may also present with nausea, vomiting, and diarrhea if they swallow toxin. Higher exposure can lead to septic shock and death.

Diagnosis: Diagnosis is clinical. Patients present with a febrile respiratory syndrome without CXR abnormalities. Large numbers of soldiers presenting with typical symptoms and signs of SEB pulmonary exposure would suggest an intentional attack with this toxin.

Treatment: Treatment is limited to supportive care. Artificial ventilation might be needed for very severe cases, and attention to fluid management is important.

Prophylaxis: Use of protective mask. There is currently no human vaccine available to prevent SEB intoxication.

Decontamination: Hypochlorite (0.5% for 10-15 minutes) and/or soap and water. Destroy any food that may have been contaminated.


Staphylococcus aureus produces a number of exotoxins, one of which is Staphylococcal enterotoxin B, or SEB. Such toxins are referred to as exotoxins since they are excreted from the organism; however, they normally exert their effects on the intestines and thereby are called enterotoxins. SEB is one of the pyrogenic toxins that commonly causes food poisoning in humans after the toxin is produced in improperly handled foodstuffs and subsequently ingested. SEB has a very broad spectrum of biological activity. This toxin causes a markedly different clinical syndrome when inhaled than it characteristically produces when ingested. Significant morbidity is produced in individuals who are exposed to SEB by either portal of entry to the body.


SEB has caused countless endemic cases of food poisoning. Often these cases have been clustered, due to common source exposure in a setting such as a church picnic or passengers eating the same toxin-contaminated food on an airliner. Although this toxin would not be likely to produce significant mortality on the battlefield, it could render up to 80 percent or more of exposed personnel clinically ill and unable to perform their mission for a fairly prolonged period of time. Therefore, even though SEB is not generally thought of as a lethal agent, it may incapacitate soldiers for up to two weeks, making it an extremely important toxin to consider.


Staphylococcal enterotoxins are extracellular products produced by coagulase-positive staphylococci. They are produced in culture media and also in foods when there is overgrowth of the staph organisms. At least five antigenically distinct enterotoxins have been identified, SEB being one of them. These toxins are heat stable. SEB causes symptoms when inhaled at very low doses in humans: a dose of several logs lower than the lethal dose by the inhaled route would be sufficient to incapacitate 50 percent of those soldiers so exposed. This toxin could also be used (theoretically) in a special forces or terrorist mode to sabotage food or low volume water supplies.


Staphylococcal enterotoxins produce a variety of toxic effects. Inhalation of SEB can induce extensive pathophysiological changes to include widespread systemic damage and even septic shock. Many of the effects of staphylococcal enterotoxins are mediated by interactions with the host's own immune system. The mechanisms of toxicity are complex, but are related to toxin binding directly to the major histocompatibility complex that subsequently stimulates the proliferation of large numbers of T cell lymphocytes. Because these exotoxins are extremely potent activators of T cells, they are commonly referred to as bacterial superantigens. These superantigens stimulate the production and secretion of various cytokines, such as tumor necrosis factor, interferon-(, interleukin-1 and interleukin-2, from immune system cells. Released cytokines are thought to mediate many of the toxic effects of SEB.


Relevant battlefield exposures to SEB are projected to cause primarily clinical illness and incapacitation. However, higher exposure levels can lead to septic shock and death. Intoxication with SEB begins 3 to 12 hours after inhalation of the toxin. Victims may experience the sudden onset of fever, headache, chills, myalgias, and a nonproductive cough. More severe cases may develop dyspnea and retrosternal chest pain. Nausea, vomiting, and diarrhea will also occur in many patients due to inadvertently swallowed toxin, and fluid losses can be marked. The fever may last up to five days and range from 103 to 106o F, with variable degrees of chills and prostration. The cough may persist up o four weeks, and patients may not be able to return to duty for two weeks.

Physical examination in patients with SEB intoxication is often unremarkable. Conjunctival injection may be present, and postural hypotension may develop due to fluid losses. Chest examination is unremarkable except in the unusual case where pulmonary edema develops. The chest X-ray is also generally normal, but in severe cases increased interstitial markings, atelectasis, and possibly overt pulmonary edema or an ARDS picture may develop.


