This post is the second in a two-part series on particularly potent venoms found in organisms not commonly renowned for their chemical fortitude. Part 1, which explored the stings of ants and wasps, can be found here.

The fact that there are a number of hymenopterans (ants, bees, and wasps) that have particularly nasty venom isn’t exactly a shocking revelation; these insects are solidly associated with their aggravation-driven stings and their painful side-effects. The degree to which some of these stings can pack a blow may be not well-appreciated, but the general public consciousness is already quite unhappily familiar with how hymenopterans liberally dispense venoms into any and all soft, unguarded tissues like it’s their goddamn job. However, there are entire groups of animals that are worryingly, intimidatingly venomous that are hardly ever even thought of as being venomous in the first place. Yet, these animals have the same chemical gift that has brought infamy to spiders, snakes, and scorpions the world over…that same Midas touch….that is, if everything King Midas touched was suddenly gripped by unbearable, electric agony and shit all over itself in screaming, fitful anguish until it died.

The first of these are animals most folks hardly think about outside the contexts of disease transmission, things that might make the family dog very unhappy, and Leno-chinned superheros in sky blue spandex. It’s likely that only if you spend substantial time in rural areas during warm weather months does this parasite ever clamber into your overall awareness. Yes, I’m talking of course about the glorious, unflinchingly, universally revered tick.

Ticks are the notorious, unabashed gourmands of the arachnid world, partaking heavily and exclusively in the reddest of wines there is; blood. Ticks get all of their nutritional requirements from the blood of vertebrates, and require blood meals to produce offspring and to transition from one developmental stage to the next, ‘leveling up’ like Mario curb stomping a mushroom. To feed on this precious elixir, ticks have to somehow pump it out of their hosts. They do this by tearing open the outer layers of skin with paired cutting mouthparts, and by plunging their “hypostome”, a rugged, practically unbreakable spear-like component of their mouth, deep into the skin. “Spear-like” really doesn’t do this anatomical atrocity justice as a descriptor, actually. Scaled up to nightmarish, non-microscopic proportions, it resembles the depraved union of Klingon weapon and a sex toy designed by a cruel and angry god. From another angle, it looks like someone glued a hedge-trimmer on a mouth harp.

Compared to things like mosquitoes and leeches, ticks aren’t nearly as gentle and considerate about making their non-consensual withdrawals from the blood bank. Rather than expertly piercing a blood vessel, and cleanly sucking up the payload through straw-like mouthparts, ticks employ a markedly inelegant strategy. The sharp mouthparts are used to saw into the skin horizontally, providing an access tunnel for the barbed hypostome. They sweep through and clear-cut tangles of tiny blood vessels like a weed-trimmer shredding a roadside thicket. The rent vessels spring forth with their delicious contents, and the flood generates a pool just under the surface of the skin from which the tick can slurp up its meal through the hypostome.

When the peckish parasite penetrates through the outermost epidermal layers of skin, that’s when the real fun begins, and the venom comes into play. Ticks are indeed venomous animals, and rely on a medley of saliva-bound toxins they inject into the wound site to keep the feeding process running smoothly. Tick venom is complex, with each component toxin targeting a specific physiological process, the multitude of them adding up to create a gestalt effect geared towards keeping the gravy train flowing into Tick Town, and the host’s body completely oblivious that something is amiss. Tick venom is very good at keeping the nutritive river running; anti-coagulants, thrombin inhibitors, small proteins that screw with platelet plug formation (a key part of clotting), and vasodilators (molecules that help widen the piping in your circulatory system) all make the host bleed like Russian royalty, growing the blood reservoir below the skin and allowing the tick to feed uninterrupted. The venom also has a whole host of anti-inflammatory components that work to shut down localized immune response to the bite and all the saliva being pumped in. These toxins are a molecular invisibility cloak, and allow the tick’s feeding to fly under the radar of the host’s immune system. This, in turn, allows the tick to guzzle on the good stuff, anchored in place, for a LONG time compared to other blood-sucking animals (we’re talking a week or more in some untreated cases). Female ticks are especially gluttonous, packing away ten times their original body mass in blood. At the end of a blood meal they, much like Marlon Brando in that 90s remake of “The Island of Dr. Moreau”, are left turgid and bloated far beyond any resemblance to their former svelte selves.

