by Greg Marley
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 inte
nsive 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.
9
FALSE MORELS
The Finnish Fugu
All mushrooms are edible,
but some only once.
TRADITIONAL CROATIAN PROVERB
I f I haven’t made it obvious before, let me set the record straight: I live along the coast of Maine, and have made this beautiful state my home since 1981. Mainers have three seasons about which we can, and generally do, boast. Spring is not one of them. Winter is a postcard-perfect scene of ice, snow, cold wind, wet boots, and mittens. Summer, though slow to arrive and impatient to leave, is a blessed time of rain and sun, lush green hillsides, and perfect sailing, and it is not too hot except for perhaps three days a year. Autumn—what can I say beyond simply perfect? Fall is when the mushroom season peaks in both abundance and diversity. Fall is crisp cool nights and blustery sunny days, sweaters, and harvest. It leaves in a blaze of color.
Then there is spring, or what we note on the calendar as spring. March 23 came this year as it always does and, on that day, I looked out my window to a snow squall that was adding even more inches to a total that had already made the ski areas proud. True spring weather was still out of sight, around the corner of next month. Every year, before spring arrives, we go through a process of thaw that we affectionately call mud season, in which the surface of the earth transforms from a frozen solid to a non-frozen solid. In between the two solid states is mud—boot-grabbing, tire-miring mud—when you carry both an umbrella and a snow shovel. On the far side of mud season is May. May is when spring truly arrives in Maine, a month when life—put on hold all winter and restrained through mud season—explodes in an ecstatic burst of greenery and rushes on to summer. May is also the month we count on seeing our first mushrooms of the season.
Unlike the morel extravaganzas of Minnesota or Michigan, spring mushrooming opportunities in most of New England are not worth planning a vacation around. In general, saprobic fungi need the earth to be warmed in order to begin the active growth of their mycelial network. The mycelium feeding through the soil duff and dead wood debris generates the biomass reserves necessary to produce fruit. And mycorrhizal species growing in symbiosis with trees and shrubs generally do not start fruiting before early summer, when they begin receiving a boost of nutrients from their host trees. There are, however, a few notable exceptions. In the spring, a northeastern mushroomer might stumble across a few eager saprobic wood rotters such as the inky caps, spring oyster mushrooms, dryad’s saddle, and later, as the spring days warm, we find wine cap stropharia fruiting on wood mulch or rich garden soil. Some beautiful and interesting cup fungi, such as the scarlet cup (Sarcoscypha austriaca), also fruit in the spring, although not in abundance. Of course, the spring mushroom that has every dedicated mycophagist holding her or his breath in anticipation is the morel. No other mushroom in North America has more wid
espread recognition and elicits more passionate anticipation. But to know the morel, one must also learn the cautionary tale of another spring mushroom: the false morel.
False morels and morels, sometimes collectively called sponge mushrooms, are both groups of sac fungi or, more scientifically speaking, members of a division of fungi known as Ascomycota. These fungi mature their spores in saclike mother cells (microscopic asci) from which they are forcibly discharged upon maturity. Asci line the surface of the pits of morels or the surface of the folded tissue on false morels. There are about twelve species of false morels in North America, all members of the genus Gyromitra. They fruit on the ground, and most species can be recognized by distinctive complexly infolded caps that resemble the surface of a brain. A few are more cup-like without a distinct stalk. The best known among them is Gyromitra esculenta, known simply in the United States as the false morel. I will refer to this species as “the” false morel to differentiate from the group as a whole.1
DESCRIPTION
The overall shape of the false morel is difficult to describe because it is so variable. The cap, up to 5 inches in diameter, is generally irregularly spherical, but it often has irregular lobes and ridges forming peaks and valleys (see #13 in the color insert). The cap color ranges from pale brown to a warm reddish brown, but gradually darkens in age or certain weather conditions. The cap surface is complexly folded into a series of ridges resulting in a brain-like effect of wrinkled convolutions. The surface is smooth and slippery and without hairs or scales. The cap curls under and attaches irregularly to a ¾–2½-inch-thick dingy white or buff-colored stalk that is also irregularly shaped and thickens toward the base. The stalk can be hollow or stuffed with cottony tissue and there is clear separation between cap and stem. Once seen side by side, one would never mistake the false morel for a true morel. The brain-like convolutions of the false morel’s cap are very distinct from the pitted surface of the morel (see #2). Morels also have a distinctly hollow stalk that merges into the cap without clear distinction.
