Relevance to Humans and Ecosystems


Mushroom Poisoning

Mushroom poisoning is caused by the consumption of raw or cooked fruiting bodies (mushrooms, toadstools) of a number of species of higher fungi. The term toadstool (from the German Todesstuhl, death's stool) is commonly given to poisonous mushrooms, but for individuals who are not experts in mushroom identification there are generally no easily recognizable differences between poisonous and nonpoisonous species. Old wives' tales notwithstanding, there is no general rule of thumb for distinguishing edible mushrooms and poisonous toadstools. The toxins involved in mushroom poisoning are produced naturally by the fungi themselves, and each individual specimen of a toxic species should be considered equally poisonous. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing. Thus, the only way to avoid poisoning is to avoid consumption of the toxic species. Poisonings in the United States occur most commonly when hunters of wild mushrooms (especially novices) misidentify and consume a toxic species, when recent immigrants collect and consume a poisonous American species that closely resembles an edible wild mushroom from their native land, or when mushrooms that contain psychoactive compounds are intentionally consumed by persons who desire these effects.

Nature of Disease

Mushroom poisonings are generally acute and are manifested by a variety of symptoms and prognoses, depending on the amount and species consumed. Because the chemistry of many of the mushroom toxins (especially the less deadly ones) is still unknown and positive identification of the mushrooms is often difficult or impossible, mushroom poisonings are generally categorized by their physiological effects. There are four categories of mushroom toxins: protoplasmic poisons (poisons that result in generalized destruction of cells, followed by organ failure); neurotoxins (compounds that cause neurological symptoms such as profuse sweating, coma, convulsions, hallucinations, excitement, depression, spastic colon); gastrointestinal irritants (compounds that produce rapid, transient nausea, vomiting, abdominal cramping, and diarrhea); and disulfiram-like toxins. Mushrooms in this last category are generally nontoxic and produce no symptoms unless alcohol is consumed within 72 hours after eating them, in which case a short-lived acute toxic syndrome is produced.

Diagnosis of Human Illness

A clinical testing procedure is currently available only for the most serious types of mushroom toxins, the amanitins. The commercially available method uses a 3H-radioimmunoassay (RIA) test kit and can detect sub-nanogram levels of toxin in urine and plasma. Unfortunately, it requires a 2-hour incubation period, and this is an excruciating delay in a type of poisoning which the clinician generally does not see until a day or two has passed. A 125I-based kit which overcomes this problem has recently been reported, but has not yet reached the clinic. A sensitive and rapid HPLC technique has been reported in the literature even more recently, but it has not yet seen clinical application. Since most clinical laboratories in this country do not use even the older RIA technique, diagnosis is based entirely on symptomology and recent dietary history. Despite the fact that cases of mushroom poisoning may be broken down into a relatively small number of categories based on symptomatology, positive botanical identification of the mushroom species consumed remains the only means of unequivocally determining the particular type of intoxication involved, and it is still vitally important to obtain such accurate identification as quickly as possible. Cases involving ingestion of more than one toxic species in which one set of symptoms masks or mimics another set are among many reasons for needing this information. Unfortunately, a number of factors (not discussed here) often make identification of the causative mushroom impossible. In such cases, diagnosis must be based on symptoms alone. In order to rule out other types of food poisoning and to conclude that the mushrooms eaten were the cause of the poisoning, it must be established that everyone who ate the suspect mushrooms became ill and that no one who did not eat the mushrooms became ill. Wild mushrooms eaten raw, cooked, or processed should always be regarded as prime suspects. After ruling out other sources of food poisoning and positively implicating mushrooms as the cause of the illness, diagnosis may proceed in two steps. The first step, outlined in Table 1, provides an early indication of the seriousness of the disease and its prognosis.

As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged.

