Briefly toxins or biotoxins are
substances produced by one organism that have a toxic action on
another organism. Toxins are extremely poisonous products of the
metabolism of living organisms including bacteria, plants, animals, and
fungi. Biotoxins are biologically active chemical compounds produced by
a specific chemical mechanism in a living organism. Chemically, they are
a wide variety of complex structures including proteins, cyclic
peptides, alkaloids, etc. In some cases after the structure of a toxin
is known, they can be prepared by chemical synthesis. Some toxins can
also be prepared by biotechnological techniques similar to those used in
the production of some drugs. There are several differences between
toxins and traditional chemical warfare agents. When compared, toxins
generally have a higher molecular weight, most of them are odourless and
not dermally active, and most of them produce immune responses in the
host. Toxins are easy to use via the inhalation route in the form of
aerosols. Their toxicity potential is much higher than highly toxic
chemical agents like sarin. As a comparison, the lethal inhalation
concentration (LCt50) of a botulinum toxin aerosol, on average, is 1000
times more toxic than sarin vapor. Toxins from plants, animals,
bacteria, cyanobacteria, algae, and fungi have potential as CW agents.
Some toxins, such as ricin (W), botulinum toxin (X), or saxitoxin (TZ),
have been weaponised. Intensive military research activity was carried
out on other toxins including palytoxin, batrachotoxin, and
tetrodotoxin.
Clostridium
botulinum produces eight antigenically distinguishable
exotoxins (A, B, C1, C2, D, E, F and G). Type A is the most potent,
followed by types B and F. Types A, B and E are commonly associated with
systemic botulism in humans. Botulinum toxins are neurotoxic. Ingestion
of toxin is characterized by descending, flaccid paralysis that can
cause respiratory failure. Early symptoms include marked fatigue,
weakness and vertigo, usually followed by blurred vision, dry mouth and
difficulty in swallowing and speaking. Vomiting, diarrhoea, constipation
and abdominal swelling may also occur. The disease can progress to
weakness in the neck and arms, after which the respiratory muscles and
muscles of the lower body are affected. There is no fever and no loss of
consciousness. Symptoms usually appear within 12 to 36 hours (within a
minimum and maximum range of 4 hours to 8 days) after exposure. By
inhalation botulism exhibits a similar clinical footprint to ingestion
botulism. The median lethal dose for humans has been estimated at 2
nanograms (0.000000002grams or 7.054788000000001×10-11
Ounces) of botulinum toxin per kilogram of bodyweight, which is
approximately 3 times greater than in ingestion cases. Following
inhalation of the toxin, symptoms become visible between 1 to 3 days,
with longer onset times for lower levels of intoxication. Symptoms
proceed in a similar manner to ingestion of botulinum toxin and
culminate in muscular paralysis and respiratory failure.
Staphylococcal enterotoxin B
is an exotoxin produced by Staphylococcus
aureus. SEB is a superantigen; it acts by stimulating
cytokine release and inflammation. Staphylococcal enterotoxin B is toxic
by inhalation and ingestion. In a biological attack, it could be
administered in food, water or as an aerosol. Symptoms include
nonspecific flu-like symptoms, including fever, chills, headache,
myalgia and varying degrees of prostration. Additional symptoms are
specific to the route of exposure. Ingestion results in gastrointestinal
signs; nausea, vomiting and diarrhea may occur. Inhalation causes
respiratory signs, including a nonproductive cough, chest pain and
dyspnea. In severe cases, there may be pulmonary oedema and respiratory
failure. Gastrointestinal signs may also be seen after an aerosol
exposure, as the toxin is swallowed during mucociliary clearance. SEB
can cause toxic shock syndrome when it occurs systemically, or erythema
and induration after skin contact.
The term saxitoxin originates from the
genus name of the butter clam (Saxidomus
catanella) from which it was first isolated. But the term
saxitoxin can also refer to the entire suite of more than 50
structurally related neurotoxins (known collectively as "saxitoxins")
produced by algae and cyanobacteria which includes saxitoxin itself
(STX), neosaxitoxin (NSTX), gonyautoxins (GTX) and decarbamoylsaxitoxin
(dcSTX). Ingestion of saxitoxin can cause numbness of the oral
mucosa as quickly as 30 minutes after exposure. In severe poisoning,
illness typically progresses rapidly and may include gastrointestinal
(nausea, vomiting) and neurological (cranial nerve dysfunction, a
floating sensation, headache, muscle weakness, parasthesias and vertigo)
signs and symptoms. Respiratory failure and death can occur from
paralysis.
