Why Are Some Animals Venomous?

A physical struggle with prey is risky. A bite that can kill without a fight lets a small animal take prey it could never overpower, and lets a slow animal avoid being injured.

The same applies defensively. A creature with no speed or armour can still make itself extremely unprofitable to attack. Both uses explain why venom appears in animals as different as snakes, spiders, jellyfish, cone snails, shrews and the male platypus.

The distinction is about delivery. Venom is injected through a wound using fangs, stingers, spines or barbs. Poison is absorbed or ingested, so it harms whatever eats or touches the animal.

A rattlesnake is venomous. A poison dart frog is poisonous. Some species are both, and a few snakes are technically neither despite being widely believed dangerous. The useful rule is that if it bites you and you get ill it is venomous, and if you bite it and you get ill it is poisonous.

Venoms are complex mixtures, often containing dozens of proteins and peptides, and they generally target one of a few systems:

• •Neurotoxins, which block nerve signals and cause paralysis
• •Haemotoxins, which affect blood clotting and damage vessels
• •Cytotoxins, which destroy tissue around the bite
• •Enzymes that break tissue down, sometimes beginning digestion

Venom systems have arisen independently in many lineages, a pattern called convergent evolution. Frequently the raw material was a gene for an ordinary protein, often a digestive enzyme, duplicated and then modified into something more damaging.

This is a common route in evolution. A copy of an existing gene is free to change without breaking the original function, which is why venom components so often look like modified versions of everyday body proteins.

Because venom molecules target specific receptors with high precision, they are a valuable source of drug leads. Several approved medicines derive from them.

Examples include a blood pressure drug developed from a Brazilian pit viper peptide, a diabetes treatment based on a compound from Gila monster saliva, and a powerful painkiller derived from cone snail venom. Researchers continue to screen venoms for compounds that act on pain, clotting and cancer pathways.

Most traditional first aid for snakebite is actively harmful, and the list of things not to do is longer than the list of things to do.

Current medical guidance is straightforward:

• •Get to medical care as quickly as possible, since antivenom is the treatment
• •Keep the person calm and the bitten limb still and below heart level
• •Remove rings and watches before swelling starts
• •Do not cut the wound, suck out venom, apply a tourniquet or use ice
• •Note the appearance of the animal if it can be done safely, but do not chase it

Venom is not free. It is built from complex proteins, and replacing a full supply can take days and a real share of an animal's energy. Many venomous animals therefore use it sparingly. Snakes can deliver a dry bite, one with little or no venom, especially when biting defensively rather than hunting. Some scorpions appear to use a milder first secretion before a more potent one, and many venomous animals rely on warnings such as rattles, hissing or bright colours first.

Antivenom is made by exploiting the immune system. Small, safe doses of venom are given to an animal, usually a horse or sheep, which produces antibodies against it. The antibodies are collected from its blood, purified and given to bitten patients, where they bind to the venom and neutralise it. Because venoms differ between species and even between regions, antivenoms are often specific, which is one reason identifying the animal can help doctors.

Where venom exists, resistance tends to evolve in the animals that face it most often. The mongoose is the classic case. Cobra venom contains neurotoxins that bind to receptors on muscles, the same receptors that normally receive signals from nerves. In mongooses a few small changes in the shape of that receptor stop the toxin attaching, while the nerve signal still works. Honey badgers and some hedgehogs carry similar changes, which helps explain why these animals can tackle venomous snakes that would kill many other mammals of their size.

Resistance can also track a particular enemy. Some populations of California ground squirrels have blood proteins that neutralise the venom of the local rattlesnakes, and the level of protection varies between areas in step with the snakes they face. The snakes, in turn, show signs of venom evolving to overcome that defence, a back and forth known as an evolutionary arms race. Venomous animals also need protection from their own weapons, which they gain through resistant receptors, tightly sealed venom glands, or both.

Venom strength is usually compared using a measure called the LD50, the dose that kills half of a group of test animals, often mice, expressed per kilogram of body weight. By that measure the inland taipan of central Australia has the most potent venom of any land snake. Yet very few people have ever died from its bite. It lives in remote, thinly populated country, it is generally shy, and bites are rare. LD50 figures also depend on the test animal. Some venoms are tuned to particular prey, such as birds or lizards, and may be weaker against mice than against the animals the snake actually eats.

The snakes that kill the most people are those that live close to them. The World Health Organization estimates that snakebite kills tens of thousands of people every year, mostly in rural farming communities in South Asia and sub-Saharan Africa, and leaves many more with lasting disabilities. In India, a group known as the big four, the Indian cobra, common krait, Russell's viper and saw-scaled viper, causes most serious bites. These species are common in fields and villages, bites often happen during farm work, at night or to bare feet, and treatment may be hours away. Danger depends on behaviour, habitat and access to antivenom, not toxicity alone.

For decades, the Komodo dragon was said to kill large prey with a mouth full of deadly bacteria, so that a bitten deer or buffalo slowly died of infection. In 2009 researchers using medical scans and chemical analysis reported venom glands in the lizard's lower jaw, producing toxins that lower blood pressure and stop blood from clotting. Later studies found that the bacteria in Komodo mouths were broadly similar to those of other meat-eating animals. Scientists still debate how much the venom contributes compared with the deep wounds from the lizard's serrated teeth, but the old infection story has largely been abandoned.

Slow lorises, small nocturnal primates from South and South East Asia, are the only primates known to be venomous. They have a gland on the inner side of each upper arm. When threatened, a loris raises its arms, licks the gland and mixes the secretion with its saliva, then delivers a painful bite with its sharp front teeth. Bites to people have caused severe swelling and, rarely, dangerous allergic shock. Researchers think lorises use the venom mainly in fights with rival lorises, and perhaps against predators and parasites, a reminder that venom in mammals is rarer and stranger than in reptiles.

Venom evolved repeatedly because injecting a chemical is a low risk way to hunt or defend, it is distinguished from poison by being delivered through a wound, and its precision has made it a genuine source of modern medicines.