Associated Foods

Mushroom poisonings are almost always caused by ingestion of wild mushrooms that have been collected by nonspecialists (although specialists have also been poisoned). Most cases occur when toxic species are confused with edible species, and a useful question to ask of the victims or their mushroom-picking benefactors is the identity of the mushroom they thought they were picking. In the absence of a well- preserved specimen, the answer to this question could narrow the possible suspects considerably. Intoxication has also occurred when reliance was placed on some folk method of distinguishing poisonous and safe species. Outbreaks have occurred after ingestion of fresh, raw mushrooms, stir-fried mushrooms, home-canned mushrooms, mushrooms cooked in tomato sauce (which rendered the sauce itself toxic, even when no mushrooms were consumed), and mushrooms that were blanched and frozen at home. Cases of poisoning by home-canned and frozen mushrooms are especially insidious because a single outbreak may easily become a multiple outbreak when the preserved toadstools are carried to another location and consumed at another time.

Specific cases of mistaken mushroom identity appears frequently. The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra. Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta. The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3. Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus, Lactarius, Russula, Tricholoma, Coprinus, Pluteus, and others. The Inky Cap Mushroom (Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned. Some other members of the genus Coprinus (Shaggy Mane, C. comatus; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided.

Most of the psychotropic mushrooms (Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom (Psilocybe cubensis) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible. Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom (Marasmius oreades) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom (Gymnopilus spectabilis), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A. pantherina varieties are the Yellow Blusher (Amanita flavorubens). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom (Armillariella mellea). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs.

Relative Frequency of Disease

Accurate figures on the relative frequency of mushroom poisonings are difficult to obtain. For the 5-year period between 1976 and 1981, 16 outbreaks involving 44 cases were reported to the Centers for Disease Control in Atlanta (Rattanvilay et al. MMWR 31(21): 287-288, 1982). The number of unreported cases is, of course, unknown. Cases are sporadic and large outbreaks are rare. Poisonings tend to be grouped in the spring and fall when most mushroom species are at the height of their fruiting stage. While the actual incidence appears to be very low, the potential exists for grave problems. Poisonous mushrooms are not limited in distribution as are other poisonous organisms (such as dinoflagellates). Intoxications may occur at any time and place, with dangerous species occurring in habitats ranging from urban lawns to deep woods. As Americans become more adventurous in their mushroom collection and consumption, poisonings are likely to increase.

Course of Disease and Complications

The normal course of the disease varies with the dose and the mushroom species eaten. Each poisonous species contains one or more toxic compounds which are unique to few other species. Therefore, cases of mushroom poisonings generally do not resembles each other unless they are caused by the same or very closely related mushroom species. Almost all mushroom poisonings may be grouped in one of the categories outlined above.



Several mushroom species, including the Death Cap or Destroying Angel (Amanita phalloides, A. virosa), the Fool's Mushroom (A. verna) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins. Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver. Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney.

Target Populations

All humans are susceptible to mushroom toxins. The poisonous species are ubiquitous, and geographical restrictions on types of poisoning that may occur in one location do not exist (except for some of the hallucinogenic LBMs, which occur primarily in the American southwest and southeast). Individual specimens of poisonous mushrooms are also characterized by individual variations in toxin content based on genetics, geographic location, and growing conditions. Intoxications may thus be more or less serious, depending not on the number of mushrooms consumed, but on the dose of toxin delivered. In addition, although most cases of poisoning by higher plants occur in children, toxic mushrooms are consumed most often by adults. Occasional accidental mushroom poisonings of children and pets have been reported, but adults are more likely to actively search for and consume wild mushrooms for culinary purposes. Children are more seriously affected by the normally nonlethal toxins than are adults and are more likely to suffer very serious consequences from ingestion of relatively smaller doses. Adults who consume mushrooms are also more likely to recall what was eaten and when, and are able to describe their symptoms more accurately than are children. Very old, very young, and debilitated persons of both sexes are more likely to become seriously ill from all types of mushroom poisoning, even those types which are generally considered to be mild.

Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected.

