Amanita phalloides
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Amanita phalloides (Template:IPAc-en Template:Respell), commonly known as the death cap, is a deadly poisonous basidiomycete fungus and mushroom, one of many in the genus Amanita. Originating in Europe<ref>Template:Cite journal</ref> but later introduced to other parts of the world since the late twentieth century,<ref name="Litten75" /><ref name="MedJAus1993" /><ref name="Kurtziana1983" /><ref>Template:Cite journal</ref> A. phalloides forms ectomycorrhizas with various broadleaved trees. In some cases, the death cap has been introduced to new regions with the cultivation of non-native species of oak, chestnut, and pine. The large fruiting bodies appear in summer and autumn; the caps are generally greenish in colour with a white stipe and gills. The cap colour is variable, including white forms, and is thus not a reliable identifier.
These toxic mushrooms resemble several edible species (most notably Caesar's mushroom and the straw mushroom) commonly consumed by humans, increasing the risk of accidental poisoning. Amatoxins, the class of toxins found in these mushrooms, are thermostable: they resist changes due to heat and cold, so their toxic effects are not reduced by cooking nor freezing.
Amanita phalloides is the most poisonous of all known mushrooms.<ref>Template:Citation</ref><ref>Template:Citation</ref><ref>Template:Citation</ref> It is estimated that as little as half a mushroom contains enough toxin to kill an adult human.<ref>Template:Citation</ref> It is also the deadliest mushroom worldwide, responsible for 90% of mushroom-related fatalities every year.<ref>Template:Cite journal</ref> It has been involved in the majority of human deaths from mushroom poisoning,<ref name="benjamin200">Benjamin, p.200.</ref> possibly including Roman Emperor Claudius in AD 54 and Holy Roman Emperor Charles VI in 1740.<ref name="wasson"/> It has also been the subject of much research and many of its biologically active agents have been isolated. The principal toxic constituent is α-Amanitin, which causes liver and kidney failure.
Taxonomy
The death cap is named in Latin as such in the correspondence between the English physician Thomas Browne and Christopher Merrett.<ref>The "fungi Phalloides" I found not very far from Norwich, large and very fetid......I have a part of one dried still by me. Letter dated August 18th 1668 in Vol 3. The Works of Sir Thomas Browne ed. Simon Wilkins 1834</ref> It was described by French botanist Sébastien Vaillant in 1727, who gave a succinct phrase name "Fungus phalloides, annulatus, sordide virescens, et patulus" (a phallus-shaped, ring-stemmed, dirty green mushroom with a large 'spreading' cap).<ref>Template:Cite book</ref>
In 1821, Elias Magnus Fries described it as Agaricus phalloides, but included all white amanitas within its description.<ref>Template:Cite book</ref> Finally, in 1833, Johann Heinrich Friedrich Link settled on the name Amanita phalloides,<ref>Template:In lang Link JHF (1833) Grundriss der Kraeuterkunde IV. Haude und Spenerschen Buchhandlung (S.J. Joseephy), Berlin</ref> after Persoon had named it Amanita viridis 30 years earlier.<ref>Template:Cite book</ref><ref>Template:Cite book</ref> Although Louis Secretan's use of the name A. phalloides predates Link's, it has been rejected for nomenclatural purposes because Secretan's works did not use binomial nomenclature consistently;<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> some taxonomists have, however, disagreed with this opinion.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>
Amanita phalloides is the type species of Amanita section Phalloideae, a group that contains all of the deadly poisonous Amanita species thus far identified. Most notable of these are the species known as destroying angels, namely A. virosa, A. bisporigera and A. ocreata, as well as the fool's mushroom (A. verna). The term "destroying angel" has been applied to A. phalloides at times, but "death cap" is by far the most common vernacular name used in English. Other common names also listed include "stinking amanita"<ref name="North67" /> and "deadly amanita".<ref name="benjamin203">Benjamin, p.203</ref>
A rarely appearing, all-white form was initially described A. phalloides f. alba by Max Britzelmayr,<ref name="tulloss">Template:Cite web</ref><ref name="Jord109">Jordan & Wheeler, p. 109</ref> though its status has been unclear. It is often found growing amid normally colored death caps. It has been described, in 2004, as a distinct variety and includes what was termed A. verna var. tarda.<ref name="Nevpoum04" /> The true A. verna fruits in spring and turns yellow with KOH solution, whereas A. phalloides never does.<ref name="tullossverna">Template:Cite web</ref>
Description
