Saturday, May 12, 2012

Tapping into Mother Nature's Toxic Warehouse


     There are many 'natural' medications in nature, some which have been used for otherwise incurable problems (see post: From Deep in the Jungle) and others growing on the side of road or in your own backyard (see post: Mother nature's Psychedelic Roadside Drugstore). But Mother Nature is not always kind and just as often as she has produced wondrous drugs, she has created deadly poisons. Humankind has taken many of these toxins and transformed them into biological weapons.
The Willow Tree-Natural Source of 'Aspirin'

     Botulinum toxin is odorless and colorless. It has been called the most toxic substance in the biological world. The toxin is produced by the bacterium Clostridium botulinum, an obligate anaerobe (needs an oxygen-poor environment to grow) but can be commonly found in its natural habitat, the soil, especially where manure has been laid down (farms) but also seen in cases of  improperly canned foods.
     The toxin is a protein which is relatively stable and can be stored in crystalline form. It can be absorbed through the mucous membranes making dispersal in aerosol, addition to a municipal water or food supplies easy ways to introduce the toxin into a population.
Botulism-'Death in a Can'

     Depending on the dosage, symptoms may present within 12 hours or may not be apparent for as long as 14 days after exposure. The first signs of botulism include blurry or double vision, vomiting and difficulty swallowing and speaking. At this point, the only hope for effective treatment would be a botulism antitoxin and only if it is administered before symptoms became further advanced.
     The protein is a neurotoxin and once the symptoms appear the damage is irreversible (usually within 48 hours). If untreated, paralysis begins to take hold, seizing up your muscles and finally leading to failure of the respiratory system.
     There are several botulinum toxin immunologically unique strains and the only treatment involves passive antibody shots against all the clostridium botulinum strains. Because of these multiple strains, immunization of a large population is not considered feasible.
     The mortality rate from exposure to this toxin is 70 percent but can be brought down to as low as 6 percent if the patient is place on a ventilator (breathing machine). But recovery takes time since the toxin binds to the point where nerve endings and muscles meet (neuro-muscular junction) which, in effect, cuts off the signal from the brain, making the muscle inoperable. To recover fully from a case of botulism, the patient actually has to grow back the nerve endings at the muscle junctions, a process that can take several months.
     Although a vaccine exists, concerns over effectiveness and side effects have been a problem in its development.
Clostridium botulinum
     One important advantages of botulinum toxin as a biological weapon, is that since its symptoms are delayed, the damage is already done before the target is aware of exposure. Victims become the 'walking dead' before they even realize what has occurred. The amount of antiserum required to treat large numbers of exposed people is not available and many people would be simply beyond saving even if given the antitoxin.
     Even though botulinum is highly toxic it would take a large quantity to reach a lethal concentration in a large city's water supply. Contamination of a food supply would be difficult, although centralized individual food processing plants would likely be targets for terrorists, presenting the opportunity to commit mass murder.
     During WW II, more than 3000 US scientists worked on biological warfare and many of the problems of dispersal of this toxin were likely solved. The toxin can also be fused, using common molecular biology techniques with other proteins which stabilize it for dispersal without decreasing its lethality or the toxin can be mixed with other protective agents (ex. trehalose, viral-glass) or it can be encapsulated in protective material providing a timed release presentation that dissolves once it is in the digestive system.
     It may also be possible to clone this clostridium toxin gene into common bacteria that inhabit the human gut, allowing the clostridium botulinum bacteria to establish themselves long enough to produce a quantity of toxin sufficient to disable the victim before their immune system would be able to respond.
Aum Shinrikyo Logo
     After the First Gulf War, the Iraqis admitted to producing more than 5000 gallons of Clostridium botulinum. Other nations such as Iran, Syria, North Korea and Libya have been suspected of being in the biological weapons production business also producing botulinum toxin and it remains unclear what has happened to the massive Soviet Union’s biological weapons’ production facilities and their stockpiles since the breakup of the Soviet Union.
     In 1990, members of the Japanese cult Aum Shinrikyo released an aerosol of botulinum toxin against several political targets but failed to cause mass deaths. Later, the cult switched to the chemical agent sarin gas in a 1995 attack, killing about a dozen people (see posts: Death Cults and Biological Warfare in the Twentieth Century) and injuring thousands.