It is through their feeding and injection of potent salivary chemicals that ticks manage to serve as vectors for a multitude of diseases. More than a dozen disease-causing microorganisms (and growing) hitch a ride inside ticks and infect the animals they bite via their chauffeur’s venomous spit. Some of them are familiar…and horrifying; Lyme disease, Rocky Mountain spotted fever, and Colorado tick fever are just a few. Many of these illnesses are knock-you-on-your-ass debilitating, and for this reason, the real health concerns of tick bites don’t come from the venom itself, but from whatever bacterial or viral horrors were tagging along. Ticks are dangerous venomous animals in the same way that mosquitoes are, simply by being the filthiest, most pestilence-ridden vampires this side of an unregulated Transylvanian bordello.

“But hold on now,” I hear you protest. “What the fuck is this tricky-dicky bullshit? Wasn’t this post about ‘surprisingly venomous’ critters and not ‘surprisingly disingenuous list entries based on a technicality’?”

Well, take a seat, unabashedly displeased reader, and get ready to untwist your knickers, because there’s another aspect of tick venom that packs a punch well beyond the fact that the stuff is basically a pathogen soup. How much of a punch? Well, some species of tick have a bite that can induce a kind of paralysis so brutal, the absence of prompt treatment can be life-threatening. Yes, tick venom, in some cases, can make you go floppier than Charles Krauthammer’s face…and then kill you dead.

The condition is known as “tick paralysis” and is known from more than forty species of tick, from all over the world. Most of the time, tick paralysis is a concern mostly for animals; dogs, cats, and livestock like horses. Fido is far more likely than (most) humans to roll around in ticky areas full of long grass, pick up a shitload of bitey blood bags, and then carry on like nothing is wrong for many days later. Dogs don’t exactly pat themselves down for ticks after a blissful summertime romp in the wilderness, so ticks are more likely to feed for longer in an undetected state.

It’s actually that extended length of time blood-feeding that is crucial in the development of tick paralysis. Symptoms, for unknown reasons, really don’t start until the tick has been gorging itself on blood for at least two or four days. Partially for this reason, in the case of humans, the highest risk group for tick paralysis are young girls, since many of them have longer hair that easily obscure a feeding tick for a long while. Children in general are far more likely to contract tick paralysis (although adults can definitely be stricken down), perhaps partially due to their smaller size (which would make the paralytic toxin more relatively potent), or due to the fact that a squirrelly 8 year-old on a hiking excursion is virtually indistinguishable from the family labradoodle in regards to restraining oneself from barreling into a weedy, off-trail blood-sucker bacchanal.

The paralysis itself is as serious as a stroke, not the least due to the similarity of the some of the symptoms to, you know, the aftermath of an actual fucking stroke. The progression of effects from the paralytic toxin, apparently not released from the tick until at least two days or more into the feeding, start off as subtle. A weak voice here. An unsteady gait there. From there, things tend to get worse by the hour. The legs lose strength and buckle, eventually becoming paralyzed entirely. The paralysis ascends up the body, soon affecting the torso and arms. In a matter of days, a person afflicted by tick paralysis can go from vigorously traipsing through the brush, high on nature, to as limp as an overcooked spaghetti noodle. If the tick is not found and removed, the paralysis may continue to the point where breathing and heart rhythm is compromised. A sufferer with an unaided, frozen diaphragm is, obviously, not long for this world.
Many decades ago, back before more sophisticated public health awareness concerning ticks existed, and back when a much higher percentage of people lived out in rural areas, death by tick paralysis was more common than it is today. There are postmortem reports of ticks being found upon examination deeply embedded into the flesh of folks who had suddenly dropped dead from an unknown paralyzing sickness. The realization that an animal the size of a lentil could slowly and incrementally sicken and kill something as big as a human being must have been difficult to tackle.