A toxin found in the seeds of the
castor bean Ricinus
communis (previously Castor ricinus). The major
symptoms of ricin poisoning depend on the route of exposure and the dose
received, though many organs may be affected in severe cases. Initial
symptoms of ricin poisoning by inhalation may occur as early as 4 to 8
hours and as late as 24 hours after exposure. Within a few hours of
inhaling significant amounts of ricin, the likely symptoms would be
respiratory distress, fever, cough, nausea, and tightness in the chest.
Heavy sweating may follow as well as pulmonary edema. This would make
breathing even more difficult, and the skin might turn blue. Finally,
low blood pressure and respiratory failure may occur, leading to death.
Ingestion: following ingestion of ricin, initial symptoms typically
occur in less than 10 hours. Swallowing a significant amount of ricin,
the victim would likely develop vomiting and diarrhea that may become
bloody. Severe dehydration may be the result, followed by low blood
pressure. Other signs or symptoms may include seizures, and blood in the
urine. Within several days, the person's liver, spleen, and kidneys
might stop working, and the person could die. Skin and eye exposure:
Ricin is unlikely to be absorbed through normal skin. Contact with ricin
powders or products may cause redness and pain of the skin and the eyes.
Death from ricin poisoning could take place within 36 to 72 hours of
exposure, depending on the route of exposure (inhalation, ingestion, or
injection) and the dose received.
A toxin that is found in the seeds of a
plant called the rosary pea or jequirity pea Abrus
precatorius. The median toxic dose for humans ranges
from 10 to 1000 micrograms per kilogram when ingested and is 3.3
micrograms per kilogram when inhaled. The major symptoms of abrin
poisoning depend on the route of exposure and the dose received, though
many organs may be affected in severe cases. In general, symptoms can
appear anywhere between several hours to several days after exposure.
Initial symptoms of abrin poisoning by inhalation may occur within 8
hours of exposure but a more typical time course is 18 to 24 hours; they
can prove fatal within 36 to 72 hours. Following ingestion of abrin,
initial symptoms usually occur rapidly, but can take up to five days to
appear. The later signs and symptoms of exposure are caused by
abrin's cytotoxic effects, killing cells in the kidney, liver, adrenal
glands, and central nervous system. Inhalation: within a few hours of
inhaling abrin, common symptoms include fever, cough, airway irritation,
chest tightness, pulmonary oedema, dyspnea and cyanosis, and
nausea. Blood pressure may drop dramatically, keeping oxygen from
reaching the brain and other vital organs causing shock, and respiratory
failure may occur, which can be fatal within 36 to 72 hours. Ingestion:
ingesting any amount of abrin can lead to severe symptoms. Early
symptoms include nausea, vomiting, pain in the mouth, throat, and
esophagus, diarrhea, dysphagia, and abdominal cramps and pain. As the
symptoms progress, bleeding and inflammation begins in the
gastrointestinal tract. The affected person can vomit up blood
(haematemesis), have blood in their faeces, which creates a black, tarry
stool called melena, and more internal bleeding. Loss of blood volume
and water from nausea, vomiting, diarrhea, and bleeding causes blood
pressure to drop and organ damage to begin, which can be seen as the
person begins to have somnolence/drowsiness, hematuria, stupor,
convulsions, polydipsia, and oliguria. This ultimately results in
multi-system organ failure, hypovolemic shock, vascular collapse, and
death. Abrin can be absorbed through broken skin or absorbed
through the skin if dissolved in certain solvents. It can also be
injected in small pellets and absorbed through contact with the eyes.
Abrin in the powder or mist form can cause redness and pain in the eyes
(i.e. conjunctivitis) in small doses. Small doses absorbed through the
eyes can also cause tearing (lachrymation). Higher doses can cause
tissue damage, severe bleeding at the back of the eye (retinal
hemorrhage), and vision impairment or blindness. A large enough dose can
be absorbed into the bloodstream and lead to systemic toxicity.
Anatoxin
A [VFDF - Very Fast Death Factor, Antx-A, Anatoxin I,
Anatoxin-a] - C10H15NO