     But botulinum toxin is not all bad. Through the use of small amounts of purified botulinum toxin, doctors are able to harness the bacteria's paralytic power to help sooth neurologic diseases (such as cerebral palsy), facial ticks and, in the area of medical cosmetics, smooth away wrinkles. In the medical world, botulinum toxin, used for therapeutic purposes, is known as Botox.


     Aflatoxins are naturally occurring mycotoxins, produced by many species of  a fungus called Aspergillus. Aflatoxins are toxic and among the most carcinogenic (cancer inducing) substances known. The fungi which produce this material grow on grain, peanuts and other rich nutrients. Aflatoxins are readily extracted with ethanol, easily concentrated and are stable in storage.
Aspergillus
     How badly a person is affected by aflatoxin mycotoxins depends on the age of the individual, gender, level of exposure, duration of exposure, health, strength of their immune system, diet and environmental factors.
     When a large amount of aflatoxin is taken in a very short time, results can be liver damage (and liver cancer), mental impairment, abdominal pain with vomiting and convulsions, edema (generalized soft tissue swelling),pulmonary edema (fluid build-up in the lungs), hemorrhaging, coma and death.
     Ingesting small amounts of aflatoxin at a time, but over a long period (chronic 'food poisoning) can result in growth and development impairment in children and liver cancer due to DNA (genetic) mutations. The aflatoxin lethal dose rate which causes 50% of a group to die for animals is between 0.5 and 10 mg/kg of the animal's weight.
Peanuts Affected with Aflatoxin Fungus
     Aflatoxins are not contagious and drugs and antibiotics do little to help. This toxin, however, damages the liver more than any other organ and also suppress the immune system.
     There is a delay between exposure and the development of the clinical disease, as well as difficulty in differentiating cancer origins between accidental and intentional exposure. Even recognizing that a target population had been attacked would be difficult, making the use of aflatoxin a 'stealth biological weapon attack'.
     The Iraqis were said to have produced about 600 gallons of concentrated aflatoxin which had been loaded into bombs and missiles.
Tetrodotoxin

     Tetrodotoxin (TTX) is another neurotoxin with no antidote. Tetrodotoxin acts by blocking action potentials in nerves by binding to the sodium channels in the membranes of nerve cells, preventing any affected nerve cells from firing.
     The name 'tetrodotoxin' derives from Tetraodontiformes, a species of fish which include the pufferfish, porcupinefish, triggerfish and ocean sunfish (mola). The toxin is also found in several other animals such as the rough-skinned newt  and blue-ringed octopus.    But none of these creatures produce the toxin themselves. The poison is is actually produced by certain species of bacteria which live within these animals.

     The toxin was first isolated and by Yoshizumi Tahara in 1909, and the structure determined by Robert Burns Woodward in 1964.
     The first documented case of poisoning with tetrodotoxin was in the log of Captain James Cook. Cook reported , his crew experiencing numbness and shortness of breath after consumption of a 'tropical fish' (pufferfish?). The remains of the fish were fed to the pigs on board, and all the pigs were found dead the next morning.
Pufferfish
     In 1996, three chefs in California experienced paralysis after eating tiny amounts of pufferfish imported from Japan. In Japan, the pufferfish is  considered a delicacy (called 'fugu', meaning 'river pig') and 50-100 poisonings are reported each year in that country (see post: JetFuel for the Sex Machine)

     Tetrodotoxin poisoning is usually a result of poorly prepared pufferfish (chefs in Japan are trained and certified to prepare pufferfish), mislabeled cans that contain pufferfish and there is also one fatal case where an individual ate a California newt.
Rough-Skinned Newt
     Tetrodotoxin is extremely toxic, usually found in the liver but sometimes even the flesh of the fish and is estimated to be between 100 and 10,000 times more toxic than cyanide and is one of the top 3 most poisonous naturally occurring molecules. The toxin induces paralysis, preventing breathing, eventually causing respiratory failure.

