A lot of things in life don’t make sense, and it seems I spend half my time trying to explain and rationalize these to my three young girls. They ask a lot of questions. A lot.
- Why do we park on a driveway?
- Why is something called a “free gift”, aren’t gifts always free?
- What’s a pineapple? There’s no pine or apple in it.
- If wizards can regrow bones, why does Harry Potter still need glasses?
- Why the hell would someone throw a pair of shoes on the power line?
They also swear, which they get from their mother. Seriously. But at least there’s one name I won’t have to explain to them: the Death Cap mushroom. Like vomitoxin, it’s self explanatory.
The Death Cap mushroom, Amanita phalloides, is a nondescript mushroom native to most of Europe and has a symbiotic relationship with many species of hardwood trees, like the chestnut, beech, and oak. The fancy scientific word for this is “mycorrhiza” and involves the fungal colonization of a plant’s roots. The fungus gets carbohydrates, the tree gets minerals. Win-win.
Though non-native to the United States, the Death Cap mushroom was likely introduced in the 19th century as spores hitchhiked across the Atlantic with chestnuts or wood products from Europe, but was not conclusively identified until the early 20th century (1). What took so long for it to be identified? Well, it’s a pretty plain looking mushroom. White stalk, annulus, and volva – don’t laugh, those are real words. The cap is white too, and turns shades of brown, yellow, and green with age. Unless you’re a well trained forager or mycologist that knows what to look for, Amanita phalloides doesn’t scream “poison, ” until it’s too late.
The poisons involved are two groups of bicyclic peptides, the amatoxins and phallotoxins, made up of eight and seven amino acids, respectively. But while the phallotoxins are present in a higher concentration, in every part of the mushroom (2), it is the amatoxins that get the blame, particularly α-amanitin. The amatoxins do their dirty work by inhibiting the enzyme RNA polymerase II (3). That sounds important…do we need one of those? Yeah, you do. One of the functions of RNA polymerase II is catalyzing the transcription of DNA to messenger RNA. That sounds important too…I suppose we need that as well? Short answer, yes. Messenger RNA is really a single-stranded copy of a gene that becomes translated into proteins – it makes you, you, and enables the growth and repair of your body.
Death Cap toxicity occurs chronologically in the systems that came into contact with the peptide poisons: the GI system first, then the liver. It’s the disruption of the GI system that clues you in that you were poisoned, but it’s the liver failure that kills you. Your liver is responsible for metabolizing and excreting the vast majority of chemicals and drugs that enter your body, and without it you die. Without your liver able to replicate and repair itself from the amatoxin induced damage, you’re in for a painful journey.
Symptoms are delayed and start approximately 6 to 12 hours after ingestion, and present with nausea, vomiting, diarrhea, and general abdominal pain. At this point people may think they have “food poisoning” and that it will pass. And it does after about 24-48 hours, like the calm before the storm, or being in the eye of a hurricane (I’ve experienced that, it’s true). But it’s during this “recovery” phase that irreparable liver damage is kicking in, with liver failure just around the corner. At this point, liver transplantation is usually the best, or only, option for survival (4). Supportive care is of course provided, but other treatments are often considered, such as antibiotics and silibinin, a chemical from milk thistle extract that may offer protection to liver cells. Silibinin has received a lot of attention in recent years, but the medical community still seems to be split on the issue (5, and for a review of current therapies).
The next obvious question is: How much is lethal? There aren’t any clinical trials for these sorts of things, or rather not many people signing up for them. But the LD50 (the amount needed to kill 50% of the population) is estimated at approximately 0.3 mg/kg for the amatoxins in various species – it could be more or less in humans, but it’s a good starting point (6). For an average 70 kg person, that’s 21 mg – or about 1 grain of rice. The cap of the Death Cap contains about 0.36 mg of amatoxins per gram of mushroom (2), so one would only need to eat 58 grams, or 2 ounces of mushroom, for it to be potentially fatal. Other portions of the fatal shroom contain higher concentrations of amatoxins, such as the ring, where only 7 grams (!) could prove lethal. Overall mortality rates range from 10% to 25%. Why the range? It depends upon course of treatment, with liver transplantation affording the best chance for survival, but also on proper identification of the mushroom ingested. I have a feeling many people become ill from eating mushrooms, but the exact species is not conclusively identified and many labeled as a Death Cap – it sounds better and makes for a better story – so their survival tends to deflate the mortality rates.
My take home message regarding picking and eating wild mushrooms is always “Don’t.” But if you feel the need, urge, or primitive desire, go for it! Just become properly trained first, your life isn’t worth a free mushroom. But another point that I touched on earlier, is that with the advent of efficient mass transit, it is easy for non-native species to “invade,” like Amanita phalloides a hundred years ago here in the States. So while an expert may be intimately familiar with poisonous mushrooms in their neck-of-the-woods, an unknown lethal one may spring up and cause confusion. So go foraging with the weapon of knowledge, and protect yourself from the evil Cap of Death.
** Homepage featured image of Amanita phalloides by Justin Pierce (CC BY-SA 3.0) **
1. Pringle, Anne, and Else C. Vellinga. “Last Chance to Know? Using Literature to Explore the Biogeography and Invasion Biology of the Death Cap Mushroom Amanita Phalloides (Vaill. Ex Fr. :Fr.) Link.” Biological Invasions 8.5 (2006): 1131-144.
2. Enjalbert, F., C. Gallion, F. Jehl, and H. Monteil. “Toxin Content, Phallotoxin and Amatoxin Composition of Amanita Phalloides Tissues.” Toxicon 31.6 (1993): 803-07.
3. Karlson-Stiber, Christine, and Hans Persson. “Cytotoxic Fungi—an Overview.” Toxicon 42.4 (2003): 339-49.
4. Broussard, C.N. et al. “Mushroom Poisoning—From Diarrhea to Liver Transplantation.” The American Journal of Gastroenterology 96:11 (2001): 3195-3198.
5. Ward, Jeanine, Kishan Kapadia, Eric Brush, and Steven D. Salhanick. “Amatoxin Poisoning: Case Reports and Review of Current Therapies.” The Journal of Emergency Medicine 44.1 (2013): 116-21.
6. Vetter, János. “Toxins of Amanita Phalloides.” Toxicon 36.1 (1998): 13-24.