The death cap has a large and imposing epigeous (aboveground) fruiting body (basidiocarp), usually with a pileus (cap) from 5 to 15 cm across (2 to 5.8 inches) across, initially rounded and hemispherical, but flattening with age.<ref name="Bresinsky">Template:Cite book</ref> The color of the cap can be pale-green, yellowish-green, olive-green, bronze, or (in one form) white; it is often paler toward the margins, which can have darker streaks;<ref>Template:Cite book</ref> it is also often paler after rain. The cap surface is sticky when wet and easily peeled—a troublesome feature, as that is allegedly a feature of edible fungi.<ref name="Jord99">Jordan & Wheeler, p.99</ref> The remains of the partial veil are seen as a skirtlike, floppy annulus usually about Template:Convert below the cap. The crowded white lamellae (gills) are free. The stipe is white with a scattering of grayish-olive scales and is Template:Convert long and Template:Convert thick, with a swollen, ragged, sac-like white volva (base).<ref name="Bresinsky"/> As the volva, which may be hidden by leaf litter, is a distinctive and diagnostic feature, it is important to remove some debris to check for it.<ref name="Jord108">Jordan & Wheeler, p.108</ref> Spores: 7-12 x 6-9 μm. Smooth, ellipsoid, amyloid.<ref>Template:Cite web</ref>
The smell has been described as initially faint and honey-sweet, but strengthening over time to become overpowering, sickly-sweet and objectionable.<ref name="Zeitl61">Zeitlmayr, p.61</ref> Young specimens first emerge from the ground resembling a white egg covered by a universal veil, which then breaks, leaving the volva as a remnant. The spore print is white, a common feature of Amanita. The transparent spores are globular to egg-shaped, measure 8–10 μm (0.3–0.4 mil) long, and stain blue with iodine.<ref name="Zeitl61"/> The gills, in contrast, stain pallid lilac or pink with concentrated sulfuric acid.<ref>Template:Cite book</ref><ref>Template:Cite web</ref>
Biochemistry
The species is now known to contain two main groups of toxins, both multicyclic (ring-shaped) peptides spread throughout the mushroom, tissue: the amatoxins and the phallotoxins. Another toxin is phallolysin, which has shown some hemolytic (red blood cell–destroying) activity in vitro. An unrelated compound, antamanide, has also been isolated.
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.<ref name="Litten75" /> Of the amatoxins, α-Amanitin is the chief component and along with β-amanitin is likely responsible for the toxic effects.<ref name="Koppel">Template:Cite journal</ref><ref name="dart">Template:Cite book</ref> 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.<ref name="Karlson-Stiber">Template:Cite journal</ref> 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.<ref name="benjamin217">Benjamin, p.217</ref> The RNA polymerase of Amanita phalloides is insensitive to the effects of amatoxins, so the mushroom does not poison itself.<ref name="Horgen">Template:Cite journal</ref>
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,<ref>Template:Cite journal</ref> they have since been found to add little to the death cap's toxicity, as they are not absorbed through the gut.<ref name="Karlson-Stiber" /> Furthermore, phalloidin is also found in the edible (and sought-after) blusher (A. rubescens).<ref name="Litten75" /> Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides.<ref name="Vetter" /> Like the phallotoxins, they do not induce any acute toxicity after ingestion in humans.<ref name="Karlson-Stiber" />
The genome of the death cap has been sequenced.<ref>Template:Cite journal</ref>
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Similarity to edible species
A. phalloides is similar to the edible paddy straw mushroom (Volvariella volvacea)<ref name="benjamin198">Benjamin, pp.198–199</ref> and A. princeps, commonly known as "white Caesar".<ref name="Atlantic 2019 article" />
Some may mistake juvenile death caps for edible puffballs<ref name="hall">Template:Cite book</ref><ref>Template:Cite journal</ref> or mature specimens for other edible Amanita species, such as A. lanei, so some authorities recommend avoiding the collecting of Amanita species for the table altogether.<ref>Template:Cite book</ref> The white form of A. phalloides may be mistaken for edible species of Agaricus, especially the young fruitbodies whose unexpanded caps conceal the telltale white gills; all mature species of Agaricus have dark-colored gills.<ref>Template:Cite web</ref>
In Europe, other similarly green-capped species collected by mushroom hunters include various green-hued brittlegills of the genus Russula and the formerly popular Tricholoma equestre, now regarded as hazardous owing to a series of restaurant poisonings in France. Brittlegills, such as Russula heterophylla, R. aeruginea, and R. virescens, can be distinguished by their brittle flesh and the lack of both volva and ring.<ref name="Zeitl62">Zeitlmayr, p.62</ref> Other similar species include A. subjunquillea in eastern Asia and A. arocheae, which ranges from Andean Colombia north at least as far as central Mexico, both of which are also poisonous.