Food Analysis

The mushroom toxins can with difficulty be recovered from poisonous fungi, cooking water, stomach contents, serum, and urine. Procedures for extraction and quantitation are generally elaborate and time-consuming, and the patient will in most cases have recovered by the time an analysis is made on the basis of toxin chemistry. The exact chemical natures of most of the toxins that produce milder symptoms are unknown. Chromatographic techniques (TLC, GLC, HPLC) exist for the amanitins, orellanine, muscimol/ibotenic acid, psilocybin, muscarine, and the gyromitrins. The amanitins may also be determined by commercially available 3H-RIA kits. The most reliable means of diagnosing a mushroom poisoning remains botanical identification of the fungus that was eaten. An accurate pre-ingestion determination of species will also prevent accidental poisoning in 100% of cases. Accurate post-ingestion analyses for specific toxins when no botanical identification is possible may be essential only in cases of suspected poisoning by the deadly Amanitas, since prompt and aggressive therapy (including lavage, activated charcoal, and plasmapheresis) can greatly reduce the mortality rate.

Selected Outbreaks

Isolated cases of mushroom poisoning have occurred throughout the continental United States.

The popular interest in gathering and eating uncultivated mushrooms has been associated with an increase in incidents of serious mushroom-related poisonings. From December 28, 1996, through January 6, 1997, nine persons in northern California required hospitalization after eating Amanita phalloides (i.e., "death cap") mushrooms; two of these persons died. Risks associated with eating these mushrooms result from a potent hepatotoxin. This report describes four cases of A. phalloides poisoning in patients admitted to a regional referral hospital in northern California during January 1997 and underscores that wild mushrooms should not be eaten unless identified as nonpoisonous by a mushroom expert.

Another one occurred in Oregon in October,1988, and involved the intoxication of five people who consumed stir-fried Amanita phalloides. The poisonings were severe, and at this writing three of the five people had undergone liver transplants for treatment of amanitin-induced liver failure.

Other cases have included the July, 1986, poisoning of a family in Philadelphia, by Chlorophyllum molybdites; the September, 1987, intoxication of seven men in Bucks County, PA, by spaghetti sauce which contained Jack O'Lantern mushroom (Omphalotus illudens); and of 14 teenage campers in Maryland by the same species (July, 1987). A report of a North Carolina outbreak of poisoning by False Morel (Gyromitra spp.) appeared in 1986. A 1985 report details a case of Chlorophyllum molybdites which occurred in Arkansas; a fatal poisoning case caused by an amanitin containing Lepiota was described in 1986.

In 1981, two Berks County, PA, people were poisoned (one fatally) after ingesting Amanita phalloides, while in the same year, seven Laotian refugees living in California were poisoned by Russula spp.

In separate 1981 incidents, several people from New York State were poisoned by Omphalotus illudens, Amanita muscaria, Entoloma lividum, and Amanita virosa.

An outbreak of gastroenterititis during a banquet for 482 people in Vancouver, British Columbia, was reported by the Vancouver Health Department in June, 1991. Seventy-seven of the guests reported symptoms consisting of early onset nausea (15-30 min), diarrhea (20 min-13 h), vomiting (20-60 min), cramps and bloated feeling. Other symptoms included feeling warm, clamminess, numbness of the tongue and extreme thirst along with two cases of hive-like rash with onset of 3-7 days. Bacteriological tests were negative. This intoxication merits special attention because it involved consumption of species normally considered not only edible but choice. The fungi involved were the morels Morchella esculenta and M. elata (M. angusticeps), which were prepared in a marinade and consumed raw. The symptoms were severe but not life threatening. Scattered reports of intoxications by these species and M. conica have appeared in anecodotal reports for many years.

Numerous other cases exist; however, the cases that appear in the literature tend to be the serious poisonings such as those causing more severe gastrointestinal symptoms, psychotropic reactions, and severe organ damage (deadly Amanita). Mild intoxications are probably grossly underreported, because of the lack of severity of symptoms and the unlikeliness of a hospital admission.

US Food and Drug Administration


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Gyromitra esculenta

Gyromitra esculenta
View the Mycomorphbox template that generates the following list
Mycological characteristics
smooth hymenium
cap is convex
hymenium attachment is not applicable
stipe is bare

spore print is yellow

to buff

ecology is saprotrophic

or mycorrhizal

edibility: choice

or deadly

Gyromitra esculenta /ˌrɵˈmtrə ˌɛskjʉˈlɛntə/, one of several species of fungi known as false morels, is an ascomycete fungus from the genus Gyromitra, widely distributed across Europe and North America. It normally sprouts in sandy soils under coniferous trees in spring and early summer. The fruiting body, or mushroom, is an irregular brain-shaped cap dark brown in colour which can reach 10 cm (4 in) high and 15 cm (6 in) wide, perched on a stout white stipe up to 6 cm (2.4 in) high.