Tick paralysis still occurs periodically in the U.S., and luckily, deaths are now very rare (although much more common in pets and livestock). So rare in fact, that when we even consider the hypothetical possibility of endogenously dangerous ticks, we have to turn them into humongous, squealing, alien monstrosities that terrorize a young Seth Green and a freshly-greased Clint Howard in a hilariously shitty 90s sci-fi/body horror flick like an army of murderous haggis:

One of the worst offenders for tick paralysis the world over is found in Australia, because of course it is. Locally, it is known as the “Australian paralysis tick” (or Ixodes holocyclus if you feel like treating this parasite with a modicum of respect and calling it by its true name). This species ranges all along the eastern coastline of the Australian continent and into Tasmania, frequenting dense, humid rainforests that characterize the region. It evolved to target large marsupial mammals as hosts; things like koalas, kangaroos, and bandicoots, but of course, humans and their furriest family members are also adequate substitutes as blood repositories.

During the first half of the 20th century, there were nearly two dozen recorded deaths in Australia from this species, a value that is, by the way, greater than deaths from more expeditiously venomous arachnids like the notorious funnel-web and red-back spiders in the same period. It was this particularly paralytic variety of tick that has inspired the most research into the causative chemical agent behind the venom’s effect, and has yielded the most information. Although, to be frank, we still know relatively little about how this venom works compared to other venomous groups of arachnids like spiders and scorpions. What we do know for certain is that once the tick is removed, the effect of the neurotoxic venom diminishes rapidly, and the paralysis can wane completely within only a day. There doesn’t seem to be much in the way of lasting effects, like you would see in the recovery period after a bite from a venomous snake or spider. You can think of tick venom as a very light, steady drip, introducing neurotoxin continuously, so that as long as the tick is in place and feeding, the paralysis builds over the hours and days. But as soon as the tick is unattached, the body expertly manages to break down whatever toxins were left behind. This is a very different system compared to most potentially fatal neurotoxic envenomations, which tend to rely on one or two injections of a catastrophic dose of venom, followed by the delayed effect on the target’s physiology. Getting bitten by a cobra, for example, is the neurotoxic equivalent of getting hit by a truck. The damage done is nearly instantly dire, and without prompt treatment, death is a near certainty. Tick envenomation is more like getting repeatedly pelted with whole cantaloupes; sure, it only hurts a little at first, but after many hours, the cumulative bruising and bleeding from hundreds of hard-shelled cantaloupe impacts can begin to take their toll. If the onslaught never ceases, then murder by melon is a very likely consequence. Tick envenomation is a regular trickle, not the firehose of single-incident destruction seen in most other venomous animals.

We also know of a small number of putative neurotoxins in tick saliva that may be directly responsible for the paralytic bite. They are known as “holocyclotoxins” and based on both the size of the compounds and the genetic sequence coding for the toxins, they appear to be very closely related to scorpion neurotoxins. There is some thought that these paralytic toxins are a hold-over from before ticks had evolved a parasitic lifestyle from spider-like, non-parasitic ancestors that would have needed potent neurotoxins in their bites to disable prey. Inadvertently killing your meal ticket isn’t exactly a winning strategy in regards to natural selection, so it’s unlikely that it has anything to do with parasitism, and more to do with an evolutionary line that is fundamentally steeped in significantly venomous ancestors.