Distribution and habitat
The death cap is native to Europe, where it is widespread.<ref>Template:Cite journal</ref> It is found from the southern coastal regions of Scandinavia in the north, to Ireland in the west, east to Poland and western Russia,<ref name="Nevpoum04">Template:Cite book</ref> and south throughout the Balkans, in Greece, Italy, Spain, and Portugal in the Mediterranean basin, and in Morocco and Algeria in north Africa.<ref name="Malber70">Template:Cite book</ref> In west Asia, it has been reported from forests of northern Iran.<ref>Asef, M.R. 2009. Poisonous mushrooms of Iran. Iran-shenasi publishing.</ref> There are records from further east in Asia but these have yet to be confirmed as A. phalloides.<ref name="Pringvell06">Template:Cite journal</ref>
By the end of the 19th century, Charles Horton Peck had reported A. phalloides in North America.<ref>Template:Cite book</ref> In 1918, samples from the eastern United States were identified as being a distinct though similar species, A. brunnescens, by George Francis Atkinson of Cornell University.<ref name="Litten75">Template:Cite journal</ref> By the 1970s, it had become clear that A. phalloides does occur in the United States, apparently having been introduced from Europe alongside chestnuts, with populations on the West and East Coasts.<ref name="Litten75" /><ref name="benjamin204">Benjamin, p.204</ref> A 2006 historical review concluded the East Coast populations were inadvertently introduced, likely on the roots of other purposely imported plants such as chestnuts.<ref>Template:Cite journal</ref> The origins of the West Coast populations remained unclear, due to scant historical records,<ref name="Pringvell06" /> but a 2009 genetic study provided strong evidence for the introduced status of the fungus on the west coast of North America.<ref>Template:Cite journal</ref> Observations of various collections of A. phalloides, from conifers rather than native forests, have led to the hypothesis that the species was introduced to North America multiple times. It is hypothesized that the various introductions led to multiple genotypes which are adapted to either oaks or conifers.<ref>Template:Cite journal</ref>
A. phalloides were conveyed to new countries across the Southern Hemisphere with the importation of hardwoods and conifers in the late twentieth century. Introduced oaks appear to have been the vector to Australia and South America; populations under oaks have been recorded from Melbourne, Canberra<ref>Template:Cite news</ref><ref>Template:Cite journal</ref><ref name="MedJAus1993">Template:Cite journal</ref> (where two people died in January 2012, of four who were poisoned),<ref>Template:Cite news</ref> Adelaide,<ref>Death cap mushrooms growing in the hills Template:Webarchive Elisa Black, AdelaideNow.com.au, 7 January 2012, accessed 8 January 2012</ref> and further observed by citizen scientists in Beechworth,<ref>Template:Cite news</ref> Sydney and Albury.<ref>Template:Cite news</ref> It has been recorded under other introduced trees in Argentina.<ref name="Kurtziana1983">Template:Cite journal</ref> Pine plantations are associated with the fungus in Tanzania<ref name="Peg77">Template:Cite book</ref> and South Africa, found under oaks and poplars in Chile,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> as well as Uruguay.<ref>Template:Cite journal</ref> A number of deaths in India have been attributed to it.<ref name="JCEH2014">Template:Cite journal</ref>
Ecology