Although potentially fatal if eaten raw, Gyromitra esculenta is a popular delicacy in Scandinavia, Eastern Europe, and the upper Great Lakes region of North America. Although popular in some districts of the eastern Pyrenees, it is prohibited from sale to the public in Spain. It may be sold fresh in Finland, but it must be accompanied by warnings and instructions on correct preparation.

Although it is still commonly parboiled before preparation, recent evidence suggests that even this procedure may not make the fungus entirely safe,[1] thus raising concerns of risk even when prepared properly. When consumed, the false morel's principal active agent, gyromitrin, is hydrolyzed into the toxic compound monomethylhydrazine (MMH). The toxin affects the liver, central nervous system, and sometimes the kidneys. Symptoms of poisoning involve vomiting and diarrhea several hours after consumption, followed by dizziness, lethargy and headache. Severe cases may lead to delirium, coma and death after 5–7 days.

Taxonomy and naming[edit]

The fungus was first described in 1800, by mycologist Christian Hendrik Persoon, as Helvella esculenta,[2] and gained its current accepted binomial name when the Swedish mycologist Elias Magnus Fries placed it in the genus Gyromitra in 1849.[3] The genus name is derived from the Greek terms gyros/γυρος "round" and mitra/μιτρα "headband".[4] Its specific epithet is derived from the Latin esculentus, "edible".[5]

It is known by a variety of common descriptive names such as "brain mushroom,"[6] "turban fungus,"[7] elephant ears,[8] or "beefsteak mushroom/morel," although beefsteak mushroom can also refer to the much less toxic Fistulina hepatica.[9] Dating from the 19th century, the German term lorchel is a result of the older lorche, itself from the 18th century Low German Lorken, aligning with the similar sounding (and similar looking) morchel.[10][11]

Gyromitra esculenta is a member of a group of fungi known as "false morels", so named for their resemblance to the highly regarded true morels of the genus Morchella. The grouping includes other species of the genus Gyromitra, such as G. infula (elfin saddle), G. caroliniana and G. gigas (snow morel). While some of these species contain little to no gyromitrin, many guidebooks recommend treating them all as poisonous, since their similar appearance and significant intraspecific variation can make reliable identification difficult.[12]

The more distantly related ascomycete mushrooms of the genus Verpa, such as V. bohemica and V. conica, are also known as false morels, early morels or thimble morels; like the Gyromitra, they are eaten by some and considered poisonous by others.[13]

The genus Gyromitra had been classically considered part of the family Helvellaceae, along with the similar-looking elfin saddles of the genus Helvella. Analysis of the ribosomal DNA of many of the Pezizales showed Gyromitra esculenta and the other false morels to be only distantly related to the other members of the Helvellaceae and instead most closely related to the genus Discina, forming a clade which also contains Pseudorhizina and Hydnotrya. Thus the four genera are now included in the family Discinaceae.[14]


A younger specimen with a less wrinkled cap

Resembling a brain, the irregularly shaped cap may be up to 10 centimetres (3.9 in) high and 15 centimetres (5.9 in) wide. Initially smooth, it becomes progressively more wrinkled as it grows and ages. The cap colour may be various shades of reddish-, chestnut-, purplish-, bay-, dark or sometimes golden-brown. Specimens from California may have more reddish-brown caps.[6] Attached to the cap at several points, the stipe is 3–6 centimetres (1.2–2.4 in) high and 2–3 centimetres (0.8–1.2 in) wide. Gyromitra esculenta has a solid stipe whereas those of true morels (Morchella spp.) are hollow.[15] The smell can be pleasant and has been described as fruity, and the fungus is mild-tasting. The spore print is whitish, with transparent spores that are elliptical and 17–22 μm in length.[16]

