8
AMANITA NIGHTMARES
The Death Cap and Destroying Angel

Among all those things that are eaten with danger, I take the mushrooms may justly be ranged in the first and principle place; true it is that they have a most pleasant and delicate taste, but discredited much they are and brought to an ill name, by occasion of the poison which Agrippina the empress conveyed unto her husband Tiberius Claudius, the Emperor, by their means a dangerous precedent given for the like practice afterwards. And verily by that fact of hers, she set on foot another poison, to the mischief of the whole world and her own bane especially (even her own sonne Nero, the Emperor, that wicked monster).

PLINY IN THE NATURAL HISTORY OF THE WORLD, A.D. 23–79

Pliny’s description of the alleged murder of Emperor Claudius in the first century A.D. is perhaps the oldest surviving record of a mushroom being used as an instrument of murder and regime change. While the cause of Claudius’ death is a matter of historical debate, according to this version of the story, the Emperor’s fourth wife (and niece), the Empress Agrippina, plotted to elevate Nero—her son from a previous marriage—to the throne. She first convinced Claudius to adopt Nero, putting Nero in line for ascension, and then laced the emperor’s dinner plate with either the juice or chopped fruit of the death cap, Amanita phalloides. Claudius, who was a well-known glutton and inordinately fond of mushrooms, thought he was eating the colorful and tasty Caesar’s mushroom, Amanita caesarea, a mushroom of high acclaim across Europe, prized by nobility of the Roman Empire, and one of his personal favorites.

According to the historian Tacitus (circa A.D. 55–117), the emperor finished his dinner and enjoyed the evening without ill effect, but got sick during the night and stayed sick for some extended time thereafter. He enjoyed a brief recovery after emptying his system, but in Tacitus’ next entry, the doctor Xenophon was called to attend to the needs of the emperor and tried to make him vomit by sticking a feather down his throat. This seems to indicate that Claudius again became ill after his initial recovery, a course of illness consistent with amatoxin poisoning. Some historians suggest that Xenophon was part of Agrippina’s plot and administered a second poison to the victim at this point, perhaps an enema of colocynth, a powerful purgative. Whatever the case, Claudius’ condition deteriorated, and after a significant delay, the death of the Emperor Claudius was announced and Nero assumed the throne.¹ Once, again, the delay before death is consistent with amatoxin poisoning taking a number of days to kill a victim.

Sad to say, the story may be true and such tales are what give mushrooms a bad name. If the goal has been to vilify mushrooms, the choice of Amanita phalloides as the poster child of mycological villainy would be ideal. The death cap, which has long been upheld as the most dangerous and deadly of mushrooms, is responsible for the majority of serious poisonings and deaths by mushrooms across the world. In Europe, it accounts for an estimated 80–90 percent of mushroom-related deaths.² In the United States, serious poisonings by Amanita mushrooms have mostly involved the death cap and the closely related destroying angels, A. bisporigera, A. virosa, and A. ocreata. (See #12 in the color insert.)

The Amanitas

The death cap is a medium-large, beautiful mushroom with greenish-beige cap commonly found in forested regions across much of Europe and Asia. Though not native to North America, it was introduced to this country in the last century, most likely as an inadvertent mycorrhizal hitchhiker on the rootstock of imported trees, especially European oaks, pines, and spruce. In the United States, it has become naturalized and common in the West Coast states of Washington, Oregon, and Central and Northern California. The death cap is also found increasingly in the Midwest, Mid-Atlantic states, and southern New England. The mushroom was recently collected in Maine for the first time. Though it seems to prefer growing with species of trees in the oak family, it also is found with species of pine, spruce, birch, hornbeam, and horse chestnut, and reportedly now with hemlock. Rod Tulloss, one of the leading authorities on the genus Amanita in North America, reports that, in the western hemisphere, the death cap has been introduced into locations from Canada to Argentina, and, therefore, few forested regions should assume they are safe from this deadly mushroom species. Once established in an area on introduced trees, it can naturalize onto native trees and shrubs, a behavior that’s been noted extensively on the West Coast. Such migration of an introduced mycorrhizal fungus onto native plant species is being increasingly referred to as mycorrhizal invasion. So far, in the Northeast the death cap has been more restricted, and has rarely spread from plantation sites where it’s been initially established.³

