Planet Earth plays host to a myriad of creatures with the ability to exude, inject or release toxins. This article gives an insight into five of these fascinatingly deadly organisms and the chemical weapons with which evolution has endowed them.
Many species, such as the black widow spider or puffer fish, have achieved an impressive level of fame thanks to their deadly prowess.
However, there are many more who are yet to receive their rightful recognition. This article aims to give a handful of the more unusual noxious organisms their fair share of the limelight.
At this stage, it seems pertinent to clear up a question that exasperates entomologists, herpetologists, toxicologists and zoologists at large: what is the difference between venom and poison?
Both venomous and poisonous animals carry a chemical that is dangerous or deadly to another organism. The major difference is the way in which the toxin is shared.
A venomous animal has a dastardly delivery mechanism – fangs or a stinger, for instance – and the toxin is generally produced in the vicinity of this implement for ease of distribution.
On the other hand, poisonous animals contain a toxic substance but have no mechanism for delivering the poison; it simply exudes or contains its weapon, like the poison dart frog and his toxic coating or the puffer fish’s poisonous internal organs.
Here, rather than focusing on the most toxic animals, we will cover five of the more surprising or unusual members of the venomous and poisonous family. In addition, we will learn how it is that their toxic capabilities can impact humans.
The blue-capped ifrit (Ifrita kowaldi) is one of the very few species of birds to have developed the use of chemical weapons; in fact, only three genera are known to carry poison, all of which live in New Guinea.
As with the other poisonous New Guinean birds, the blue-capped ifrit does not manufacture its poison; it embezzles it from its food.
The bird consumes beetles of the genus Choresine, which contain high levels of homobatrachotoxins, a type of batrachotoxin – potent neurotoxic steroidal alkaloids.
By snacking on these poisonous beetles, the bird manages to assimilate the batrachotoxins into its skin and feathers. This sequestering of weaponry is thought to ward off predators and potential free-loading parasites.
For humans, simply handling the birds can produce numbness, tingling and sneezing.
Batrachotoxins are some of the most toxic natural substances known to man. Colombian arrow frogs are coated with the same chemical, and, like the ifrit, the frogs develop their toxic overcoat from the beetles they consume.
These toxins are lipid-soluble and work directly on the sodium ion channels of nerves, irreversibly bonding to them and jamming them open. This makes transduction of nerve signals from the spine to the muscles impossible, leading to paralysis.
Batrachotoxins also have significant effects on the heart muscles, causing abnormal rhythmic patterns and, eventually, cardiac arrest.
Currently, there is no antidote to batrachotoxin. Counterintuitively, the poison from the highly toxic pufferfish – tetrodotoxin – can help minimize its effects. Tetrodotoxin blocks the same channels that the batrachotoxins jam open, effectively reversing the damage.
The blue-ringed octopuses consist of at least three species of the genus Hapalochlaena and live in the balmy waters of the Pacific and Indian Oceans. They are considered to be planet Earth’s most venomous marine animals.
The octopus’ beautiful coloration and serene manner is a rouse; they must be admired from afar. Unless provoked, the octopus is more inclined to flee than fight, but trapping them in a corner is ill-advised.
At a push, the blue-ringed octopus reaches just 20 cm in length, but they still harbor enough toxic chemicals to kill 26 adult humans.
To add insult to injury, there is no antivenom, and, because the bite is so small, many people do not realize that they have been envenomated until the symptoms begin. By then, the trouble is well underway.
If you are unfortunate enough to be bitten, you will receive a smorgasbord of chemicals that include tetrodotoxin, tryptamine, histamine, octopamine, acetylcholine, taurine and dopamine.
The most sinister of these components is tetrodotoxin, considered to be at least 1,000 times more deadly than cyanide. Tetrodotoxin is produced by bacteria in the blue-ringed octopus’ salivary glands. When released into a mammalian blood stream, it blocks sodium channels, and, like getting the wrong key stuck in a door, the channels are left open, making nerve conduction impossible.