G. esculenta resembles the various species of true morel, although the latter are more symmetric and look more like pitted gray, tan, or brown sponges. Its cap is generally darker and larger.[17]

Distribution and habitat[edit]

Gyromitra esculenta grows on sandy soil in Temperate coniferous forest and occasionally in deciduous woodlands. Among conifers it is mostly found under pines (Pinus spp.), but also sometimes under aspen (Populus spp.).[18] The hunting period is from April to July, earlier than for other species, and the fungus may even sprout up with the melting snow.[6] It can be abundant in some years and rare in others. The mushroom is more commonly found in places where ground has been disturbed, such as openings, rivulets, washes, timber clearings, plowed openings, forest fire clearings, and roadsides.[15] Enthusiasts in Finland have been reported burying newspaper inoculated with the fungus in the ground in autumn and returning the following spring to collect mushrooms.[19]

Although more abundant in montane and northern coniferous woodlands such as the Sierra Nevada and the Cascade Range in northwestern North America, Gyromitra esculenta is found widely across the continent,[6] as far south as Mexico.[20] It is also common in Central Europe, less abundant in the east, and more in montane areas than lowlands.[7] It has been recorded from Northern Ireland,[21] from Uşak Province in Western Turkey,[22] and from the vicinity of Kaş in the Antalya Province of Turkey's southern coast.[23]


For sale with warning sign, Market Square, Helsinki

Toxic reactions have been known for at least a hundred years. Experts speculated the reaction was more of an allergic one specific to the consumer, or a misidentification, rather than innate toxicity of the fungus, due to the wide range in effects seen. Some would suffer severely or perish while others exhibited no symptoms after eating similar amounts of mushrooms from the same dish. Yet others would be poisoned after eating Gyromitra esculenta for many years without ill-effects.[24] However, the fungus is now widely recognized as potentially deadly.[25]

Gyromitra esculenta contains levels of the poison gyromitrin that vary locally among populations; although these mushrooms are only rarely involved in poisonings in either North America or Western Europe, intoxications are seen frequently in eastern Europe and Scandinavia.[26] A 1971 Polish study reported at the time that the species accounted for up to 23% of mushroom fatalities each year.[27] Death rates have dropped since the mid-twentieth century; in Sweden poisoning is common, though life-threatening poisonings have not been detected and there was no fatality reported over the 50 years from 1952 to 2002.[28] Gyromitra poisonings are rare in Spain, due to the widespread practice of drying the mushrooms before preparation and consumption,[29] but has a mortality rate of about 25%.[30]

A lethal dose of gyromitrin has been estimated to be 10–30 mg/kg for children and 20–50 mg/kg in adults. These doses correspond to around 0.2–0.6 kilograms (0.4–1.3 lb) and 0.4–1 kilogram (0.9–2.2 lb) of fresh mushroom respectively.[31] However, individual responses may vary and people who have ingested similar amounts may develop anything from minimal to severe toxicity.[32] Evidence suggests that children are more severely affected; it is unclear whether this is due to a larger weight consumed per body mass ratio or to differences in enzyme and metabolic activity.[33] Although the amount of gyromitrin present can be significantly reduced through parboiling, there is evidence that repeated consumption can increase risk of toxicity.[32]

Geographical variation[edit]

Populations of Gyromitra esculenta appear to vary geographically in their toxicity. A French study has shown that mushrooms collected at higher altitudes have lower concentrations of toxin than those from lower elevations,[33] and there is some evidence that fungi west of the Rocky Mountains in North America contain less toxin than those to the east.[34] However, poisonings in the west have been reported,[35] although less frequently than in Europe.[36]


MMH (CH3N2H3), a toxic metabolite

The identity of the toxic constituents eluded researchers until 1968, when acetaldehyde N-methyl-N-formylhydrazone, better known as gyromitrin, was isolated.[37] Gyromitrin is a volatile water-soluble hydrazine compound hydrolyzed in the body into monomethylhydrazine (MMH). Other N-methyl-N-formylhydrazone derivatives have been isolated in subsequent research, although they are present in smaller amounts. These other compounds would also produce monomethylhydrazine when hydrolyzed, although it remains unclear how much each contributes to the false morel's toxicity.[38]