The death cap is so dangerous, in part, because it resembles several edible members of Amanita, as well as edible species of the genus Volvariella. The paddy straw mushroom, Volvariella volvacea, is a popular edible mushroom of the tropics, especially in Asia, where it is widely cultivated on rice straw. It is frequently used in Asian cooking and is widely available canned in the United States. A second species, the common volvariella, Volvariella speciosa, is an edible mushroom regularly found in gardens and fields. Both of these species share the characteristic distinctive volva of the amanita, a cup of tissue surrounding the base of the stem that is the remnants of the universal veil, a sac fully enclosing the young mushroom in the button stage. Because the edible volvariellas are normally collected and consumed in the firm button stage, enclosed within or barely out of the universal sac, they look a great deal like young amanitas in the button stage. Several families who have mistakenly eaten the death cap have been recent Asian immigrants to the United States and naïve about the wild mushrooms in their adopted country, believing they were collecting edible mushrooms. This scenario—of new immigrants collecting and eating mushrooms resembling a known edible back home—is one of the most common situations in which deadly amanitas are eaten in America. A significant proportion of amatoxin poisonings in America in recent years involve newly arrived or first-generation immigrants.

As with many groups of mushrooms, the taxonomy of the genus Amanita is complex and the understanding of the relationships among species is in flux. Many current mushroom guides refer to the North American species of destroying angels as Amanita virosa or A. verna. Recent taxonomic studies suggest that both of these names refer to European species and that the majority of pure white Amanita species in our northeastern woods belong to the species Amanita bisporigera.⁴ The genus Amanita is quite large worldwide, encompassing more than 500 “named species” according to Amanita expert Rod Tulloss, and mycologists generally agree that the North American amanitas are not well understood. I recall a conversation with Tulloss at the 2007 Northeast Mycological Federation Foray in Orono, Maine, in which he recalled his state of mind at the onset of his Amanita studies. He said that, at the time, he felt that it would be a good project of relatively short duration. Now, many years later, he regularly comes across specimens that don’t correspond with any known species and admits that a revision of the group is nowhere near completion.

The Toxins: Amatoxins

Amatoxins, the liver-destroying toxins found in amanitas, are so potent that it takes as little as 0.1 milligram (mg) of alpha-amanitin per kilogram of body weight to kill a person. A lethal dose for the average-sized adult is only 6–7 mg. Analyses of mushrooms show that Amanita phalloides caps contain between 0.5 and 1.5 mg of alpha-amanitin per gram of tissue, with the greatest concentration in the gills of the mushroom. Since the cap of A. phalloides can easily weigh 50–60 grams, a cap that is four inches in diameter could contain enough toxin to kill several people!⁵ The cap of a destroying angel, Amanita bisporigera, contains, on average, about half the concentration of alpha-amanitin as a death cap, which makes it less potent, though still capable of causing death. Concentrations of the toxins can vary according to the age of the mushrooms, between mushrooms found in different locales, and even between individual mushrooms growing together in the same locale.

By way of comparison, consider the standard dosages of several common products: In general, it takes 200–400 mg of Ibuprofen or 325–650 mg of aspirin to treat a headache. To treat an infection like strep throat, we may take 200–500 mg of an antibiotic twice a day for ten days. And a 16-ounce Starbucks regular drip coffee delivers, on average, 320 mg of caffeine. Yet only 6 mg of amanitin will kill 50 percent of the adults who consume it.

Amatoxins kill people by shutting down protein synthesis in affected organs. More specifically, alpha-amanitin binds with an enzyme known as RNA polymerase II and prevents it from functioning. RNA polymerase II is responsible for assisting the body in building proteins as directed by our cellular DNA architecture. When protein production stops, cell division shuts down. When somebody eats a death cap, amanitins are absorbed through the gut, pass through the bloodstream, and end up concentrated in organs that need proteins to rapidly replace cells, primarily the liver and secondarily the kidneys. These organs bear the brunt of early amatoxin damage; death and near death experienced from eating amanitas is typically due to liver failure.⁶

The Course of Amatoxin Poisoning

By all accounts from the people who survived to tell us about it, the deadly amanitas are tasty and will be enjoyed in direct proportion to the skill of the cook. The first sign of difficulty begins six to twelve hours after eating the mushroom. A more rapid onset of symptoms of amatoxin poisoning often signals a greater intake of toxins and a poorer prognosis, as was the case with a woman in New York State who died in 2009 following a meal of at least a dozen Amanita bisporegera and who was reported to have the onset of illness in four to five hours. The delayed onset of symptoms is typical in amatoxin poisoning and a hallmark indicator of the potential severity of the poisoning.

