Ecology

Associations

In Great Britain and/or Ireland:
Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita virosa is ectomycorrhizal with live root of Betula
Remarks: Other: uncertain

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita virosa is ectomycorrhizal with live root of Fagus
Remarks: Other: uncertain

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita virosa is ectomycorrhizal with live root of Quercus
Remarks: Other: uncertain

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita virosa is ectomycorrhizal with live root of Castanea sativa
Remarks: Other: uncertain

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Relevance to Humans and Ecosystems

Risks

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.

PROTOPLASMIC POISON

Amatoxins

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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Wikipedia

Amanita virosa

Amanita virosa
View the Mycomorphbox template that generates the following list
Mycological characteristics
gills on hymenium

cap is convex

or flat
hymenium is free
stipe has a ring and volva
spore print is white
ecology is mycorrhizal
edibility: deadly

Amanita virosa, commonly known as the European destroying angel, is a deadly poisonous basidiomycete fungus, one of many in the genus Amanita. Occurring in Europe, A. virosa associates with various deciduous and coniferous trees. The large fruiting bodies (i.e., the mushrooms) appear in summer and autumn; the caps, stipes and gills are all white in colour.

Immature specimens of A. virosa resemble several edible species commonly consumed by humans, increasing the risk of accidental poisoning. Along with its geographical namesakes, A. virosa is one of the most poisonous of all known poisonous mushrooms; its principal toxic constituent α-amanitin damages the liver and kidneys, often fatally.

Taxonomy and naming[edit]

The common name of destroying angel is applied to several all-white species of poisonous Amanita, to this species in Europe and to Amanita bisporiga in eastern North America, and A. ocreata in the west. A. virosa was first collected and described by Elias Magnus Fries in Sweden. Its specific epithet virosa derived from the Latin adjective virōsus 'toxic'[1][2] (compare virus).

Amanita virosa is very similar to several other species of all-white amanitas known as destroying angels, which has led to confusion over which occurs where. This specific name has been applied to all-white destroying angels occurring in North America, though others propose these all belong to A. bisporiga and other rarer species instead. There has been some question over whether Amanita verna is a valid species.

Description[edit]

A. virosa first appears as a white egg-shaped object covered with a universal veil. As it grows, the mushroom breaks free, though there may be ragged patches of veil at the cap edges. The cap is initially conical with inturned edges, before becoming hemispherical and flattening with a diameter up to 12 cm (4½ in). The cap often has a distinctive boss; it is able to be peeled and white, though the centre may be ivory in colour. The crowded free gills are white, as is the stipe and volva. The thin stipe is up to 15 cm (6 in) tall, with a hanging grooved ring. The spore print is white and the spores egg-shaped conical and 7–10 μm long. They stain blue with iodine. The flesh is white, with a taste reminiscent of radishes, and turns bright yellow with sodium hydroxide.[3]

This fungus highlights the danger of picking immature fungi as it resembles the edible mushrooms Agaricus arvensis and A. campestris, and the puffballs (Lycoperdon spp. ) before the caps have opened and the gills have become visible.

The ability to be peeled has been taken as a sign of edibility in mushrooming, which is a potentially lethal mistake in this species. It is unclear why this fungus, which more closely resembles edible species, has been implicated in fewer deaths than the death cap, though its rarity may contribute to this.[4]

Distribution and habitat[edit]

A. virosa is found in mixed woodland, especially in association with beech, on mossy ground in summer and autumn.[3] Most Amanita species form ectomycorrhizal relationships with the roots of certain trees.

Toxicity[edit]

young fruiting bodies showing conical caps

Amanita virosa is highly toxic, and has been responsible for severe mushroom poisonings.[5] Like the closely related death cap (A. phalloides), it contains the highly toxic amatoxins, as well as phallotoxins. Some authorities strongly advise against putting these fungi in the same basket with those collected for the table and to avoid touching them.[6][7]

Amatoxins consist of at least eight compounds with a similar structure, that of eight amino-acid rings; they were isolated in 1941 by Heinrich O. Wieland and Rudolf Hallermayer of the University of Munich.[8] Of the amatoxins, α-amanitin is the chief component and along with β-amanitin is likely responsible for the toxic effects.[9][10] Their major toxic mechanism is the inhibition of RNA polymerase II, a vital enzyme in the synthesis of messenger RNA (mRNA), microRNA, and small nuclear RNA (snRNA). Without mRNA essential protein synthesis and hence cell metabolism grind to a halt and the cell dies.[11] The liver is the principal organ affected, as it is the organ which is first encountered after absorption in the gastrointestinal tract, though other organs, especially the kidneys, are susceptible.[12]

