10 Venenos mortais do Mundo

10 Deadliest Poisons in the World
Poison of any kind, be it chemical, food borne or naturally occurring, has been the subject of everything from the news to chemical warfare and even been the antagonist for plenty of mystery writers in their works of fiction. There are hundreds of deadly poisons known to man; many of which have been used nefariously to commit murder, genocide and acts of terrorism. Some of those poisons are on this list; shockingly others, used to such devastating effect, are not. Whether these poisons were produced synthetically for purposes other than causing death, whether they occur naturally in the plants and animals of the world, or whether they are a by product of some other lab experiment, one thing is certain; they will all kill you, and they will all kill you in painful, horrific ways.

10. Cyanide

A well-known toxin, Cyanide is a deadly poison that affects the central nervous system (CNS) as well as the heart. Even if a small dose of cyanide enters the body, the poison will attack the blood stream and bind to the iron in the blood, thus prohibiting oxygen to flow through the body, resulting in death in minutes. Though there are different forms of Cyanide, Hydrogen Cyanide, is by far the deadliest of them. Considered a chemical weapon as a gas, Hydrogen Cyanide is incredibly deadly, killing a human in less than ten minutes. In fact, the poison was used as such to devastating effect during the First World War, before chemical weapons were banned under the Geneva Convention. Today, Cyanide is predominantly used as a method of murder, suicide, or as a plot device in fiction.

Antidote:
Hydroxocobalamin reacts with cyanide to form cyanocobalamin, which can be safely eliminated by the kidneys. This method has the advantage of avoiding the formation of methemoglobin (see below). This antidote kit is sold under the brand name Cyanokit and was approved by the FDA in 2006.

An older cyanide antidote kit included administration of three substances: amyl nitrite pearls (administered by inhalation), sodium nitrite, and sodium thiosulfate. The goal of the antidote was to generate a large pool of ferric iron (Fe3+) to compete for cyanide with cytochrome a3 (so that cyanide will bind to the antidote rather that the enzyme). The nitrites oxidize hemoglobin to methemoglobin, which competes with cytochrome oxidase for the cyanide ion. Cyanmethemoglobin is formed and the cytochrome oxidase enzyme is restored. The major mechanism to remove the cyanide from the body is by enzymatic conversion to thiocyanate by the mitochondrial enzyme rhodanese. Thiocyanate is a relatively non-toxic molecule and is excreted by the kidneys. To accelerate this detoxification, sodium thiosulfate is administered to provide a sulfur donor for rhodanese, needed in order to produce thiocyanate.

9. Anthrax

Perhaps the most famous post 9/11 poison, Anthrax was seemingly in the media every day in the early years of the new millennium due to a series of Anthrax-infected letters that were mailed to unsuspecting victims across the United States in the weeks after 9/11. All told five people died and 17 more were injured in the Anthrax attacks, while millions more were affected by the paranoia it sparked. A new Anthrax scare arose everywhere, from major cities to small towns across the United States. The fear the poison elicited was widespread, and for good reason. Essentially a disease caused by bacteria, Anthrax must be inhaled to infect someone as it spreads by spores released into the air. After becoming infected, a minor cold will quickly turn into massive respiratory failure as the Anthrax shuts down a person’s breathing. The mortality rate from Anthrax is nearly 90% within a week of infection.

Anthrax vaccines:
Vaccines against the livestock and human disease anthrax—caused by the bacterium Bacillus anthracis—have had a prominent place in the history of medicine, from Pasteur’s pioneering 19th-century work with cattle (the first effective bacterial vaccine and the second effective vaccine ever) to the controversial late 20th century use of a modern product to protect American troops against the use of anthrax in biological warfare. Human anthrax vaccines were developed by the Soviet Union in the late 1930s and in the US and UK in the 1950s. The current vaccine approved by the U.S. Food and Drug Administration (FDA) was formulated in the 1960s.