     Death occurs within 4-6 hours and since there is no antidote, the mortality rate is over 50%.  Because of its extreme toxicity, the Japanese Imperial Army investigated it as a biological during WWII and its potency was tested in labs. It has been used in Japan to treat pain from migraines and terminal cancer and, in animals, combined with bupivicaine, works well as an anesthetic.
Fugu Sashimi
     The toxin was artificially synthesized in Nagoya University, Japan in 1972.
     Tetrodotoxin can enter the body by ingestion, injection, inhalation and through skin abrasions. Toxicity varies between species of fish and, at times, during different seasons and at different geographic localities, the flesh of many pufferfish may not be dangerously toxic. Ingestion of the toxin is not always fatal but at near-lethal doses, it can leave a person in a state of near-death for several days, all the while remaining fully conscious. TTX has been alleged as an ingredient in Haitian Voodoo and the closest approximation of zombieism.
Haitian Voodoo Zombie

     Symptoms of TTX poisoning develop within 20-30 minutes of ingestion but, at times, can be delayed up to four hours. Numbness of the lips and tongue is followed by increased salivation, sweating, headache, weakness, lethargy, loss of coordination, tremor, paralysis, blotchy skin changes, difficulty swallowing, seizures, breathing problems and eventually respiratory failure, and coma.
     Nausea, vomiting, diarrhea, and abdominal pain often appear early on and heart irregularities may precede complete respiratory failure and cardiovascular collapse. Death usually occurs within 4 to 6 hours, with a range of about 20 minutes to 8 hours. If the patient survives 24 hours, recovery without any residual effects will usually occur over several days.
     No antidote has been developed for teradotoxin poisoning but a monoclonal antibody specific to tetrodotoxin, developed by USAMRIID has been shown to be effective for reducing lethality.
Staphyloccocu aureus
     

     Staphylococcal enterotoxin B (SEB) is a toxin produced by the bacterium Staphyloccocu aureus and commonly causes food poisoning, with severe intestinal cramping, diarrhea and nausea often starting within a few hours of ingestion. The toxin is very stable and can remain active even after the contaminating bacteria are killed and can even withstand boiling at 100°C for a short time.
     The effects of the SEB toxin act through the body's own immune system, causing the immune system to release a large amount of cytokines (inflammatory chemicals) that lead to significant inflammatory reaction.
     The bacteria that produce this toxin are associated with human beings and other warm blooded mammals. Staphylococcus aureus can be easily isolated from nose, armpits or anal swabs of the people around you and about 50% of these isolates can produce this toxin.
     Symptoms of SEB intoxication include a sudden onset of fever, about 40 degrees (Celsius), chills, headache, muscle pains, and a non-productive cough. Some patients may develop shortness of breath and chest pain. Fever may last 2-5 days and cough may continue for up to one month.
     Nausea, vomiting, and diarrhea usually are a prominent feature when the toxin is swallowed. Soldiers in stressful combat situations, may have symptoms which are much more severe, resulting in vasodilation and severe drop in blood pressure, respiratory distress, shock and death within 40-60 hours of exposure.
     Staphylococcal enterotoxin B is a potential agent of bioterrorism because of its easy production and dispersion, a delayed onset of symptoms, its ability to cause high morbidity and, because SEB is an organism seen in so many normal individuals, there can be great difficulty in discerning whether the poisoning was accidental/natural or intentional.
     It is believed that the US Army Chemical Warfare Service may have supplied a vial of SEB to OSS (the forerunner of the CIA) agents during WW II to incapacitate a Nazi agent in North Africa at the time of the D-Day invasion.
     The United States certainly did weaponize SEB originally as agent PG during the Cold War. It was anticipated to have a rate-of-action of several hours and a duration-of-action of 1 - 2 days. There was a program to deliver a usable weapon, and there was also a plan to use it in the opening hours of the invasion of Cuba during the Cuban Missile Crisis.
     Ricin is a protein toxin (see post: Biological Weapons in the Twentieth Century) derived from seeds of the castor bean plant. Ricin kills by destroying an important component of the protein synthesizing machinery of cells, the ribosome.
     Its effects act like a slow poison, gradually causing a total body collapse as necessary proteins are not replaced. Since both the structure and mechanism of action of ricin is well understood, the toxin is an excellent candidate for genetic manipulation.
Castor Bean Plant

     Ricin may be useful as a 'magic bullet', an agent that might selectively destroy cancer cells. But this same technology could easily be applied to improving its use as a biological weapon.
     If ricin is chemically bound to antibodies that only bind to a certain type of cancer cell, the attached ricin should only kill the targeted cancer cells. In theory, therefore, the altered ricin could be made specific enough to target a distinct genetic makeup, that is, a specific and single individual for assassination.
     Victims of ricin poisoning present with nausea, diarrhea, rapid heart rate, low blood pressure and seizures persisting for up to a week.