With amatoxin poisoning, the initial symptom phase is marked by severe gastrointestinal distress including copious, watery, or even bloody diarrhea, cramps, nausea, and vomiting. These symptoms generally last 24–40 hours before slowly abating, leaving the victim weak, worn, and fragile. At this point, victims who have sought medical attention are sometimes sent home to complete their recovery, especially if the medical providers don’t know they have a case of amatoxin poisoning on their hands. Thus begins the secondary latency period, a honeymoon phase lasting another 24–48 hours and ending with the onset of symptoms of organ deterioration or failure. The gastrointestinal symptoms start again with new bouts of cramps and diarrhea and the individual will appear jaundiced. Laboratory tests show signs of a compromised liver or liver failure and possibly compromised or failing kidneys. In severe cases, without proper and timely medical intervention, the course will progress to convulsions, coma, and death due to liver or multiple organ failure, which generally happens, on average, six to eight days after the person ate the mushrooms.⁷

Prompt medical attention is the key to saving lives. The appropriate blood tests to assess liver function can indicate early signs of liver distress during the initial gastrointestinal phase, giving medical staff the opportunity to support liver function as they work to prevent absorption of toxins and maintain hydration and healthy blood chemistry. Knowing the identity of the mushrooms that the victim ate greatly aids in the early treatment and improves their chances of survival. However, accurate identification can present a problem. Given the delayed onset of symptoms, there is often no remaining uneaten food and any that has been eaten has already passed through the victim’s digestive tract. In some cases, mushroom identification can be made from an analysis of spores in the victim’s vomit or stool samples. Treatment should never be delayed pending identification. Treat the symptoms present!

Synopsis of Treatment Priorities for Amatoxin Poisoning
The medical interventions practiced by alert and prepared medical teams reduce toxin intake and absorption and support bodily systems through:⁸

• Early monitoring of liver function through lab tests.

• Efforts to prevent or minimize toxin absorbtion through the use of:

• Activated charcoal to bind toxins remaining in the GI tract

• Silymarin (milk thistle extract sold under the trade name Legalon), shown to decrease the binding of the toxins in the liver and responsible for saving lives in Europe and recently in the United States⁹

• Penicillin G in massive doses that helps to reduce toxin reuptake

• Support of adequate hydration through the use of IV fluids to replace fluids lost through gastrointestinal disturbance and increased urine flow.

• Liver albumin dialysis through the use of a Molecular Absorbent Recirculating System (MARS) to filter toxins from the blood and cleanse the liver, giving it an opportunity to regenerate or time to wait for a transplant.¹⁰ This has been practiced primarily in Europe.

The initial latency period prior to the onset of symptoms also allows much of the toxin to pass beyond the gut and therefore beyond “recall” from gastric lavage or the use of activated charcoal to absorb the toxins. Studies have shown that the kidneys remove amanitin from the blood and it is excreted in urine. Therefore treatment always includes hydration to increase urine production and maintain electrolyte balance in light of the losses from gastrointestinal distress. In addition, massive doses of penicillin G have been shown to be effective in reducing the reuptake of the toxin from the bile, where it concentrates following passage through the liver.

Because the death cap is native to Europe and quite common there, and because far more continental Europeans than Americans hunt and eat mushrooms, European medical authorities have developed extensive experience and more sophisticated methods of treating amanitin victims than have North American doctors. For some years, Europeans have acknowledged the availability and use of injectable silymarin (milk thistle extract) for dramatic improvement in outcomes of severe amatoxin poisonings. Although it has not been approved for regular use in this country, the Food and Drug Administration granted approval for its emergency use in a 2007 California case involving four people who nearly died following the ingestion of death cap mushrooms. Although one elderly patient later died of kidney failure, the others experienced dramatic improvement in liver functioning following the silymarin treatment and recovered.¹¹ Mushroom poisoning experts and the medical personnel addressing the rare cases of amatoxin poisoning hope that injectable silymarin will be granted approval for use in the United States. The rare occurrence of such poisoning in the United States, coupled with the deadliness of amatoxin, does not lend itself to the clinical trials required by the FDA for approval of new drugs or the development of new intervention techniques.

As doctors and researchers begin to understand more about the remarkable regenerative ability of liver tissue, the Europeans have also increasingly been using a technique called liver albumin dialysis that uses a Molecular Absorbent Recirculating System (MARS).¹² MARS therapy assists in the removal of toxins from the blood, temporarily replacing the function of the liver, which has shown the ability to return to full functioning if bodily functions can be supported while it has time to rejuvenate. The MARS system was approved for use by the FDA in 2005 and should now become available for use in poisoning cases in the United States. The kidneys have far less regenerative ability than the liver, and amatoxin victims often live with chronic compromised kidney function following a poisoning.