Once injected, tetrodotoxin leads to a complete paralysis of the muscles, including those necessary for breathing; in a rather sinister twist, the bitten individual will remain fully aware of their surroundings as the paralysis progresses.
Because these deadly effects can arrive just minutes after a bite, the victim’s only hope is artificial respiration. If breathing can be maintained, the body will slowly metabolize the tetrodotoxin and, if they survive the first 24 hours, a full recovery can be expected.
The platypus (Ornithorhynchus anatinus), colloquially referred to as the duck-billed platypus, is one of nature’s strangest creations. One of only five extant species of monotreme, the platypus is a resident of the most easterly fringes of Australia.
Despite being a mammal, the platypus lays eggs; it stores fat in its tail, hunts using electroreception, walks more like a reptile than a mammal, has fish-like eyes and sleeps for 14 hours a day.
To add to this list of odd characteristics, the male platypus is one of very few mammals to produce venom; this venom is secreted from spurs on the hind limbs and is only produced by males during mating season.
The platypus’ movable spurs can unleash a range of at least 19 peptides and a host of other non-proteinous chemicals.
Of the peptides, most fall into three categories: defensin-like peptides (similar to toxins used by reptiles), C-type natriuretic peptides (involved in changes in blood pressure) and nerve growth factor.
Platypus venom can paralyze small animals (such as a rival male) and, although it is not quite potent enough to do the same to a human, an attack is surprisingly painful and incapacitating. The wound and surrounding area rapidly swells as blood flow spikes.
Unlike many other animal toxins, there is no necrotic (tissue death) component to a platypus envenomation; instead, the crowning glory of the platypus’ attack is the production of sheer, unadulterated agony.
The pain normally lasts a few days or weeks, but it has been known to last months. To make matters worse, the pain does not respond well to morphine.
In 1991, an Australian ex-military man – Keith Payne – made the mistake of trying to free a trapped platypus and caught the sharp end of his spur. According to Payne, the pain was worse than being hit by shrapnel. One month on and the injury was still very much alive; 15 years later and the wound continued to cause discomfort when carrying out certain tasks.
The first description of a platypus envenomation to be published in scientific literature arrived courtesy of William Webb Spicer in 1876:
“[…] the pain was intense and almost paralyzing. But for the administration of small doses of brandy, he would have fainted on the spot; as it was, it was half an hour before he could stand without support, by that time the arm was swollen to the shoulder, and quite useless, and the pain in the hand very severe.”
Platypus venom is believed to act directly on pain receptors (nociceptors) coercing them into producing the most intensely painful experience. Because platypus attacks on humans are rare, no specific treatment has been developed to alleviate this discomfort.
Thankfully, the vast majority of humans will never visit the regions of Oceania inhabited by these striking, semi-aquatic wonders.
Cone snails are a family of predatory, sea-dwelling mollusks comprising around 700 species, many of which wear attractive patterned shells. This enchanting outerwear tempts the occasional diver to pick them up, an instantly regrettable decision.
Sporting a needle-like modified radula tooth, some cone snail species pack a fearsome punch. Using the radula as a harpoon, they fire it into their prey and exude their poison; once paralysis has struck, the mollusk hauls in its quarry. The snail’s harpoon is so powerful, it is capable of piercing a wetsuit.
Each species of cone snail contains a venom consisting of hundreds, if not thousands, of different compounds.
Smaller species can only inflict minor damage to humans, similar in scale to a bee sting, but larger species are capable of delivering a fatal blow.
The selection of neurotoxic peptides produced by cone snails are referred to as conotoxins, and there is a dazzling array. Even between individuals of the same species, the cocktail of chemicals can be highly varied.
This variety means that the human impact of an attack can also be varied; generally, however, the pattern of reaction starts with pain, swelling, numbness and vomiting.
It then progresses to paralysis, changes in vision, respiratory failure and potentially death (although only 15 confirmed deaths have occurred from cone snails to date).