The toxins react with pyridoxal-5-phosphate—the activated form of pyridoxine—and form a hydrazone. This reduces production of the neurotransmitter GABA via decreased activity of glutamic acid decarboxylase,[39] producing the neurological symptoms. MMH also causes oxidative stress leading to methemoglobinemia.[31] Additionally during the metabolism of MMH, N-methyl-N-formylhydrazine is produced; this then undergoes cytochrome p450 regulated oxidative metabolism which via reactive nitrosamide intermediates leads to formation of methyl radicals which lead to liver necrosis.[40][41] Inhibition of diamine oxidase (histaminase) elevates histamine levels resulting in headaches, nausea, vomiting, and abdominal pain.[42]


The symptoms of poisoning are typically gastrointestinal and neurological.[28] Symptoms occur within 6–12 hours of consumption, although cases of more severe poisoning may present sooner—as little as 2 hours after ingestion. Initial symptoms are gastrointestinal, with sudden onset of nausea, vomiting, and watery diarrhea which may be bloodstained. Dehydration may develop if the vomiting or diarrhea is severe. Dizziness, lethargy, vertigo, tremor, ataxia, nystagmus, and headaches develop soon after;[28] fever often occurs, a distinctive feature which does not develop after poisoning by other types of mushrooms.[43] In most cases of poisoning, symptoms do not progress from these initial symptoms, and patients recover after 2–6 days of illness.[27]

In some cases there may be an asymptomatic phase following the initial symptoms which is then followed by more significant toxicity including kidney damage,[44] liver damage, and neurological dysfunction including seizures and coma.[31] These signs usually develop within 1–3 days in serious cases.[28] The patient develops jaundice and the liver and spleen become enlarged, in some cases blood sugar levels will rise (hyperglycemia) and then fall (hypoglycemia) and liver toxicity is seen. Additionally intravascular hemolysis causes destruction of red blood cells resulting in increase in free hemoglobin and hemoglobinuria which can lead to renal toxicity or renal failure. Methemoglobinemia may also occur in some cases. This is where higher than normal levels of methemoglobin, which is a form of hemoglobin that can not carry oxygen, are found in the blood. It causes the patient to become short of breath and cyanotic.[45] Cases of severe poisoning may progress to a terminal neurological phase, with delirium, muscle fasciculations and seizures, and mydriasis progressing to coma, circulatory collapse, and respiratory arrest.[46] Death may occur from five to seven days after consumption.[47]


Treatment is mainly supportive; gastric decontamination with activated charcoal may be beneficial if medical attention is sought within a few hours of consumption. However, symptoms often take longer than this to develop, and patients do not usually present for treatment until many hours after ingestion, thus limiting its effectiveness.[48] Patients with severe vomiting or diarrhea can be rehydrated with intravenous fluids.[27] Monitoring of biochemical parameters such as methemoglobin levels, electrolytes, liver and kidney function, urinalysis, and complete blood count is undertaken and any abnormalities are corrected. Dialysis can be used if kidney function is impaired or the kidneys are failing. Hemolysis may require a blood transfusion to replace the lost red blood cells, while methemoglobinemia is treated with intravenous methylene blue.[49]

Pyridoxine, also known as vitamin B6, can be used to counteract the inhibition by MMH on the pyridoxine-dependent step in the synthesis of the neurotransmitter GABA. Thus GABA synthesis can continue and symptoms are relieved.[50] Pyridoxine, which is only useful for the neurological symptoms and does not decrease hepatic toxicity,[41][51] is given at a dose of 25 mg/kg; this can be repeated up to a maximum total of 15 to 30 g daily if symptoms do not improve.[52] Benzodiazepines are given to control seizures; as they also modulate GABA receptors they may potentially increase the effect of pyridoxine. Additionally MMH inhibits the chemical transformation of folic acid into its active form, folinic acid, this can be treated by folinic acid given at 20–200 mg daily.[31]