Currently administered human anthrax vaccines include acellular (USA, UK) and live spore (Russia) varieties. All currently used anthrax vaccines show considerable local and general reactogenicity (erythema, induration, soreness, fever) and serious adverse reactions occur in about 1% of recipients. New third-generation vaccines being researched include recombinant live vaccines and recombinant sub-unit vaccines

8. Sarin

Considered a weapon of mass destruction, and rightfully so, the nerve gas Sarin will kill you in an agonizing way. From a tight chest to complete suffocation before your body shuts down, Sarin does its handiwork on the human body in an interminably long 60 seconds. That is all it can take; a meagre minute, a single, torturous minute to die. Though Sarin production as a weapon has been outlawed since 1993, there have been many instances since where the poison has been used in terrorist attacks or chemical warfare, particularly during the Tokyo Subway attack in 1995, and the insurgencies in Iraq and Syria, the latter where the chemical agent was employed on civilians killing anywhere from 330 and 1,800 people.

7. Amatoxin

Amatoxin is a type of poison found in the world’s deadliest mushrooms. You know, the one’s they tell you not to eat when camping. The poison is extremely volatile; if ingested the Amatoxin enters the blood stream and makes a beeline for the liver or the kidney, resulting in extreme illness as the poison attacks the cells of the organ, shutting them down over a matter of days. Amatoxins can attack the heart as well; a sure bet that without proper treatment, usually consisting of high amounts of Penicillin, those who have ingested the poison will fall into a coma within days, and ultimately die of heart or liver failure.

Treatment:
Treatment involves high dose penicillin as well as supportive care in cases of hepatic and renal injury. Silibinin, a product found in milk thistle, is a potential antidote to amatoxin poisoning, although more data needs to be collected. Cautious attention is given to maintaining hemodynamic stability, although if hepatorenal syndrome has developed the prognosis is guarded at best.

6. Strychnine

Used as a pesticide meant to kill small animals, Strychnine is one of the deadliest poisons on earth. Though found naturally in certain trees in Asia, Strychnine is also created synthetically in labs (ironically winning a Nobel Prize for the first successful attempt). The poison can infect a person in a myriad of ways, whether through ingestion, inhalation, or absorption. Upon entering the body, within a few minutes the muscles begin contracting, while nausea and vomiting overwhelm the victim. As more and more muscles in the body begin to convulse and spasm, they lead to asphyxiation. The entire lethal process from ingestion to death takes roughly a half an hour.

Treatment:
There is no specific antidote for strychnine but recovery from strychnine exposure is possible with early hospital treatment. Treatment consists of removing the drug from the body (decontamination) and getting supportive medical care in a hospital setting. Supportive care includes intravenous fluids, medications against convulsions and spasms, and cooling measures for high temperature. The patient should be kept in a quiet and darkened room, because excessive manipulation and loud noises may cause convulsions. Because these convulsions are extremely painful, an appropriate painkiller should be given. Treatment of strychnine poisoning involves an oral administration of activated charcoal which adsorbs any strychnine within the digestive tract. Unabsorbed strychnine can be removed from the stomach by gastric lavage with tannic acid or potassium permanganate solutions to oxidize strychnine. Seizures are controlled by anticonvulsants, such as phenobarbital or diazepam, along with muscle relaxants such as dantrolene to combat muscle rigidity. Chloroform or heavy doses of chloral, bromide, urethane or amyl nitrate can also be used to restrain the convulsions. Because diazepam, as the anticonvulsant of choice, is not effective in all cases, a combination with midazolam, fentanyl, or pancuronium is recommended for controlling the convulsions. Strychnine poisoning demands an aggressive management with early intubation, control of muscle tremors, and prevention of rhabdomyolysis and renal failure. If the patient survives the first 24 hours after poisoning then recovery is probable. Also, George Harley (1829–1896) showed in 1850 that Curare (wourali) was effective for the treatment of tetanus and strychnine poisoning.

5. Mercury

Remember in science class when the teacher implored you not to break the thermometer? Well, for good reason. A heavy metal, Mercury is incredibly toxic to the human body when touched or inhaled. Had you or any of your classmates broken that thermometer and gotten some of the Mercury on your body, your skin would have started itching, burning and even peeling off within minutes. If ingested or inhaled, Mercury is altogether even more unpleasant, causing memory loss, loss of vision, kidney failure and brain damage. Eventually Mercury poisoning will shut down the CNS and result in death.