The phallotoxins consist of at least seven compounds, all of which have seven similar peptide rings. Phalloidin was isolated in 1937 by Feodor Lynen, Heinrich Wieland's student and son-in-law, and Ulrich Wieland of the University of Munich. Though phallotoxins are highly toxic to liver cells,[13] they have since been found to have little input into the destroying angel's toxicity as they are not absorbed through the gut.[11] Furthermore, phalloidin is also found in the edible (and sought-after) Blusher (Amanita rubescens).[8] Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides.[14] Like the phallotoxins they do not exert any acute toxicity after ingestion in humans.[11]

Treatment[edit]

Consumption of Amanita virosa is a medical emergency requiring hospitalization. There are four main categories of therapy for poisoning: preliminary medical care, supportive measures, specific treatments, and liver transplantation.[15]

Preliminary care consists of gastric decontamination with either activated carbon or gastric lavage. However, due to the delay between ingestion and the first symptoms of poisoning, it is commonplace for patients to arrive for treatment many hours after ingestion, potentially reducing the efficacy of these interventions.[15][16] Supportive measures are directed towards treating the dehydration which results from fluid loss during the gastrointestinal phase of intoxication and correction of metabolic acidosis, hypoglycemia, electrolyte imbalances, and impaired coagulation.[15]

No definitive antidote for amatoxin poisoning is available, but some specific treatments have been shown to improve survivability. High-dose continuous intravenous penicillin G has been reported to be of benefit, though the exact mechanism is unknown,[17] and trials with cephalosporins show promise.[18][19] There is some evidence that intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of death cap poisoning. Silibinin prevents the uptake of amatoxins by hepatocytes, thereby protecting undamaged hepatic tissue; it also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.[20][21][22] N-acetylcysteine has shown promise in combination with other therapies.[23] Animal studies indicate the amatoxins deplete hepatic glutathione;[24] N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage.[25] None of the antidotes used have undergone prospective, randomized clinical trials, and only anecdotal support is available. Silibinin and N-acetylcysteine appear to be the therapies with the most potential benefit.[15] Repeated doses of activated carbon may be helpful by absorbing any toxins that are returned to the gastrointestinal tract following enterohepatic circulation.[26] Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis,[27] hemoperfusion,[28] plasmapheresis,[29] and peritoneal dialysis[30] have occasionally yielded success but overall do not appear to improve outcome.[11]

In patients developing liver failure, a liver transplant is often the only option to prevent death. Liver transplants have become a well-established option in amatoxin poisoning.[31][32][33] This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant.[15] That being the case, there has been a reassessment of criteria such as onset of symptoms, prothrombin time (PTT), serum bilirubin, and presence of encephalopathy for determining at what point a transplant becomes necessary for survival.[34][35][36] Evidence suggests that, although survival rates have improved with modern medical treatment, in patients with moderate to severe poisoning up to half of those who did recover suffered permanent liver damage.[37] However, a follow-up study has shown that most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion.[38]

See also[edit]

References[edit]