As is the case with botulinum toxins, intoxication due to SEB inhalation is a clinical and epidemiologic diagnosis.  Because the symptoms of SEB intoxication may be similar to several respiratory pathogens such as influenza, adenovirus, and mycoplasma, the diagnosis may initially be unclear. All of these might present with fever, nonproductive cough, myalgia, and headache. SEB attack would cause cases to present in large numbers over a very short period of time, probably within a single 24 hour period. Naturally occurring pneumonias or influenza would involve patients presenting over a more prolonged interval of time. Naturally occurring staphylococcal food poisoning cases would not present with pulmonary symptoms. SEB intoxication tends to progress rapidly to a fairly stable clinical state, whereas pulmonary anthrax, tularemia pneumonia, or pneumonic plague would all progress if left untreated. Tularemia and plague, as well as Q fever, would be associated with infiltrates on chest radiographs.

Nerve agent intoxication would cause fasciculations and copious secretions, and mustard would cause skin lesions in addition to pulmonary findings; SEB inhalation would not be characterized by these findings. The dyspnea associated with botulinum intoxication is associated with obvious signs of muscular paralysis, bulbar palsies, lack of fever, and a dry pulmonary tree due to cholinergic blockade; respiratory difficulties occur late rather than early as with SEB inhalation.

Laboratory findings are not very helpful in the diagnosis of SEB intoxication. A nonspecific neutrophilic leukocytosis and an elevated erythrocyte sedimentation rate may be seen, but these abnormalities are present in many illnesses. Toxin is very difficult to detect in the serum by the time symptoms occur; however, a serum specimen should be drawn as early as possible after exposure. Data from rabbit studies clearly show that SEB in the serum is transient; however, it accumulates in the urine and can be detected for several hours post exposure. Therefore, urine samples should be obtained and tested for SEB. High SEB concentrations inhibit kidney function. Because most patients will develop a significant antibody response to the toxin, acute and convalescent serum should be drawn which may be helpful retrospectively in the diagnosis.


Currently, therapy is limited to supportive care. Close attention to oxygenation and hydration are important, and in severe cases with pulmonary edema, ventilation with positive end expiratory pressure and diuretics might be necessary. Acetaminophen for fever, and cough suppressants may make the patient more comfortable. The value of steroids is unknown. Most patients would be expected to do quite well after the initial acute phase of their illness, but most would generally be unfit for duty for one to two weeks.


Although there is currently no human vaccine for immunization against SEB intoxication, several vaccine candidates are in development. Preliminary animal studies have been encouraging and a vaccine candidate is nearing transition to advanced development and safety and immunogenicity testing in man. Experimentally, passive immunotherapy can reduce mortality, but only when given within 4-8 hours after inhaling SEB.




Signs and Symptoms: Weakness, fever, cough and pulmonary edema occur 18-24 hours after inhalation exposure, followed by severe respiratory distress and death from hypoxemia in 36-72 hours.

Diagnosis: Signs and symptoms noted above in large numbers of geographically clustered patients could suggest an exposure to aerosolized ricin. The rapid time course to severe symptoms and death would be unusual for infectious agents. Laboratory findings are nonspecific but similar to other pulmonary irritants which cause pulmonary edema. Specific serum ELISA is available. Acute and convalescent sera should be collected.

Treatment: Management is supportive and should include treatment for pulmonary edema. Gastric decontamination measures should be used if ingested.

Prophylaxis: There is currently no vaccine or prophylactic antitoxin available for human use, although immunization appears promising in animal models. Use of the protective mask is currently the best protection against inhalation.

Decontamination: Weak hypochlorite solutions and/or soap and water can decontaminate skin surfaces. Ricin is not volatile, so secondary aerosols are generally not a danger to health care providers.


Ricin is a potent protein toxin derived from the beans of the castor plant (Ricinus communis ). Castor beans are ubiquitous worldwide, and the toxin is fairly easily produced from them. Ricin is therefore a potentially widely available toxin. When inhaled as a small particle aerosol, this toxin may produce pathologic changes within 8 hours and severe respiratory symptoms followed by acute hypoxic respiratory failure in 36-72 hours. When ingested, ricin causes severe gastrointestinal symptoms followed as well by vascular collapse and death. This toxin may also cause disseminated intravascular coagulation, microcirculatory failure and multiple organ failure if given intravenously in laboratory animals.