Amatoxin Poisoning in the United States

Between 2003 and 2007, an unusually high number of cases of Amanita poisonings occurred across North America. Sixteen incidents involving seventy-one people poisoned by amatoxin-containing species were reported. These cases resulted in twenty-three deaths, a number almost unheard of in North America.¹³ (Until 2003, there had been an average of less than one death per year from all mushroom poisonings in the United States.) Of the total number, four of the deaths were in the United States and Canada, and eighteen were in Mexico. Michael Beug of NAMA reported his concern that the markedly higher death rate in Mexico was due to the lack of availability of liver transplants and the intensive medical support reviewed above. A liver transplant is the final life-saving intervention when a person’s liver function collapses and death is imminent. In countries with responsive and knowledgeable medical infrastructures, the death rate from amatoxin poisoning is around 10 percent. In countries where modern medical facilities are less available, the death rate, in the absence of intensive medical intervention, is closer to 50 percent.¹⁴

Any abrupt rise in the number of deaths attributed to mycophagy in North America is disconcerting, to say the least. Although it is too soon to discern a long-term trend or to make clear meaning from this recent increase, a few questions are in order. Does the trend reflect an increase in eating wild mushrooms and if so, are there specific groups of people that can be identified as at greater risk? Outreach is needed to educate recent Asian immigrants to alert them to the resemblance between edible paddy straw mushrooms and the death cap. In many European countries with extensive history of mycophagy and a larger percentage of the population collecting and eating wild mushrooms, the incidence of minor and severe poisonings is much higher than in North America. Are we likely to continue to see an upward trend in the number of poisoning cases as America increases use of wild mushrooms? It could be that the increasing cases of severe poisonings are due primarily to the spread of the death cap in North America. Over time we can gather the information needed to tell whether this is indeed a trend or just a tragic anomaly. Whatever the case, the good news for those worried about toxic mushrooms is that there exists a fairly foolproof way to avoid those amanitas containing amatoxins: don’t eat any species from the genus or look-alike groups. For some people, it turns out, this can prove rather difficult.

A couple of years ago I got a call from my friend Dan one late summer afternoon. Dan had taken one of my mushroom identification courses and had quickly become quite seriously infected with the mushroom foraging bug. Dan was a cancer survivor and he incorporated many medicinal mushrooms into his diet to help maintain his health. Foraging mushrooms became a perfect complement to daily nature walks and as a practitioner of Qi Gong, his walking meditations served as an ideal way to be present in the moment and the beauty of the natural world. That summer and fall, however, Dan was often distracted by the presence of great edible and medicinal mushrooms along his walk routes.

On this day, he called to consult me about a batch of blusher mushrooms, Amanita rubescens, that he’d found that morning and was inclined to cook up for dinner. His description over the phone seemed clear and I agreed that he likely had a basket of blushers. According to most field guides, this is a good edible species, though most authors also caution readers to avoid this mushroom (and all other amanitas) due to its deadly cousins. Dan told me he intended to eat them, but his nervous tone belied his uncertainty. He quickly added, “What do you think I should do?”

Dan was caught up in an evolutionary phase that is part of the maturation most mushroom hunters pass through. “If the books call it an edible species, I should eat it” or “the more the merrier.” As food-driven collectors become familiar with the common mushrooms and grow increasingly comfortable identifying different species, they often seem to feel an internal pressure to increase the number of edible mushrooms they’ve tried. Some risk-taking collectors develop an element of “extreme mushrooming,” the need to collect and eat an ever-increasing number of mushrooms. When this competitive nature is applied to amanitas, Michael Kuo refers to it as amanita bravado, a behavioral disorder. “Sometimes, mushroom hunters with considerable identification skills are able to successfully identify and eat some of the nonpoisonous amanitas without experiencing ill effects.” Kuo goes further in expressing his concern that following a dinner of amanitas, the mushroom hunter brags of his exploits to more novice hunters who may lack the identification skills needed to safely collect and eat from this high-risk group of mushrooms. “This is a dangerous state of affairs for obvious reasons, and the people involved have made little social progress since high school. If you have enjoyed a nice meal of amanitas, keep it to yourself. Bragging about it only creates social pressure for others, with less identification experience, to make a potentially fatal mistake.”¹⁵

I told Dan that even though I was quite confident in my ability to recognize blushers from many yards down a woodland path, I had never eaten them. In keeping with my painfully gained, somewhat conservative philosophy of foraging for edible mushrooms, I replied to my friend, “Why bother?” Why bother collecting and eating amanita mushrooms, no matter how edible, when they are so closely related to the deadliest mushrooms in the world? Especially during high mushroom season when there are great edibles practically leaping into the collecting basket. And especially if you have compromised health.

Dan took my advice about his basket of blushers and later told me that the conversation had taken root. He was, thereafter, less driven to convert every potentially edible mushroom into dinner. His wife, who had been growing increasingly alarmed with what she considered his risk-taking, was relieved and encouraged by the tempering of his enthusiasm. Being a good forager does not require an ever increasing “life list” of edible mushroom species.