Ticks’ venom, much like the venom of the hymenopterans I mentioned in Part 1 of this post series (like jack jumper ants and Philippine hornets), is still something that is actively, consciously, and maliciously injected. The hymenopterans have stingers, and the tick has its awl-shaped mouth; both tools that require a fairly direct decision to effectively wield. For example, no one gets stung by a wasp by accidentally bumping into the stinger. The wasp has to actively drive its stinger into a victim. But there are plenty of surprisingly venomous animals that are more passively venomous, allowing bold and naive attackers to make the mistake of doing the envenomation for them, adorning themselves with armor made of hypodermic needles full of biochemical napalm, primed and ready, capable of inducing horrific pain with the slightest pin prick. Stonefish and prickly, venomous caterpillars are among the creatures that come to mind. But there are others, particularly beneath the crashing waves of the tropics, that possess strong (perhaps unexpectedly so) toxins that they can unleash if someone were to unwisely place their hands somewhere they really, really shouldn’t.

Sea urchins are not the most huggable animals in the ocean. Close relatives of sea stars and sea cucumbers (they are all Echinoderms, a term that means “spiny skin”), they are characteristically blanketed in countless hard spines. Urchins exist as little more than a bony globe surrounding huge gonads, a small, but rugged set of teeth, a smattering of gummy tube feet, and a shitload of prickles, plates, and poky bits. Many of these porcupines of the sea tend to do alright against predators by just being tough, unappetizing balls of thorns. But some have incorporated venom right into their spines, and by doing so, become the most regret-filled meals since KFC’s “Double Down Dog”, a culinary abortion so grotesque that I’d tell it to go fuck itself if it didn’t look like it already had.

Living in Hawai`i, and spending a lot of time in the water around the coral reefs here, I am familiar with a few varieties of these venomous urchins. One of them, the banded sea urchin (Echinothrix calamaris), is a fairly common sight on the reef, their striking white and black ringed spines waggling slowly from their protected position in holes and outcrops. In the Hawaiian language, they are called “wana” (pronounced ‘vah-na’), and are the sole reason I wear protective boots or tabis before I ever wade into the water along a rocky shoreline.

Wana have a set of spines interspersed with their long, banded ones that are shorter and thinner and far more brittle. These spines easily puncture skin and break off under the slightest amount of pressure, and are finely barbed, allowing them to introduce a flood of venom as they stick stubbornly in you. Last year my girlfriend got to experience the venom of the banded urchin quite literally first-hand, when during a bit of volunteer work leading elementary school children around an exploratory look in the intertidal, she picked up what she thought was one of the harmless species of urchin. It was not a harmless species of urchin. Not even close. The price for her mistake was a quiver of purple to black lances thrust deeply into her finger, making her look like she strayed too close to a mechanical pencil factory during a hurricane.

After pulling out the spines, the intense pain in her finger quickly faded, and the swelling and pain decreased for about a week. But the urchin wasn’t done with her yet, and a few weeks later, pain and stiffness returned to the disfigured phalanx before finally abating for good.

While the hot fire poker pain of a run-of-the-mill venomous urchin spine seems bad, trust me, in the world of venomous urchins, it can get a LOT worse. Far exceeding the potency of the banded sea urchin are the flower urchins, which consist of four species in the genus Toxopneustes. They are found in shallow reef habitats in the tropical and subtropical Indo-Pacific, ranging from East Africa, through the Indo-Australian Archipelago, and throughout the Pacific and across to the coastlines of California and Central and South America. Do not be fooled by the deceptively benign common name. The “flower” moniker refers to the urchin’s numerous flower or cup-shaped “pedicellariae” structures, which are typically small and claw-shaped in other urchins…bear in mind that its scientific name, Toxopneustes means “poison breath”, so that should be a solid indication that it is a dangerous sea beast devoid of warmth or joy. Also, it is those very elegant, delicate-looking “flowers” that administer this urchin’s toxic ruination.