Ricin's significance as a potential biological warfare toxin relates in part to its wide availability. Worldwide, one million tons of castor beans are processed annually in the production of castor oil; the waste mash from this process is approximately five percent ricin by weight. The toxin is also quite stable and extremely toxic by several routes of exposure, including the respiratory route. Ricin is said to have been used in the assassination of Bulgarian exile Georgi Markov in London in 1978. Markov was attacked with a specially engineered weapon disguised as an umbrella which implanted a ricin- containing pellet into his body.


Ricin is actually made up of two hemagglutinins and two toxins. The toxins, RCL III and RCL IV, are dimers of about 66,000 daltons molecular weight. The toxins are made up of two polypeptide chains, an A and a B chain, which are joined by a disulfide bond. Ricin can be produced relatively easily and inexpensively in large quantities in a fairly low technology setting. It is of marginal toxicity in terms of its LD50 in comparison to toxins such as botulinum and SEB (incapacitating dose), so an enemy would have to produce it in larger quantities to cover a significant area on the battlefield (see Figure 1, Appendix A). This might limit large-scale use of ricin by an adversary. Ricin can be prepared in liquid or crystalline form, or it can be lyophilized to make it a dry powder. It could be disseminated by an enemy as an aerosol, or it could be used as a sabotage, assassination, or terrorist weapon.


Ricin is very toxic to cells. It acts by inhibiting protein synthesis. The B chain binds to cell surface receptors and the toxin-receptor complex is taken into the cell; the A chain has endonuclease activity and extremely low concentrations will inhibit protein synthesis. In rodents, the histopathology of aerosol exposure is characterized by necrotizing airway lesions causing tracheitis, bronchitis, bronchiolitis, and interstitial pneumonia with perivascular and alveolar edema. There is a latent period of 8 hours post inhalation exposure before histologic lesions were observed in animal models. In rodents, ricin is more toxic by the aerosol route compared to other routes of exposure.

There is little toxicity data in humans. The exact cause of morbidity and mortality would be dependent upon the route of exposure. Aerosol exposure in man would be expected to cause acute lung injury, pulmonary edema secondary to increased capillary permeability, and eventual acute hypoxic respiratory failure.


The clinical picture in intoxicated victims would depend on the route of exposure. After aerosol exposure, signs and symptoms would depend on the dose inhaled. Accidental sublethal aerosol exposures which occurred in humans in the 1940's were characterized by onset of the following symptoms in four to eight hours: fever, chest tightness, cough, dyspnea, nausea, and arthralgias. The onset of profuse sweating some hours later was commonly the sign of termination of most of the symptoms. Although lethal human aerosol exposures have not been described, the severe pathophysiologic changes seen in the animal respiratory tract, including necrosis and severe alveolar flooding, are probably sufficient to cause if enough toxin is inhaled. Time to death in experimental animals is dose dependent, occurring 36-72 hours post inhalation exposure. Humans would be expected to develop severe lung inflammation with progressive cough, dyspnea, cyanosis and pulmonary edema.

By other routes of exposure, ricin is not a direct lung irritant; however, intravascular injection can cause minimal pulmonary perivascular edema due to vascular endothelial injury. Ingestion causes gastrointestinal hemorrhage with hepatic, splenic, and renal necrosis. Intramuscular administration causes severe local necrosis of muscle and regional lymph nodes with moderate visceral organ involvement.


An attack with aerosolized ricin would be, as with many biological warfare agents, primarily diagnosed by the clinical and epidemiological setting. Acute lung injury affecting a large number of cases in a war zone where an attack could occur should raise suspicion of an attack with a pulmonary irritant such as ricin, although other pulmonary pathogens could present with similar signs and symptoms. Other biological threats, such as SEB, Q fever, tularemia, plague, and some chemical warfare agents like phosgene, need to be included in a differential diagnosis. Ricin intoxication would be expected to progress despite treatment with antibiotics, as opposed to an infectious process. There would be no mediastinitis as seen with inhalation anthrax. SEB would be different in that most patients would not progress to a life-threatening syndrome but would tend to plateau clinically. Phosgene-induced acute lung injury would progress much faster than that caused by ricin.