Monomethylhydrazine,[53] as well as its precursors methylformylhydrazine[54][55] and gyromitrin[56] and raw Gyromitra esculenta,[57] have been shown to be carcinogenic in experimental animals. Although Gyromitra esculenta has not been observed to cause cancer in humans,[58] it is possible there is a carcinogenic risk for people who ingest these types of mushrooms.[54] The toxins may be cumulative[32] and even small amounts may have a carcinogenic effect.[59] At least 11 different hydrazines have been isolated from Gyromitra esculenta, and it is not known if the potential carcinogens can be completely removed by parboiling.[1]


For sale in Helsinki

Despite its recognized toxicity, Gyromitra esculenta is marketed and consumed in several countries or states in Europe and North America. It was previously consumed in Germany, with fungi picked in and exported from Poland; more recently, however, Germany and Switzerland discouraged consumption by prohibiting its sale.[16][58] Similarly in Sweden, the Swedish National Food Administration warns it is not fit for human consumption,[60] and restricts purchase of fresh mushrooms to restaurants alone.[61] The mushroom is still highly regarded and consumed in Bulgaria, being sold in markets and picked for export there.[62] In some countries such as Spain, especially in the eastern Pyrenees, they are traditionally considered a delicacy, and many people report consuming them for many years with no ill effects.[63] Despite this, the false morel is listed as hazardous in official mushroom lists published by the Catalan Government[12] and sale to the public is prohibited throughout Spain.[64] Selling and purchasing fresh false morels is legal in Finland, where it is highly regarded.[65] However, the mushrooms are required by law to be accompanied with a warning that they are poisonous and legally prescribed preparation instructions.[66] False morels are also sold prepared and canned, in which case they are ready to be used. Official figures from the Finnish Ministry of Agriculture and Forestry report a total amount of false morels sold in Finland of 21.9 tonnes in 2006 and 32.7 tonnes, noted as being above average, in 2007.[67] In 2002, the Finnish Food Safety Authority estimated annual consumption of false morels to be hundreds of tonnes in plentiful years.[68] Outside of Europe, Gyromitra esculenta is consumed in the Great Lakes region and some western states in the United States.[69]

In Finnish cuisine, false morels may be cooked in an omelette, or gently sautéed in butter in a saucepan, flour and milk added to make a bechamel sauce, or pie filling. Alternatively, more fluid can be added for a false morel soup. Typical condiments added for flavour include parsley, chives, dill and black pepper.[70][71]


Cooked in a cream sauce

Most of the gyromitrin must be removed to render false morels edible. The recommended procedure involves either first drying and then boiling the mushrooms, or boiling the fresh mushrooms directly.[72] To prepare fresh mushroom it is recommended that they are cut into small pieces and parboiled twice in copious amounts of water, at least three parts water to one part chopped mushrooms, for at least five minutes, after each boiling the mushroom should be rinsed thoroughly in clean water.[72] Each round of parboiling reduces the gyromitrin contents to a tenth.[73] The gyromitrin is leached into the water where it will remain, therefore the parboiling water must be discarded and replaced with fresh water after each round of boiling. Drying the mushrooms can also reduce the concentration of gyromitrin; ten days of open air desiccation leads to the loss of 90% of gyromitrin.[32] However it is still recommended that the mushroom be boiled after drying.[72]

MMH boils at 87.5 °C (190 °F) and thus readily vaporizes into the air when water containing fresh false morels is boiled.[35] Poorly ventilated spaces allow vapor to accumulate, resulting in gyromitrin poisoning. If boiling the mushrooms indoors, care should be taken to ensure adequate ventilation, and, if symptoms of gyromitrin poisoning appear, immediately seek fresh air.[74] Even after boiling, small amounts of gyromitrin remain in the mushrooms. Given the possibility of accumulation of toxins, repeated consumption is not recommended.[75]

Prospects for cultivation[edit]

Strains with much lower concentrations of gyromitrin have been discovered, and the fungus has been successfully grown to fruiting in culture.[76] Thus there is scope for future research into cultivation of safer strains.[77]

See also[edit]


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