Every suction cup-shaped pedicellaria is equipped with three sharp claws, derived from the grasping appendages more commonly seen in pedicellaria in other urchin species, and looks like some surreal marriage of grappling hook and toilet plunger. Each recurved fang connects to a venom gland. When disturbed, the cup of the pedicellaria snaps shut, like a Venus fly trap, and the fangs overlap with one another, turning the round tip of the pedicellaria closed and more triangle-shaped. The fast and forceful collapse of the pedicellaria tip plunges the three fangs deep into whatever unfortunate fleshy bit (like a human hand, for example) that triggered the reflex. The snapping action automatically opens up a valve in the stem of the claw, and the urchin sends a stream of venom right into the puncture site, like some kind of vindictive, ferocious sea cauliflower.

Things tend to go downhill rapidly after that. The claws don’t relax and release on their own, and the stalks for the venomous pedicellaria are brittle, so even a passing brush can not only land you with a dozen “bites” from the world’s most venomous version of those cheap, sticky suction cup ball toys, but the grip of the cups can cause them to break off and stay stubbornly stuck to your skin, where they continue to pump in cascades of burning venom.

This is a pretty goddamn awful situation to be in, because Toxopneustes venom, by urchin standards, really doesn’t fuck around. There appears to be two principal toxin components of the venom nailed down at this point. One of these is peditoxin (comprised of pedoxin and pedin, the former of which, on its own, causes sedation, coma, convulsions, and death in test animals), which, once purified from flower urchin venom, fairly easily kills mice in low doses by inducing a kind of anaphylaxis-like shock. In addition to this, another toxin, contractin A, is known to induce contractions in smooth muscles. It’s not clear how contractin A actually plays out in a whole, living animal (the study used tracheal smooth muscle isolated from a rodent), but it’s important to remember that smooth muscle is found in some fairly important places….like in the walls of major blood vessels, or in the respiratory tract. Having your circulatory or respiratory system seize up, especially while out swimming in the ocean (where a sting is most likely to occur) can be a one-way ticket to Davy Jones’ locker.

And indeed, there are a handful of reports of people drowning after an unfavorable encounter with a Toxopneustes urchin, supposedly caused by the intense flood of envenomation symptoms: the disorientation caused by the electric pain, combined with respiratory distress, muscle weakness, and wide ranging numbness and paralysis, which together overwhelm the water competency of the victim. However, no purported “deaths-by-urchin” have been definitively confirmed. That being said, it’s best not to test this one if out and about on the reef. The peak of flower urchin envenomation effects are apparently short-lived, with the worst pain and paralysis ceasing within the first half hour of the sting, but one must remember that it only takes seconds to minutes to drown…something not exactly helped when the ability to breathe, tread water, and think clearly are shot to shit.

If the harsh sting of the Koosh Ball of Agony wasn’t unexpectedly dangerous enough for a creature that looks more like a dog’s squeaky toy than a real animal, then get a load of the last entry in this post; an animal that appears so benign and motionless that it registers in the brain as more plant or mineral than anything else.

Imagine you’re on the vacation of a lifetime, SCUBA diving off the equatorial coasts of Indonesia’s island of Sulawesi. You are some forty feet below the surface, surrounded by the serenity of some of the richest and most diverse coral reefs in the world, the only sound your rhythmic breathing and the rush of bubbles from your regulator. Towering coral pinnacles flank your gliding path along the reef, great, complex, stony structures of purple, yellow, and navy blue. Clouds of minuscule, neon green damselfish undulate and contort around their stationary place above a coral head as you approach. The water is a warm 82 degrees, and isn’t much cooler below the surface, so you are only wearing a short-sleeved wetsuit. You catch a glimpse of something big, fast, and deep blue blazing off to your right. It’s a humphead parrotfish. You signal to your dive buddy and follow cautiously, watching it slow down and maneuver around a field of broad, olive-yellow, branching corals. It disappears through a hole, but you know it has popped out the other side. You know you need to rise up above the wall of branching corals in front of you, so you ascend slightly, attempting to peek over the edge. You can hear the parrotfish feeding just on the other side, so you need to move as slowly as possible, so you don’t scare it away. You ready your camera, and reach out to steady yourself by grabbing onto one of the thicker regions of the weird, smooth, lacey coral in front of you. You stop, remembering that Kent, the divemaster, had specifically directed you and your buddy to not touch any wildlife if possible…ESPECIALLY not the sensitive corals. Kent is a 42 year-old white man with dreadlocks, a DMB logo arm tattoo, who talks incessantly about his recent “juice cleanse” and the “spiritual awakening” he had volunteering and (inadequately) constructing school houses in Uganda. Fuck Kent, you think to yourself, and firmly grab onto the coral with your bare left hand and pull your weightless body upwards.  You snap some amazing photos of your parrotfish subject, and continue on your way, finishing up your dive shortly. As you ascend with your dive group to the boat, you notice a burning sensation in your left hand. You shake it out a bit and stretch your fingers back and forth. The pain gets worse, and by the time you flop back onto the boat, the stinging radiates through your entire palm. This is just the beginning of a week-long ordeal of pain, irritation, and suffering.

On your dive you unknowingly made a grave error; touching fire coral (Millepora), incurring its venomous wrath straight into your soft, unprotected hand.

The term “fire coral” is actually misleading. The fifty or so species of Millepora, found across the Indo-Pacific (except for Hawai`i) and the tropical Atlantic and Caribbean, are not corals at all, and are actually quite distantly related to them. While both “fire coral” and standard stony corals are colonial animals in the phylum Cnidaria (a group that also contains jellies and sea anemones), they are in entirely different taxonomic classes. True stony corals are what we call “anthozoans” (a term meaning ‘flower animals’), and are close relatives of things like anemones and sea pens. “Fire coral”, in contrast, is a “hydrozoan”, and is closely related to things like freshwater hydras, colonial siphonophores like the Portuguese Man ‘o War, and the by-the-wind sailor. Millepora is a member of a group of cnidarians that includes creatures that look and act a lot like “true” jellies, class Scyphozoa (“jellyfish” or “jelly” is a term that is applied to many groups of free-swimming, bell-shaped cnidarians, whatever their evolutionary lineage)….yet, to the untrained eye, looks indistinguishable from any of the corals that make up the reef.

However, looking closer at these vast colonies of hydrozoans helps illustrate just how different they are.

Both Millepora and true stony corals are colonial organisms, meaning that their big, branching structures are made up of many multitudes of single organisms (called “polyps”), articulated and fused together like the apartments making up a high-rise skyscraper. Coral polyps are like very, very tiny sea anemones in overall shape; little mounds with soft tentacles surrounding a mouth hole. They are, however, encased in a hard aragonite skeleton (a “corallite”), with the feeding tentacles (which are covered in “cnidocytes”, the explosive, venomous harpoon-primed stinging cells found in all cnidarian groups) alternating between being exposed to the water, or retracted within the skeleton. Corals feed on planktonic bits that stray into their outstretched tentacles, and most shallow water species are also supplemented by symbiotic unicellular algae (“zooxanthellae”) that live inside of the polyps and provide food energy via their own photosynthesis.
Millepora also harbor zooxanthellae and derive energy from them, but the structural units by which they generate their giant colonies are markedly different. Instead of distinct polyps sheathed in a rigid corallite, the surface of a fire coral colony looks like close-up of Edward James Olmos’s face. It is a plain of diminutive pores and pockmarks (“millepora” means “thousand pores”), each housing a polyp. However, in fire coral, the polyps fall into a number of different types. The two most common types are gastrozoids and dactylozoids. Gastrozoids are the feeding polyps, and in this way, are similar to what you’d see in a coral polyp. Most of the time, gastrozoids are retracted deep below the surface of the colonial skeleton, where they are connected to one another by a network of canals, so nutrients can be distributed between individuals. The dactylozoids are strange by comparison; mouthless, their job is to catch prey and feed it to the gastrozoids. They have long, thin, wispy, transparent tentacles that stick straight out, making the colony look like it stole its hair style directly from Bernie Sanders. These dactylozoids and their tentacles are the ones armed with the stinging cells that dole out the pain to microscopic plankton and misplaced human limbs alike.

Contact with the dactylozoid tentacles causes the cnidocytes to do their one and only job; shoot out a barbed harpoon at blistering, impossible speeds directly into whatever triggered it. How impossible? The discharge of the stinging cells takes roughly 700 nanoseconds, which is an acceleration so stupidly huge that the harpoon is subjected to more than five million times the force of gravity….some 5,410,000 g. This mechanism produces, far and away, the highest acceleration of any animal on the planet. To put that value in perspective, for a human to experience that g-force on a standard merry-go-round with a 15 meter radius, you would have to be spinning around at more than 182,000,000 miles per hour. This is so fast that you would travel the equivalent of the Earth’s circumference in less than half a second. Not only would the force nearly instantly liquefy you, even down to the collagen that holds your tissues together…but the air friction generated from such speeds would incinerate whatever remained.

Basically, what I’m trying to say is that the spring-loaded harpoon of a discharging cnidocyst is fast.

Once that harpoon tip hits its target, venom is injected into the puncture site through the hollow tubule that runs from inside of the harpoon, down the thread, and into the capsule of the cnidocyte. Cnidarian stings vary widely in how seriously they impact human physiology. Many sea anemones have mildly irritating stings, while some cubozoans (box jellies), like the sea wasp (Chironex fleckeri) has sting that has been implicated in human fatalities. Fire coral falls somewhere in the middle. For Millepora, it takes usually at least a few minutes for the first symptoms to show up after a sting. Hot, burning pain is the predominant shit you would have to deal with, and it is the first to rear its head. Red, irritated welts and blisters raise on the skin in the impacted area, and in some cases, in the hours following the sting, the sufferer may experience nausea so strongly they end up barfing a bit. The pain eventually gives way to intense itching after a while, and the red rash can remain for a week or more. The sting’s effects are certainly unpleasant, a little like mosquito bites on top of poison ivy on top of a gnarly sunburn, but they are, at least, not life-threatening. Barring a rare allergic reaction, fire coral ain’t going to kill you. Really, a much more likely scenario to be cause for concern is if someone came in contact with Millepora by getting scratched or cut by it. Cuts sustained from coral or Millepora are exposed to mucus from the coral, full of irritating proteins, as well as tiny chunks of calcified skeleton. This, together with the cut being submerged in a marine soup of microorganisms, means that coral scrapes are particularly slow to heal and infection-prone. If the skin is broken, essentially, the most dangerous element of a fire coral encounter potentially has nothing to do with the venomous colonial critter itself.

So, it’s just good policy to not touch anything that looks like it could be coral. Touching pisses the coral off and/or kills it, and touching coral can end up indirectly hurting you, and THAT pisses YOU off. There’s not a lot of winning here.
Don’t touch urchins, either. Even if they look like they are made entirely out of gelatin trumpets. Actually, especially if they look like that.

Venom has evolved in a hell of a lot more critters than snakes, scorpions, and spiders. Some of them are brightly-colored buzzing nightmares, some are underestimated miniature vampires, and some don’t even look like animals at all. Takeaway from all of this? If you are out in our big world and see a new beastie thing, and you desperately want to pet the thing, remember that maybe you really shouldn’t pet the thing.

Image credits: Intro flower urchin, tick hypostome, tick before and after feeding, Toxopneustes, flower urchin pedicellaria, fire coral scene (Derek Keats), fire coral tentacles (Eric Burgers)

© Jacob Buehler and “Shit You Didn’t Know About Biology”, 2012-2015. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Jacob Buehler and “Shit You Didn’t Know About Biology” with appropriate and specific direction to the original content.