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Snakebite can kill over 100,000 people each year and is considered one of the world's deadliest neglected health issues. But what does venom actually do to you?
Venom is thought to have evolved independently at least 100 times. Today there are thousands of venomous animals thriving around the world and over time their venoms have evolved to do specific jobs in the animals they envenomate.
Discover what snake venom does, why some species have incredibly potent venom, and why speed is so important when treating snakebite.
Lots of animals use venom for predation, killing or immobilising their prey before eating it. It is also commonly used for defence, serving would-be predators with a painful and memorable warning.
There are about 700 species of front-fanged venomous snakes, almost all of which belong to the families Viperidae and Elapidae. There are an additional 1,800 rear-fanged species which belong to the family Colubridae. Many of these are likely to be venomous too, though this group generally poses less of a threat to humans, with a few exceptions.
Almost all snakes evolved venom to help them hunt but some will also use it defend themselves.
There are several other less common uses for venom. For example, male platypuses use their venomous spurs against their competition in the breeding season, tawny crazy ants use theirs as an antidote to the venom of fire ants and some species, such as shrews, are thought to use their venom to preserve food.
Two groups of venomous snakes are particularly well known: vipers (Viperidae) and elapids (Elapidae). Broadly speaking, the venoms in these two groups do different things to a bite victim.
Vipers, which includes adders and rattlesnakes, have venoms that are generally haemotoxic. This means they attack the circulatory system. They can cause bleeding or interfere with the blood's ability to clot.
Many famously venomous snakes are elapids, such as cobras, mambas, kraits and taipans. Their venom is typically neurotoxic, which means that it interferes with the transmission of nerve impulses. It generally has an immobilising effect, either making a victim's body turn rigid or become limp.
Neurotoxicity and haemotoxicity are not the only effects venoms can have, nor are they mutually exclusive.
Taipans, for example, have immobilising neurotoxic venom which also has very fast-acting blood clotting abilities.
Rattlesnakes can cause horrible bleeding, but their venom is also cytotoxic (tissue destructive) and can cause wounds and necrosis. Some rattlesnake venom also has neurotoxic properties.
Venoms may also have other notable abilities when they contain myotoxins (skeletal muscle destroying), cardiotoxins (which specifically affect the heart) or sarafotoxins (blood vessel constricting) for example.
Karl P Schmidt was an American herpetologist (amphibian and reptile expert) who was fatally bitten by a boomslang (Dispholidus typus) in 1957.
Boomslangs are highly venomous snakes found in Africa, but they are not in the elapid or viper family. Boomslangs are part of Colubridae and are a rear-fanged species, meaning their venom delivering teeth are at the back of the mouth.
Schmidt kept a detailed diary of his symptoms, from a bite to the fleshy part of his thumb to the hours leading up to his death. He reported a fever, violent nausea, vomiting, pain and bleeding from the gums, nose and bowels and a variety of other side effects.
He died within 24 hours and an autopsy revealed extensive internal bleeding.
A group of components at work in boomslang venom are snake venom metalloproteinases (SVMPs).
Ronald Jenner, a venom researcher at the Museum, explains, 'These are enzymes. They are a broad family of toxins that have all evolved to do different things, but they all interact in bad ways with the blood-clotting system and the integrity of blood vessels.'
SVMPs are also particularly present in viper venoms. They can destroy the outer membrane of capillary vessels, causing internal bleeding. In some cases they can also activate the blood clotting system, causing clots around the circulatory system. These have the ability to block blood vessels and induce a stroke or heart attack.
'If they don't do that and you get a good biteful of these blood-activating toxins, they will use up your blood clotting factors, and if that happens you have a big problem. It basically means that your blood can't clot,' says Ronald.
With the damage these toxins can do to the integrity of blood vessels and their over-stimulation of the clotting system, SVMPs can result in uncontrollable internal bleeding that is ultimately fatal.
A bite from a venomous snake isn't always deadly for people. The effects of some species' bites can be quite mild. But several snakes are household names thanks to their ultra-powerful venoms.