Additional supportive clinical or diagnostic features after aerosol exposure to ricin may include the following: bilateral infiltrates on chest radiographs, arterial hypoxemia, neutrophilic leukocytosis, and a bronchial aspirate rich in protein compared to plasma which is characteristic of high permeability pulmonary edema. Specific ELISA testing on serum or immunohistochemical techniques for direct tissue analysis may be used where available to confirm the diagnosis.  Ricin is an extremely immunogenic toxin, and acute as well as convalescent sera should be obtained from survivors for measurement of antibody response.


Management of ricin intoxicated patients again depends on the route of exposure. Patients with pulmonary intoxication are managed by appropriate treatment for pulmonary edema and respiratory support as indicated.  Gastrointestinal intoxication is best managed by vigorous gastric decontamination with lavage and superactivated charcoal, followed by use of cathartics such as magnesium citrate. Volume replacement of GI fluid losses is important. In percutaneous exposures, treatment would be primarily supportive.


The protective mask is effective when worn in preventing aerosol exposure. Although a vaccine is not currently available, candidate vaccines are under development which are immunogenic and confer protection against lethal aerosol exposures in animals. Prophylaxis with such a vaccine is the most promising defense against a biological warfare attack with ricin.




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 results in prostration, weakness, ataxia, collapse, shock, and death.

Diagnosis: 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.

Treatment: There is no specific antidote. Superactivated charcoal should be given orally if swallowed.

Prophylaxis: 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.

Decontamination: The outer uniform 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.


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 in the literature. 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 500o F for 30 minutes is required for inactivation, while brief exposure to NaOH 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 baked into bread that was ingested by civilians. Some developed a protracted lethal illness called alimentary toxic aleukia (ATA) 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 and 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.


Mycotoxins allegedly have been used in aerosol form ("yellow rain") to produce lethal and nonlethal casualties in Laos (1975-81), Kampuchea (1979-81), and Afghanistan (1979-81). 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 protected with masks and chemical 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. Much controversy has centered about the veracity of eyewitness and victim accounts, but there is enough evidence to make agent use in these areas highly probable.


T2 and other mycotoxins may enter the body through the skin and aerodigestive 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 (T2), the toxin(s) will adhere to and penetrate skin, be inhaled, and swallowed. Clothing will be contaminated and serve as a reservoir for further toxin exposure. Early symptoms beginning within minutes of exposure 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/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 crampy 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 commonest symptoms were 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 an odor, are visible, 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, 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 0.1-1.0 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 discarded within 4 hours and decontaminated by exposure to 5% hypochlorite for 6-10 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. Superactive 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 iscurrently field available. All therapy is symptomatic and supportive.


Physical protection of the skin and airway are the only proven effective methods of protection during an attack. Immunological (vaccines) and chemoprotective pretreatments are being studied in animal models, but are not available for field use by the warfighter.



The American Spectator-- James Ring Adams--   What terror weapon is Saddam Hussein hiding from U.N. inspectors, even at the risk of renewed U.S. bombing? The evidence points to a new form of one of the nastiest villains of the Cold War, Yellow Rain.

This blistering, highly lethal agent, scientifically a "mycotoxin," a form of poison produced by microscopic fungi, emerged at the beginning of the 1980's in Soviet surrogate attacks on anti-Communist insurgents in Laos and Afghanistan. Strong complaints from the Reagan State Department apparently persuaded the Soviet Union to stop using it. But U.S. diplomats were scarred by a loud counter attack from 'Western apologists unwilling to admit that Moscow was violating a major treaty against biological Weapons. '[his threat is back, along with a more widely acknowledged range of biological weapons, hut the psychological denial by the disarmament lobby has left the West largely helpless to deal with it.

The arms inspectors at the U.N. Special Commission (UNSCOM) now say outright they were on the trail of a major biological weapons system when Saddam Hussein cut them off this January. But they clam up when pressed for more specifics. UNSCOM spokesman Ewen Buchanan explains that they don't want to tip Iraq to what they know, which he hints is quite a lot.

The Aflatoxin Bomb

But it was Iraq itself which put Yellow Rain back on the terror weapon hot list and presented LINSCOM with its great est mystery. In July 1995, officials in Baghdad revealed to the inspectors that not only had they experimented with a sub stance called Aflatoxin, but they had loaded it into missile warheads and gravity bombs during the Gulf War and given commanders pre-delegated authority to use it. After the cease-fire, their stockpile was destroyed, the Iraqis added.