     Known by some as the 'toxin from hell', USAMRIID is reported to have shown an interest in the toxins produced by the microbe Pfiesteria piscicida. Toxins produced by this unicellular organism cause a variety of symptoms including disorientation, memory loss, loss of ability to concentrate, loss of motor coordination and impairment of a variety of other mental functions and have been demonstrated to be effective both airborne and on contact.
Pfiesteria piscicida
   
Pfiesteria is a dinoflagellate, a group of plant-like one-celled microoragnisms which are free-swimming and have the ability to create energy, like plants, by photosynthesis. But Pfiesteria piscicida is an exception to the rule in that, although it is classified as a dinoflagellate, it is toxic and can be both plant-like (by performing photosynthesis) and animal-like by consuming other organisms.
     Pfiesteria piscicida was only recently discovered in 1988, by Dr. JoAnn Burkholder, an aquatic ecologist at North Carolina State University. The 'piscicida' part of the name translates to 'fish killer' and since its discovery, the organism has killed more than one billion fish. Pfiesteria piscicida  is a small organism and goes through  24 different stages in its life cycle. Several of these stages may produce toxins.

     In its nontoxic forms, the organism is quite harmless and may masquerade as a plant or it may feed on bacteria and algae. In the presence of fish excreta and secretions, however, it is stimulated to morph into a killer. Once triggered, Pfiesteria piscicida emits a neurotoxin into the water which subdues the fish and eats through their skin.
     This dinoflagellate then feeds on the weak and exposed skin, blood, and tissue,, eventually killing the fish, not through the invasion by Pfiesteria piscicida but by suffocation (the toxins cause paralysis of muscles) or by infection (bacteria and foreign objects can enter the fish through the open wounds).
Lesions on Fish Killed by Pfiesteria piscicida

     After the fish die, the dinoflagellates may continue to feed on the fish or change forms and disappear, leaving, as the only evidence of its presence, open, 2 cm.-sized lesions on the fish carcasses.
     Initially, the fish stricken by the toxin exhibit peculiar behavior such as disorientation and abnormal swimming or they may beach themselves or float near the surface of the water. Within fifteen minutes, the fish is dead and the feeding begins.
     Humans can be affected by the toxin as well. Clinical symptoms of exposure to Pfiesteria toxins include memory loss, confusion, acute skin burning (on direct contact with water) as well as headaches, skin rash, eye irritation, upper respiratory irritation, muscle cramps, and gastrointestinal complaints (i.e., nausea, vomiting, diarrhea, and/or abdominal cramps).
     The strongest evidence of adverse human health effects comes from case studies of two research scientists who were both overcome in their laboratory in 1993. To this day, they complain of on-going difficulties such as adverse effects on their cognitive abilities, particularly after exercising.
      In rats, studies have shown that the toxin appeared to slow learning but did not affect memory.
     There has been renewed interest in the past few years in tricholthecene mycotoxins produced by toxic black mold for use in biological weapons. These toxins are extremely poisonous and difficult to destroy. There are over 60 types of trichothecene mycotoxins. It is produced by a number of molds including the mold Stachybotrys chartarum ('black mold') but also by other species such as Fusarium which grows on grains such as maize, oats and wheat.
Toxic Black Mold

     The ravages of toxic black mold have been recorded in the Bible (chapter 14 of the Book of Leviticus) where it was recommended that if toxic black mold was found on a stone within a house, the stone was to be removed and taken outside of the city. All who had lived or had eaten in the house had to wash themselves and if the mold appeared on more stones in the house after this, then the house was to be destroyed and the stones taken outside of city limits.
     The Czech mycologist August Carl Joseph Corda originally described toxic black mold in 1837 after he had found the mold growing on a wall of a house in Prague. In the 1930s and 1940s, farm animals in Eastern Europe mysteriously began to die from a strange new disease with symptoms of bleeding, immune system suppression, infection, nervous system disorder and shock. The illness was caused by toxic black mold, growing on the animal's wet hay and feed.