Treatment:
Research on the treatment of mercury poisoning is limited. Currently available drugs for acute mercurial poisoning include chelators N-acetyl-D, L-penicillamine (NAP), British Anti-Lewisite (BAL), 2,3-dimercapto-1-propanesulfonic acid (DMPS), and dimercaptosuccinic acid (DMSA). In one small study including 11 construction workers exposed to elemental mercury, patients were treated with DMSA and NAP. Chelation therapy with both drugs resulted in the mobilization of a small fraction of the total estimated body mercury. DMSA was able to increase the excretion of mercury to a greater extent than NAP.

4. Tetrodotoxin

The infamous poison that dwells deep within the puffer fish, that many sushi connoisseurs pay a premium to eat in hopes it is prepared correctly, and the poison that almost killed Homer Simpson, Tetrodotoxin is lethal. Symptoms, of which there are a multitude, usually occur 30 minutes after consuming the poison. First, your mouth will become paralyzed; next swallowing will become a chore. Soon, your coordination and speech will become disabled. Following that, seizures and convulsions may set in, eventually leading to coma and death. Death most commonly occurs after about 6 hours, but Tetrodotoxin has been known to kill within 17 minutes, clearly making it one of the deadliest poisons on earth.

Symptoms and treatment:
The diagnosis of pufferfish poisoning is based on the observed symptomology and recent dietary history.

Symptoms typically develop within 30 minutes of ingestion, but may be delayed by up to four hours; however, death once occurred within 17 minutes of ingestion. Paresthesia of the lips and tongue is followed by hypersalivation, sweating, headache, weakness, lethargy, incoordination, tremor, paralysis, cyanosis, aphonia, dysphagia, seizures, dyspnea, bronchorrhea, bronchospasm, respiratory failure, coma, and hypotension. Gastroenteric symptoms are often severe and include nausea, vomiting, diarrhea, and abdominal pain. Cardiac arrhythmias may precede complete respiratory failure and cardiovascular collapse.

The first symptom of intoxication is a slight numbness of the lips and tongue, appearing between 20 minutes and three hours after eating poisonous pufferfish. The next symptom is increasing paresthesia in the face and extremities, which may be followed by sensations of lightness or floating. Headache, epigastric pain, nausea, diarrhea, and/or vomiting may occur. Occasionally, some reeling or difficulty in walking may occur. The second stage of the intoxication is increasing paralysis. Many victims are unable to move; even sitting may be difficult. There is increasing respiratory distress. Speech is affected, and the victim usually exhibits dyspnea, cyanosis, and hypotension. Paralysis increases, and convulsions, mental impairment, and cardiac arrhythmia may occur. The victim, although completely paralyzed, may be conscious and in some cases completely lucid until shortly before death. Death usually occurs within 4 to 6 hours, with a known 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.

Therapy is supportive and based on symptoms, with aggressive early airway management. If ingested, treatment can consist of emptying the stomach, feeding the victim activated charcoal to bind the toxin, and taking standard life-support measures to keep the victim alive until the effect of the poison has worn off. Alpha adrenergic agonists are recommended in addition to intravenous fluids to combat hypotension. Anticholinesterase agents have been used with mixed success. No antidote has been developed and approved for human use; but a monoclonal antibody specific to tetrodotoxin has been developed by USAMRIID and was shown to be effective for reducing lethality in tests on mice.

3. Ricin

Ricin has become the new poison of choice when mailing toxic letters, supplanting Anthrax with that dubious distinction. While the fervour surrounding such events may venture into the land of paranoia in the general public sometimes, the serious precautions taken by law enforcement with Ricin are wholly justified. Found in the bean of the Castor Oil Plant, Ricin is incredibly lethal, as it attacks protein production in the body, ultimately shutting it down completely. Most deadly when inhaled, hence the powdered form mail in letters, a quantity no larger than a sprinkle of table salt can kill. Knowing all this, it is no wonder Ricin has been studied as an option for chemical warfare by everyone from the United States military to Al-Qaeda.

2. VX  (nerve agent)
The most dangerous nerve gas on the planet, this former pesticide became a prime target for militaries across the globe to stockpile, despite its label as a banned weapon of mass destruction. There truly is no use for VX other than as a chemical agent in war. So toxic is VX that one drop of the poison coming into contact with exposed skin will kill a human. Inhalation being the most common form of exposure, symptoms from VX poisoning will range from flu-like symptoms with mild exposure to paralysis and full respiratory failure leading to death when exposed to a lethal dose.