Nothing about this story added up. Baghdad's count of the number munitions loaded with Aflatoxin kept changing, fluctuating up and down from the original report of four al-Hussein missiles and seven R-4oo gravity bombs. Then the reported production facility at Fudaliyah seemed totally inadequate to growing the quantity Ira(l said it held. But the biggest question of all was: Why Aflatoxin?

It was simply a lousy candidate for a battlefield weapon. The toxin could ruin your peanut crop, as it sometimes does in the U.S.. and in the long run might cause liver cancer in humans. But it didn't have the immediate drop-dead action that could make a difference in a fight. It was no cinch to handle, either. It was hard to dissolve, even for a mycotoxin, so you wound up making a munition filled with solvent. As one UNSCOM specialist was food of saying, you would get hurt by an Aflatox in bomb mainly if it fell on your head

Yet there's a plausible report that an agent of this sort was turned on American forces during the Gulf War, and it did harm. At 3 am, on January 19, 1991, flash of red light and a loud shock wave woke nearly 750 Seabees of the 24th Naval Mobile Construction Battalion camped near al Jitbayl in northern Saudi Arabia. A general alarm sounded, with a radio message warning of "a confirmed chemical agent." As troops struggled into their masks and rubberized suits, they noticed a "dense yellowish mist" float ing over the camp. Those who didn't suit in time began to choke and felt a burning on their skin. Exposed areas later broke out in rashes and blisters, which turned to ulcerating sores. The New York Times surveyed 152 veterans of the unit in Sep tember 1996 and found that 114 report ed chronic post war illness.

The Pentagon said Patriot missiles caused the explosion and blamed the symptoms on a toxic propellant released from an Iraqi SCUD as it broke up in the air. But the details don't fit For one thing, the nitric acid propellant should have corroded the rubber suits, but they were unaffected. According to a paper by Jonathan Tucker of the Monterey Institute of Inter national Studies in California, no SCUD attacks were reported that night. Tucker finds it possible instead that Patriot missiles were launched against an aircraft equipped to spray a biological weapon. Unit veterans strongly suspect a cover-up. A communications officer later stated in an affidavit that radio operators in the command bunkers were ordered to burn the log pages covering the incident.

Explanations of these mysteries were lacking until this spring, when a former UNSCOM inspector named Terry Taylor spilled the beans. At a symposium in London he remarked that Iraq's "Aflatoxin bomb" looked like a cover for another agent, a quick-acting battlefield toxin, was produced with the same fermenting process. UNSCOM officials don't hide their annoyance that their hand was tipped even this much. When one asks them about the likely candidate for the secret substance, one or more of the chothecenes, they roll their eyes.

Peanut Mold or Yellow Rain?

The txichothecene family of mycotoxins produced what the Reagan Administration identified as the active agent in Yellow Rain, and it is nasty. These toxins immediately attack eyes, skin, and respiration. As blistering agents, they do up to forty times more damage than the Lewisite and mustard gas of World War I. The skin forms pus-filled welts and sloughs off, giving rise to symptoms like those noted at al-Jubayl. As the toxins bum their way through throat, stomach, and intestines, they cause vomiting and bloody diarrhea. Depending on exposure, death can come in minutes. Lesser amounts can cause long-term suppression of the immune system.

Unlike Aflatoxin, the trichothecenes dissolve fairly readily. (The term "yellow rain" referred to the dispersal agent used in the early 1980's, which spread the toxin in oily, sticky yellow droplets.) But UNSCOM specialists doubt that this weapon has returned in its original form. The toxin then most frequently identified, T-2, was considered a battlefield failure since its dispersal radius was still limited. There are other choices, however

Some mycotoxins are named for the species of fungus that produces them, but the trichothecenes are classed together by their chemical structure. One type of toxin can be produced by several different species, and a prolific species like fusarium, stachybotris, and, yes, penicilliurn can produce several different trichothecenes. These fungi are easily found in nature. (Stachybotris made a name for itself in New York City recently when a bloom of the mold closed down a newly renovated public library on Staten Island.)