Black mambas (Dendroaspis polylepis) and inland taipans (Oxyuranus microlepidotus) often top lists of the world's most venomous snakes. But their venoms may seem like overkill as their diets are primarily small mammals and birds. So why are they so strong?
'It needs to be quick,' explains Ronald.
'If it takes half an hour for pain to kick in, a predator could still eat the snake. When they use it for predation, they don't want to give their prey time to escape. In terms of athletic ability, a snake is no match for a bird, for example.
'Some mambas have venom that delivers a one-two punch. First it quickly makes the prey go rigid, then slower acting neurotoxins completely destroy nerve impulse transmission and the prey goes from rigid to floppy.'
The need for speed is similar for taipans. It's often noted that these snakes could kill thousands of mice with a single bite, but their venom didn't evolve for this purpose. Instead, their sledgehammer-like venom is for quickly taking down feisty prey like bandicoots that could cause the snake harm if they had a chance to fight back.
Administering antivenom can be vital for the survival of a bite victim. Antivenom binds to the components of a venom and obstructs them, preventing them from reaching their target. It doesn't reverse the effects of venom but prevents further damage being done by filtering out unused toxins.
Getting medical assistance as fast as possible is crucial if you are bitten by a venomous snake. If there is a prolonged window before antivenom is received, any damage caused in that time will need additional treatments.
Antivenom does come with some risk, however. It's made by injecting an animal, such as a horse, with dilute venom to promote the production of antibodies. These are extracted and used to treat envenomation in humans. However, the non-human origin of these antibodies means that injecting them into a human patient comes with a heightened risk of allergic reaction, anaphylactic shock and even death. The less you need to inject to neutralise the venom, the better.
There are two types of antivenom: monovalent and polyvalent.
Monovalent antivenoms are formulated to work on the venom of one species. But the effectiveness of it relies on being absolutely certain of the identity of the snake responsible for a bite. Even closely related snakes can have venoms that are drastically different from one another. Venoms of a single species may even differ based on the region they live in. This has been seen in the monocled cobra (Naja kaouthia), for instance.
'If someone arrives at a hospital and says, "a small, brown thing bit me", that's not very specific. If you only have monovalent antivenoms, it's going to be a Russian roulette of which one to use,' explains Ronald.
Polyvalent antivenoms, however, are formulated to work on the venoms of multiple snake species. But as the components for targeting the toxin cocktail of a species in these antivenoms are diluted by the presence of those that would work on other species' venoms, more vials may be needed, raising the risk for a patient.
Between 81,000-138,000 people die from snakebite each year. Many more survive but may do so with lasting disabilities or disfigurement.
Most snake bites occur in low-income areas in Africa, Asia and Latin America, with agricultural workers and children most often affected. For many of those who need it, lifesaving antivenoms can be physically and financially out of reach.
Treating snakebite can reportedly cost over $500 (£368). This can be an impossible price, especially in areas where people earn less than £1 a day.
Medical facilities in some areas may also be too far away or be limited in the help they can provide. Some may lack the refrigeration facilities needed for storing most antivenoms, for example.
Despite the high number of snakebites, which are also known to be underreported in some areas, low demand has meant that several companies have ceased production of important antivenoms and prices have risen.
In 2017, the World Health Organisation designated snakebite as a highest priority neglected tropical disease. It has since set a target to reach a 50% reduction in snakebite mortality and morbidity by 2030.
While animals evolved venom to help them survive, people have co-opted it for their own ends throughout history.
With today's ability to focus in on specific components of a venom, there are some that can be isolated and used to heal rather than harm. For example, a hormone-like peptide in Gila monster saliva was used to develop treatments for diabetes.
Some snake venoms also have medicinal applications. For example, synthesised jararaca (Bothrops jararaca) venom is used in Captopril, which treats hypertension and congestive heart failure, and saw-scaled vipers (Echis carinatus) have contributed to the blood-clotting inhibitor Tirofiban.
Very few snake venoms have been approved for use in pharmaceutical drugs so far. But these complex toxin cocktails are expansive 'bio-libraries' and there may yet be many more components that are found to be of use to people in the future.
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