The geography cone (Conus geographus) is known as the “cigarette snail” because, once stung, you have enough time to smoke a cigarette before you die.
Although the exact method of each drug’s action is not understood, conotoxins are known to directly affect specific subtypes of ion channels. Because of the venom’s swift action and high specificity to individual receptor types, it has sparked much interest from pharmaceutical researchers.
Harvard University’s Dr. Eric Chivian, an assistant clinical professor of psychiatry, claims that these creatures have:
“The largest and most clinically important pharmacopeia of any genus in nature.”
The drug ziconotide, a non-addictive pain reliever 1,000 times stronger than morphine, was first isolated from cone snails. Current research using cone snail chemicals is investigating potential medications for Alzheimer’s and Parkinson’s disease, depression, epilepsy and even smoking cessation.
The Komodo dragons (Varanus komodoensis) are the largest living reptiles on earth; they reside on just five Indonesian islands (the island of Komodo being one). They cut a mean figure, reaching 3 m in length and weighing in at 70 kg.
Historically, the Komodo dragon was considered to be a non-venomous species; now, however, the question of the reptile’s toxicity has sparked a lively discussion.
The bite of the Komodo dragon has long been known to cause rapid swelling, disruption of blood clotting and shooting pain in the vicinity of the bite.
This physical reaction was considered to be due in part to shock, but also because of large amounts of bacteria being passed from the Komodo dragon’s mouth into the animal’s circulation. However, some scientists wondered if there might be more to it.
Also, the Komodo dragon does not have a particularly heavy skull or powerful bite, yet it can bring down substantial prey, 40 kg Sunda deer, for instance. Could the Komodo dragon have another weapon in its arsenal?
A Komodo dragon’s prey has been noted to remain “unusually quiet” after being bitten, a reaction that hints at something more than a slow-growing sepsis from bacterial infection.
In 2009, a terminally ill Komodo dragon called Nora from Singapore Zoological Gardens was investigated for the presence of venom. The animal had a pair of glands removed from its lower jaw which, when dissected, were found to host a selection of toxic proteins.
The investigators inspected and analyzed the products found in the glands and concluded that the excretions might help reduce prey’s ability to escape:
- Phospholipase A2: similar to compounds found in snake venom; induces anticoagulative effects and hypotension
- CRISP (cysteine-rich secretory protein): smooth muscle inhibitors found in snake venom; capable of reducing blood pressure
- Kallikrein: enzymes present in mammals that reduce blood pressure when injected
- Natriuretic toxins: cause an increase in vascular permeability and dilation, leading to low blood pressure
- AVIT toxins: thought to cause painful muscle contractions immobilizing the prey.
Not everyone is convinced by the Komodo dragon’s toxicology report. To some, the findings are not evidence for the direct use of these proteins as a weapon; the debate is ongoing.
Kurt Schwenk, an evolutionary biologist at the University of Connecticut, states that the discovery of venom-like proteins does not necessarily mean that they are used as venom. He believes the blood loss and shock produced by a Komodo dragon’s bite is enough to kill large prey, he says:
“I guarantee that if you had a 10-foot lizard jump out of the bushes and rip your guts out, you’d be somewhat still and quiet for a bit, at least until you keeled over from shock and blood loss owing to the fact that your intestines were spread out on the ground in front of you.”
Other dissenters from Washington State University, including Biologist Kenneth V. Kardong and toxicologists Scott A. Weinstein, state that the allegations that the Komodo dragon is venomous “has had the effect of underestimating the variety of complex roles played by oral secretions in the biology of reptiles, produced a very narrow view of oral secretions and resulted in misinterpretation of reptilian evolution.”
Although the debate is sure to rage on until further evidence is unearthed on either side, it makes for an interesting conversation. The question of whether the Komodo dragon is capable of envenomation and disemboweling, or simply disemboweling, will have to go unanswered for now.
If we have learned just one thing from this brief wander through the annals of nature’s poisoners, it is that chemical warfare is not a human invention.