Their poisons can be even more dead ly when combined together or mixed in a "cocktail" with chemicals like mustard gas. Agricultural researchers have found that aflatoxin potentiates both T-2 and another "yellow rain" component called DAS (diacetoxyscirpenol), meaning that the harm caused by the agents together is more severe than each would cause alone. The toxins can be synthesized or altered with artificial ingredients. Any number of breakthroughs could have occurred in the thirteen years since "yellow rain" went underground. And there is a nagging, still unrefuted report that Iraq is feeding off the work of the masterminds of this terror weapon, the biological warriors of the former Soviet Union.

Incident at Majnoon

A battle from the most desperate days of the Iran-Iraq war hangs over this whole issue. At the end of 1983, Iranian human wave attacks were pushing Iraqi forces back through the marshes around Majnoon Island when Iraq unleashed a new chemical weapon. European doctors reported mustard gas, canisters of which were later found by a U.N. mission, but they also detected trace amounts of T-2. At the same time, Israeli intelligence leaked a report about Iraqi negotiations with the Soviet Union for some spectacular new weapon to break the stalemate with Iraq.

According to this analysis, Iraq asked specifically for a CBW system during the November 14, 1983 visit to Baghdad of Vladimir Mordvinov, deputy chairman of the USSR Committee for Foreign Economic Relations. Mordvinov kicked the request back to Moscow, and two weeks later his boss Yakov Ryahov flew to Baghdad to make arrangements. Radio Moscow reported with fine irony that the talks "provided for help in reclaiming an oil held."

This account fits the chronology of Iraq's homegrown biowar program, which it claims didn't begin in earnest until 1985. It also explains why Iraq was able to make what UNSCOM called such remarkable gains in such a short time.

It implies, bluntly, that Baghdad learned the secrets of Yellow Rain from its Soviet friends. This report quickly became a hot potato and remains one to this day.

Central Intelligence Agency sources warned reporters not to trust the findings of the Belgian specialist Aubin Heyndrickx who was treating the Iranian victims of Majnoon. Senior Israeli officials repudiated the work of their own analyst. The State Department fell silent about Yellow Rain. It was almost as if some secret deal had been struck to abandon the issue if the attacks ceased.

The Cold War's Biggest Secret With the advent of Mikhail Gorbachev and perestroika, the issue was forgotten, until a major defection brought it suddenly to the fore. In October 1989, a scientist from Leningrad named Vladimir Pasechnik arrived in Toulouse, France, to buy chemical equipment for his research laboratory, the Institute of Ultra Pure Biochemical Preparations. in the course of fifteen years spent building this institute, Pasechnik had discovered that he was part of a vast military project called the Biopreparat, devoted to developing new biological weapons. Conscience stricken, he called the British embassy in Paris, and was quickly hustled across the channel. His debriefing confirmed the worst fears of western intelligence. The Soviet military was spending bil lions of rubles and employing 15,000 workers in plants capable of mass producing biological weapons. Biopreparat researchers had used genetic engineering to produce new antibiotic-resistant strains of diseases such as tularemia and pneumonic plague. The revelations prompted British Prime Minister Margaret Thatcher and U.S. President George Bush to confront Gorbachev directly.

With the breakup of the Soviet Union, the allies continued to pressure Russian President Boris Yeltsin, who promised to dismantle the Biopreparat. The whole Soviet project was a blatant violation of the 1972 Biological and Toxin Weapons Convention, but the West softened its public complaints for fear of causing Yeltsin problems with his military.'

In spite of Yeltsin's promise, there are worries that he had neither the will nor the control to carry it out. He delegated the job to the notorious General Anatoly Kuntsevich, the former chemical troops commander and political hard-liner. Kuntsevich was fired in 1994 and later fell under suspicion of illegally selling chemical weapons precursors to Syria.

Editor:  Balaam's Ass Speaks--  This article contained more, and I don't expect to get it later.  I think this is enough to satisfy you that War with any Middle Eastern country would unleash a holocaust against the USA which we absolutely are NOT prepared to resist or to survive.  Millions could be taken out with these and other biological agents. We also see how the bible test below could be fulfilled in our time:

Speaking of the future destruction of Babylon:  Isaiah 13:8 And they shall be afraid: pangs and sorrows shall take hold of them; they shall be in pain as a woman that travaileth: they shall be amazed one at another; their faces shall be as flames.




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SMALLPOX-- NO CURE-- Prelude to Armageddon