Treatment:
Primary consideration should be given to removal of the liquid agent from the skin before removal of the individual to an uncontaminated area or atmosphere. After removal from the contaminated area, the casualty will be decontaminated by washing the contaminated areas with household bleach and flushing with clean water. After decontamination, the contaminated clothing is removed and skin contamination washed away. If possible, decontamination is completed before the casualty is taken for further medical treatment.

An individual who has received a known nerve-agent exposure or who exhibits definite signs or symptoms of nerve-agent exposure should immediately have the nerve agent antidote drugs atropine and pralidoxime (2-PAM), and a sedative/antiepileptic such as diazepam injected. In several nations the nerve agent antidotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK.

Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the buildup of acetylcholine produced by loss of the acetylcholinesterase function can no longer affect their target.

VX (and other organophosphates) block the enzymatic activity of acetylcholinesterase (AChE) by binding to the active site of the enzyme. The phosphate group on VX is then transferred from VX to AChE, inactivating the enzyme and producing an inactive metabolite of VX. The injection of pralidoxime (2-PAM) removes the phosphate group from AChE, reactivating it, thereby reversing the effects of VX. If pralidoxime is not given soon enough, the inactivated enzyme will "age", resulting in a much stronger AChEW-phosphate that pralidoxime cannot reverse.

1. Botulinum Toxin

Botulinum toxin is a protein and neurotoxin produced by the bacterium Clostridium botulinum. It is the most acutely lethal toxin known, with an estimated human median lethal dose (LD-50) of 1.3–2.1 ng/kg intravenously or intramuscularly and 10–13 ng/kg when inhaled.
The deadliest poison on earth, a single cap full of Botulinum Toxin could potentially kill hundreds of thousands of people if let loose on the world by causing botulism, a disease that can shut down the CNS. Ironically enough however, Botulinum Toxin has many practical applications in everything from Botox treatment, to the treatment of migraines. That said, even some Botox patients have died as a result of their procedures involving Botulinum Toxin. Mortality rates in poisoning from Botulinum Toxin hover around 50% in untreated patients, while the remainder of those treated may suffer debilitating complications from their illness for years after treatment. Due to its volatile and readily available nature, Botulinum Toxin is the deadliest poison in the world.

Treatment of botulinum poisoning:
If the symptoms of botulism are diagnosed early, an equine antitoxin, use of enemas, and extracorporeal removal of the gut contents can be used to treat the food-borne illness. Wound infections can be treated surgically. Information regarding methods of safe canning, and public education about the disease are methods of prevention. Tests to detect botulism include a brain scan, a nerve conduction test, and a tensilon test for myasthenia gravis to differentiate botulism from other diseases that manifest in the same way. Electromyography can be used to differentiate myasthenia gravis and Guillain-Barré syndrome, diseases that botulism often mimics. Toxicity testing of serum specimens, wound tissue cultures, and toxicity testing, and stool specimen cultures are the best methods for identifying botulism. Laboratory tests of the patient's serum or stool, which are then injected into mice, are also indicative of botulism. The faster way to detect botulinum toxin in people, however, is using the mass spectrometer technology, because it reduces testing time to three or four hours and at the same time can identify the type of toxin present.

The case fatality rate for botulinum poisoning between 1950 and 1996 was 15.5%, down from about 60% over the previous 50 years. Death is generally secondary to respiratory failure due to paralysis of the respiratory muscles, so treatment consists of antitoxin administration and artificial ventilation until the neurotoxins are excreted or metabolised. If initiated on time, these treatments are quite effective, although antisera can not affect BoNT polypeptides that have already entered cells. Occasionally, functional recovery may take several weeks to months or more.

Two primary botulinum antitoxins are available for treatment of botulism:
Trivalent (A,B,E) botulinum antitoxin is derived from equine sources using whole antibodies (Fab and Fc portions). This antitoxin is available from the local health department via the CDC in the USA.

The second antitoxin is Heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, which is derived from "despeciated" equine IgG antibodies, which have had the Fc portion cleaved off, leaving the F(ab')2 portions. This less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated, and is available from the United States Army.

Source: http://www.therichest.com/rich-list/the-biggest/the-10-deadliest-poisons-in-the-world/

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