  1. ^ Simpson, D.P. (1979). Cassell's Latin Dictionary (5 ed.). London: Cassell Ltd. p. 883. ISBN 0-304-52257-0. 
  2. ^ Nilson, Sven; Olle Persson (1977). Fungi of Northern Europe 2: Gill-Fungi. Penguin. p. 54. ISBN 0-14-063006-6. 
  3. ^ a b Zeitlmayr, Linus (1976). Wild Mushrooms:An Illustrated Handbook. Hertfordshire: Garden City Press. pp. 62–63. ISBN 0-584-10324-7. 
  4. ^ Ramsbottom J (1953). Mushrooms & Toadstools. Collins. p. 39. ISBN 1-870630-09-2. 
  5. ^ Benjamin.p200
  6. ^ Jordan & Wheeler. p99
  7. ^ Carluccio A (2003). The Complete Mushroom Book. London: Quadrille. p. 224. ISBN 1-84400-040-0. 
  8. ^ a b Litten, W. (March 1975). "The most poisonous mushrooms". Scientific American 232 (3): 90–101. doi:10.1038/scientificamerican0375-90. PMID 1114308. 
  9. ^ Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40. doi:10.1016/0041-0101(93)90337-I. PMID 8146866. 
  10. ^ Dart, RC (2004). "Mushrooms". Medical toxicology. Philadelphia: Williams & Wilkins. pp. 1719–35. ISBN 0-7817-2845-2. 
  11. ^ a b c d Karlson-Stiber C, Persson H (2003). "Cytotoxic fungi - an overview". Toxicon 42 (4): 339–49. doi:10.1016/S0041-0101(03)00238-1. PMID 14505933. 
  12. ^ Benjamin.p217
  13. ^ Wieland T, Govindan VM (1974). "Phallotoxins bind to actins". FEBS Lett. 46 (1): 351–53. doi:10.1016/0014-5793(74)80404-7. PMID 4429639. 
  14. ^ Vetter, János (January 1998). "Toxins of Amanita phalloides". Toxicon 36 (1): 13–24. doi:10.1016/S0041-0101(97)00074-3. PMID 9604278. 
  15. ^ a b c d e Enjalbert F, Rapior S, Nouguier-Soulé J, Guillon S, Amouroux N, Cabot C (2002). "Treatment of amatoxin poisoning: 20-year retrospective analysis". Journal of Toxicology - Clinical Toxicology 40 (6): 715–57. doi:10.1081/CLT-120014646. PMID 12475187. 
  16. ^ Vesconi S, Langer M, Iapichino G, Costantino D, Busi C, Fiume L (1985). "Therapy of cytotoxic mushroom intoxication". Critical Care Medicine 13 (5): 402–6. doi:10.1097/00003246-198505000-00007. PMID 3987318. 
  17. ^ Floerscheim, G.L.; O. Weber, P. Tschumi & M. Ulbrich (August 1982). "Die klinische knollenblatterpilzvergiftung (Amanita Phalloides): prognostische faktoren und therapeutische massnahmen (Clinical death-cap (Amanita phalloides) poisoning: prognostic factors and therapeutic measures.)". Schweizerische medizinische Wochenschrift (in German) 112 (34): 1164–77. PMID 6291147. 
  18. ^ Benjamin.p227
  19. ^ Neftel, K. et al. (January 1988). "(Are cephalosporins more active than penicillin G in poisoning with the deadly Amanita?)". Schweizerische medizinische Wochenschrift (in German) 118 (2): 49–51. PMID 3278370. 
  20. ^ Hruby K, Csomos G, Fuhrmann M, Thaler H (1983). "Chemotherapy of Amanita phalloides poisoning with intravenous silibinin". Human toxicology 2 (2): 183–95. doi:10.1177/096032718300200203. PMID 6862461. 
  21. ^ Carducci, R. et al. (May 1996). "Amanita_phalloides (cmd-click)">Silibinin and acute poisoning with ''Amanita phalloides''". Minerva Anestesiologica (in Italian) 62 (5): 187–93. PMID 8937042. 
  22. ^ Jahn, W. (1980). "Pharmacokinetics of {3H}-methyl-dehydroxymethyl-amanitin in the isolated perfused rat liver, and the influence of several drugs". In Helmuth Faulstich, B. Kommerell & Theodore Wieland. Amanita toxins and poisoning. Baden-Baden: Witzstrock. pp. 80–85. ISBN 3-87921-132-9. 
  23. ^ Montanini S, Sinardi D, Praticò C, Sinardi A, Trimarchi G (1999). "Use of acetylcysteine as the life-saving antidote in Amanita phalloides (death cap) poisoning. Case report on 11 patients". Arzneimittel-Forschung 49 (12): 1044–7. doi:10.1055/s-0031-1300549. PMID 10635453. 
  24. ^ Kawaji A, Sone T, Natsuki R, Isobe M, Takabatake E, Yamaura Y (1990). "In vitro toxicity test of poisonous mushroom extracts with isolated rat hepatocytes". The Journal of toxicological sciences 15 (3): 145–56. doi:10.2131/jts.15.145. PMID 2243367. 
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Sources[edit]

  • Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company. ISBN 0-7167-2600-9. 
  • Jordan Peter, Wheeler Steven. (2001). The Ultimate Mushroom Book. London: Hermes House. ISBN 1-85967-092-X. 
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