August Carl Joseph Corda
     The first reports of humans, affected by toxic black mold were in Russia in the 1940s. Farm workers who were in contact with grain infested with the mold became sick with symptoms including skin irritation, bleeding, inflammation of the airways, fever and fatigue.
     In Chicago, in 1986, a family had been living in a home for five years with toxic black mold growing inside and had on-going symptoms of skin and throat irritation, headaches, sickness, flu and cold symptoms, diarrhea and tiredness (sick building syndrome). The mold was found growing on building materials in the home and on some organic materials. Trichothecenes were also found in the air.
     In 1993-1994, 30 infants developed pulmonary hemorrhage in Cleveland, Ohio after their homes were flooded. Several of the infants died from the lung disease.
     It is estimated that over 500 000 people in America die each year because of toxic black mold.
     Trichothecene mycotoxin poisoning is disabling with symptoms of dry eyes, diarrhea, abdominal pain, bleeding, rash, mental impairment and fatigue.
Fusarium Graminearum
(Mycotoxin-Producing) Mold on Grain
     This type of poison is amongst the most toxic types of all mold-produced toxins. The lethal dose may be as little as 1 to 7 mg/kg depending on the specific type of trichothecene.
     These mycotoxins can remain toxic for years in a normal environment, they are not soluble in water (making them difficult to wash off) and are not destroyed by ultraviolet. Trichothecenes can withstand freezing and, in order to be destroyed, require elevated temperatures of 500 degrees Fahrenheit for 30 minutes or a solution of 5% sodium hydrochlorite (bleach).
     The only difference between the mycotoxins used in biological weapons and the mycotoxins found in homes infested with toxic mold is the concentration level. T-2 trichothecene mycotoxins are the only mycotoxins that have been used in biological weapons. Several countries have grown toxic mold to harvest concentrated T-2 mycotoxins for biological weapons. This T-2 variety can be produced easily and cheaply and is extremely toxic with no antidote or vaccine available.  These toxins are also the only substances used in biological warfare that can be absorbed through the skin.
Yellow Rain Biological Attack or 'Bee Droppings'?

     The United States military is reportedly doing 90% of its current biological weapons research in T-2 mycotoxins. The Yellow Rain biological attacks used in Vietnam and Afghanistan were concentrated T-2 mycotoxins and Gulf War syndrome is believed, by some, to be caused by American soldiers' exposure to T-2 mycotoxins during biological attacks in Desert Storm.
     During the Vietnam War, concentrated T-2 trichothecene mycotoxins were released (by the Russians?) over remote jungle areas in Laos. This caused over 6300 deaths between 1975 and 1981. These biological attacks were called Yellow Rain because of the descriptions of a yellow oily liquid being released from low flying aircraft.
     Yellow Rain attacks also occurred in Kampuchea (Cambodia) during 1979 to 1981 leading to over 1000 deaths and were used by the Soviet Union in Afghanistan from 1979 to 1981 resulting in over 3000 deaths.
     During the Gulf War in 1991, Iraq allegedly used biological weapons containing T-2 mycotoxins against American soldiers and after an Iraqi missile was detonated over an American military base in Saudi Arabia, the American soldiers reported symptoms highly suggestive of trichothecene mycotoxins exposure. It is thought by some researchers that Gulf War Syndrome may be partly caused by exposure to T-2 mycotoxins. This same toxin was also by Iraq used against Iran in the Iran-Iraq War (1980-1988).
     But for many military people, wanting to be 'ahead of the enemy', using human micro-organisms or animal cross-over microbes is not enough. Poisoning the enemy or their food supply or even using toxins - poisons created by Mother Nature's Toxic Warehouse, made by nature, straight and 'simple' - still may not allow military superiority. And that is why some scientists and politicians search for ways to 'improve' on nature's existing deadly designs.
   
     * Toxins as Biological Weapons: subject of research for the novel Vaccine - Amazon Kindle.

1 comment: