Fungi.

Quite possibly the most overlooked of the eukaryotic kingdoms. Not as mobile as their animalian close cousins, and they tend to be more discrete than the giant, showy plants. For most of us, at their best, they are an edible foodstuff, adding a bit of gummy texture to stir-fries. At their worst, they ruin an old strawberry or cause a bit of itchy feet, much to the chagrin of John Madden. They are the completely benign decomposers of the shadows, the wood-rotting, spongey, alien-like denizens of coastal forests and poorly ventilated bathrooms. Soft. Passive. Life’s unassuming and dutiful janitorial crew. Wouldn’t hurt a fly.

The unfortunate insects above, now reduced to crumbling husks, were parasitized by a species of Cordyceps fungus. More closely allied with common bread mold than your average forest mushroom, Cordyceps make a decent living out of selectively infiltrating the bodies of various insects, growing inside of them, and eventually killing them and erupting through their exoskeletons. Some can even impact the minds of their insect hosts, making them into little zombies that position their bodies in such a way so that when they succumb to their insides being turned into a palatable slurry, the spore producing fruiting body (or “stroma”) of the fungus can have an advantageous location over the forest below, allowing for the maximum amount of exposure possible to other unwitting victims. Observe below:

Sir David Attenborough’s soothing narration, coupled with the music, make this video far more creepy than necessary. There’s something vaguely nightmarish about those wailing strings and circus-tent music playing alongside images of death-by-killer-fungus. Cordyceps are found worldwide, but enjoy higher density and diversity in the lower latitudes. As far as we know, they tend to go after insects only.

Humans, predictably, have found utility in all this grotesque carnage. In the highlands of southeast Asia and on the Tibetan Plateau, Cordyceps sinensis, also known as “caterpillar fungus” and “yartsa gunbu” in Tibetan, parasitizes the caterpillars of the ghost moth Thitarodes. The fungal spores infilitrate the caterpillar, germinate, and grow inside, killing the caterpillar and making it shrivel like a prune while the stroma shoots out of its forehead, making the poor larva into a dark, twisted, mummified fungi-corn. These dead, fungus-filled caterpillars are then harvested and are believed to have medicinal properties. For hundreds of years, the people of Tibet, Nepal, Bhutan, and China have used the fungus-caterpillar combo as an aphrodesiac, as well as a treatment for general fatigue and cancer. Modern research has confirmed that many previously described beneficial effects may occur, but the evidence is tenuous at best. Either way, the demand for yartsa gunbu is very high, and prices for the medicinal duo are quickly rising. A kilogram of caterpillars can easily sell for the equivalent of several thousand US dollars, depending on the quality of the harvest. The value of yartsa gunbu is so high, that conflicts over access to grassland for harvesting purposes are commonplace in rural Tibet these days. People have even been killed in these conflicts.

Fungi can also be predatory in other, more microscopic, insidious ways. A distant relative of Cordyceps, Arthrobotrys anconia has evolved a unique way of dispatching microscopic nematodes (tiny worm-like animals found virtually everywhere, especially in soil). Basically, a bit of fungal hyphae (a filament of fungal cells) forms a three-cell ring. A nematode eventually slides into the ring, and mechanical stimulation of the struggling nematode causes the cells’ pre-made perforations to rip open, causing water to rush in, swelling the cells like a balloon and making the grip of the trap even tighter. Eventually, the constriction by this fungal python becomes too much for the nematode’s outer layers, and the trap pinches through into its guts. The nematode dies, for obvious reasons, and the trap cells germinate hyphae into the crushed body of the nematode, and digest its innards over the course of 12 to 24 hours. Yes, Arthrobotrys anconia uses a lasso to catch mobile, wormy prey…and is effectively a more realistic cowboy than George Bush ever was.

A close relative, Arthrobotrys oligospora, generates microscopic adhesive nets spread across the substrate…making a deadly hellscape of sticky landmines for a helpless, and blind, prey. Some species of Pleurotus use chemical warfare, and make bags of toxins that attach to the outside of blundering nematodes, and then secrete their poisonous cocktail all over the nematode, incapacitating the micro-beast long enough for the fungus to start “eating” it. Those poison bags, of course, function as spores once empty, so digestion gets a pretty early start. It’s like if you go out and shoot a deer, and the bullet starts growing and eating the deer from the inside out before you even catch up to the kill. Coprinus cornatus, a species of edible mushroom, also kills soil nematodes for consumption. Because adhesive webbing and drug-filled water balloons weren’t cruel enough, Coprinus one-upped other fungi by making ‘spiky balls’ (actually the mycological name) that jab into the side of a nematode, injecting poison through hundreds of hypodermic needles. Pleasant.

Yes, the world of fungi looks pretty damn threatening if you are an insect or a nematode. But larger animals can just as easily fall victim to a fungal sneak-attack.

These bats don’t have white faces because they’ve been hitting the cocaine (although that might explain their nocturnal habits) or because they had a hankerin’ for powdered doughnuts. These bats are infected with the fungus that causes “white nose syndrome”, Geomyces destructans. As you can probably infer from the species name, this particular mold is a doozy. First showing up in caves in the NE United States about four years ago, WNS grows on the snout and ears and interferes with normal winter hibernation patterns (leading to starvation). The effect has been staggering; infected caves have had die-off rates of around 90%, and are currently threatening recently common bats with extinction. While this may be good news if you are a particularly jumpy spelunker, it’s generally going to make things shittier for everyone else. It’s estimated that several million pounds of insects will go uneaten due to the bat die-off in New England, which means a big-ass burden on crops, and increased food prices. Also, if you’ve spent any time in anywhere NOT covered in concrete in the Northeast during the warmer months, you’ll acknowledge the last thing the region needs is more mosquitos. Efforts to control the fungus are mounting. Here’s hoping Gold Bond does the trick…

Oh boo hoo, you say, weakling bats can’t even handle a bit of white fuzz! I’m a big strong human with thumbs and shit and etc. etc. etc. The truth is, we Big Awesome Hairless Apes (I like to call us BAHAs) are every bit as vulnerable to fungal infestation. Nothing’s going to turn us into a mindless drone and burst out of eye holes like with Cordyceps (yet)…but what does go after us tends to be pretty damn ugly. And there’s a whole host of them. I’m not posting pictures for a good reason; if you want to initiate a lovely mix of blinding terror and dry heaves, Google images of the following afflictions: chromoblastomycosis, lobomycosis, basidiobolomycosis, histoplasmosis, coccidiomycosis, and blastomycosis. I took 400-level mycology and cannot unsee what has been seen, but your fate does not need to match mine. For those that chose to wisely heed my warning, basically, the most vicious fungal infections in humans make leprosy look like wind burn. Also, another bit of uplifting info: the fungi that cause a good portion of those flesh-melting illnesses are endemic to the US. Histoplasmosis can be picked up in the Ohio River basin. Coccidiomycosis is a disease endemic to the San Joaquin Valley in California, and throughout the Southwest. Blastomycosis is contracted chiefly in the eastern US, and appears to be associated with rotting vegetation. The other three are pretty much limited to the tropics and are usually associated with dirty wounds, so only if you get a nasty splinter on your trip to Brazil should you start sweating. Although, sometimes a fly bite can inject the fungus into your skin…and we all know how easy those are to avoid in the tropics.

My home region, the Pacific Northwest, is no stranger to fungi. Stand in one place too long during the winter and you’ll start growing criminis out of your ears. It’s also no safe haven from the people-killing variety. Cryptococcus gattii has been making waves in our rainy corner since the late 90s, infecting over 200 humans and animals with a potentially deadly lung infection that can spread to the nervous system. It is likely introduced, since it was only previously known in Australia and appeared to hang out around eucalyptus trees. Now that it’s in the states, and associating with native trees, and infecting and killing Oregonians and Washingtonians…Cryptococcus gattii is proving to be the nastiest Ozzie scourge since Rupert Murdoch.

Even our pets aren’t safe. To date, dogs, cats, ferrets, llamas, parrots, horses, and a porpoise have all contracted a C. gattii infection. How a fucking porpoise inhaled the deadly spores is beyond me, seeing as how the fungus lives in the soil and bark of trees. Seems like our flippered friends have been keeping secrets from us.

Well, you say, at least I have my food! No death-mold in my sammich! I’ll just sit in my house with all the windows cellophaned closed, in my hazmat suit and eat PBJs all day! And rye toast!

The rye above is covered in the spore-making parts of the fungus Claviceps purpurea, more commonly known as ergot. Ergot can pretty easily infect a rye crop around harvest time, and ingestion of infected grain leads to ergotism. You see, ergot contains a cocktail of alkaloid toxins that do quite a number on human physiology. One compound, ergotamine, causes the arteries to constrict and limit blood flow to relatively important things…like digits and limbs. This causes gangrene to develop, and the decayed parts eventually fall off. This, combined with the burning sensation caused by the toxin led to people in Europe during the Middle Ages to name the phenomenon “St. Anthony’s fire”, an invisible, holy fire that slowly burned its victims’ limbs off. Ergotism outbreaks were common in the poorer classes in medievel Europe, as these people were more likely to consume old or poor-quality grains. Pieter Brueghel’s “The Beggars” from 1568 records the disproportionate de-footening of the poor quite vividly:

Another alkaloid, ergine, can be broken down into lysergic acid diethylamide…also known as LSD. As you can imagine, this causes a whole other class of wacky symptoms to occur. Some scholars think that ergotism may partially, or wholly, explain the rash of witch trials in Europe and the American colonies between 1500 and 1700, seeing as how most of them occurred in places that depended on rye as a major food source. That, and you know, runaway religious paranoia and misogyny, but sure.

Of course, LSD was isolated from ergot compounds in the 1930s by Swiss scientist Albert Hofmann. It was first isolated for potential pharmaceutical use, but in 1943, after coming back to LSD research, he accidentally absorbed some of the synthesized LSD through his fingertips…and became the first person to have a legitimate acid trip.

He described the experience as being: “… affected by a remarkable restlessness, combined with a slight dizziness. At home I lay down and sank into a not unpleasant intoxicated-like condition, characterized by an extremely stimulated imagination. In a dreamlike state, with eyes closed (I found the daylight to be unpleasantly glaring), I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors. After some two hours this condition faded away.”

I’m convinced that biochemical research was simply far more badass back then…

If you live in the modern Western world, unintentional ergot poisoning isn’t a huge problem for you. But, most of the foods you eat daily can make you ill or kill you from fungal mycotoxins. One such toxin, T-2 toxin, is caused by various Fusarium infestations of grains like corn, wheat, barley, rice, and oats. The symptoms of the toxin are similar to a non-contagious Ebola. Ochratoxin-A, made by various “molds”, can be found in poultry, pork, grapes, and raisins. This toxin is nephrotoxic, meaning it attacks your kidneys, and quite efficiently so. It’s been shown to be carcinogenic in mice, and has been linked to kidney cancers in humans. These are just two of many types of mycotoxins that show up in our food in trace amounts, or sometimes more. Take comfort in knowing that the European Union regulates ochratoxin-A levels in food, as well as several other dangerous toxins. The FDA, on the other hand, doesn’t regulate ochratoxin-A or T-2 or…well, most mycotoxins. God bless America.

Damn, you say, I’ll just have to eat them before they can kill me! I’ll just eat ’em! While most everyone knows that there are “edible” mushrooms and “poisonous” mushrooms, not many know just how BAD a bad mushroom actually is. The death cap, Amanita phalloides, one of the most famous and most readily, and tragically, misidentified of North America’s toxic mushrooms is a good example of this. Eating a death cap isn’t going to place you in the John for a day or two, give you the chills, and have you come out a little more wary of wild mushrooms. Amatoxin, the principle toxin in a death cap, is very, very potent. The LD50 value, or the amount of toxin required to kill 50% of adult humans, is roughly 0.1mg/kg of body weight…so about 6-7 mg for a full grown adult. The concentration of amatoxin in mushroom tissue is a whopping 0.5 to 1.5 mg/g…and an average size death cap mushroom weighs in at about 60 g. In other words, a quarter-nibble of the wrong type of mushroom and you’ll be flirting with death, let alone eating a plate full.

If you are unfortunate enough to eat a death cap, you’ll be puking and crapping furiously about 10 hours later. 24 hours after ingestion, you’ll start feeling better, and start kicking yourself for being an ignorant ‘shroomer, and you’ll be thankful you’re alive. Then, Mother Nature, being the wickedly cruel force she can be, pulls a fast one on you. For the next two days, while you’re experiencing a new appreciation for life, the amatoxin is rapidly turning your liver into pudding. Three days after you ate the mushroom, your guts rebel again, and you spiral into liver failure. Hospital treatment by this point is useless, coma and death follow swiftly.

A more benign, and curious, mushroom toxin comes from the ink cap, Coprinopsis atramentaria. It is called coprine, and it is only toxic within hours of the consumption of alcohol; this has led to ink cap being called “tippler’s bane.” The effect is extreme nausea and vomiting, as well as facial reddening and tingling in the limbs. This isn’t life-threatening, and just serves as a time machine to what would have went down the next morning had you been able to actually drink. This mushroom grows all over the Northern Hemisphere. If you just finished a meal of wild mushrooms you collected earlier in the day, and you’re about to take a swig of a microbrew, you better be sure no ink caps rest in your belly. This particular warning is mostly geared towards my Oregonian brethren.

An even weirder mycotoxin affects our wooly friends (sometimes more-than-friends), the sheep. It’s called sporidesmin, and it comes with ingesting the fungus Pithomyces chartarum. Sporidesmin causes a disease known as “facial eczema,” which causes extreme skin irritation and the loss of fur from the face. The weird part is that the toxin doesn’t actually do anything to the skin itself. Sporidesmin works on the liver and gastrointestinal tract, causing the incomplete breakdown of chlorophyll from the grass the sheep eat. This chlorophyll, along with other waste products and bile, build up in the bloodstream. The chlorophyll is activated by exposure to sunlight, causing the skin irritation and peeling.

Facial eczema, by itself, isn’t dangerous. But the stress on the animal can lead to lowered immunity to other infections, and Pithomyces has had a major impact on total production of sheep in hard-hit places like New Zealand. There’s not a whole lot you can do to combat facial eczema, except hope for cloudy weather.

I’m a little wary of any compound that causes irritation and skin-sloughing in farm animals. The prospect of corpseified, aggro demon ewes keeps me awake at night.

Anyways. Fungi can be delicious, cool looking, and a little gross. It can also kill you.

© Jacob Buehler and “Shit You Didn’t Know About Biology”, 2012-2014. 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.