It is ectomycorrhizally associated with several tree species and is symbiotic with them. In Europe, these include hardwood and, less frequently, conifer species. It appears most commonly under oaks, but also under beeches, chestnuts, horse-chestnuts, birches, filberts, hornbeams, pines, and spruces.<ref name="tulloss" /> In other areas, A. phalloides may also be associated with these trees or with only some species. In coastal California, for example, A. phalloides is associated with coast live oak.<ref name=Arora1986>Template:Cite book</ref> In countries where it has been introduced, it has been restricted to those exotic trees with which it would associate in its natural range. There is, however, evidence of A. phalloides associating with hemlock and with genera of the Myrtaceae: Eucalyptus in Tanzania<ref name="Peg77" /> and Algeria,<ref name="Malber70" /> and Leptospermum and Kunzea in New Zealand,<ref name="tulloss" /><ref name="Rid91">Template:Cite journal</ref> suggesting that the species may have invasive potential.<ref name="Pringvell06" /> It may have also been anthropogenically introduced to the island of Cyprus, where it has been documented to fruit within Corylus avellana plantations.<ref>Loizides M, Bellanger JM, Yiangou Y, Moreau PA. (2018). Preliminary phylogenetic investigations into the genus Amanita (Agaricales) in Cyprus, with a review of previous records and poisoning incidents. Documents Mycologiques 37, 201–218.</ref>
Toxicity
The fungus is highly toxic, and is responsible for the majority of fatal mushroom poisonings worldwide.<ref name="benjamin200"/><ref>Death Cap Mushroom Soup Claims Fourth Victim</ref> Its biochemistry has been researched intensively for decades,<ref name="Litten75"/> and Template:Convert, or half a cap, of this mushroom is estimated to be enough to kill a human.<ref name="benjamin211">Benjamin, p.211</ref> On average, one person dies a year in North America from death cap ingestion.<ref name="Atlantic 2019 article">Template:Cite news</ref> The toxins of the death cap mushrooms primarily target the liver, but other organs, such as the kidneys, are also affected. Symptoms of death cap mushroom toxicity usually occur 6 to 12 hours after ingestion.<ref>Template:Cite book</ref> Symptoms of ingestion of the death cap mushroom may include nausea and vomiting, which is then followed by jaundice, seizures, and coma, which will lead to death. The mortality rate of ingestion of the death cap mushroom is believed to be around 10–30%.<ref>Template:Cite journal</ref>
Some authorities strongly advise against putting suspected death caps in the same basket with fungi collected for the table and to avoid even touching them.<ref name="Jord99"/><ref>Template:Cite book</ref> Furthermore, the toxicity is not reduced by cooking, freezing, or drying.<ref name="trim99">Template:Cite journal</ref>
Poisoning incidents usually result from errors in identification. Recent cases highlight the issue of the similarity of A. phalloides to the edible paddy straw mushroom (Volvariella volvacea), with East and Southeast Asian immigrants in Australia and the West Coast of the U.S. falling victim. In an episode in Oregon, four members of a Korean family required liver transplants.<ref name="benjamin198" /> Many North American incidents of death cap poisoning have occurred among Laotian and Hmong immigrants, since it is easily confused with A. princeps ("white Caesar"), a popular mushroom in their native countries.<ref name="Atlantic 2019 article" /> Of the nine people poisoned in Australia's Canberra region between 1988 and 2011, three were from Laos and two were from China.<ref name="trim99" /> In January 2012, four people were accidentally poisoned when death caps (reportedly misidentified as straw mushrooms, which are popular in Chinese and other Asian dishes) were served for dinner in Canberra; all the victims required hospital treatment and two of them died, with a third requiring a liver transplant.<ref>Template:Cite news</ref>
Detection
The so-called Meixner test is used to detect the presence of amatoxins in a sample. The test gives false positive results for psilocin, psilocybin, and 5-substituted tryptamines.<ref>Template:Cite journal</ref>
Signs and symptoms
Death caps have been reported to taste pleasant.<ref name="Litten75"/><ref name="Clel76">Template:Cite book</ref> This, coupled with the delay in the appearance of symptoms—during which time internal organs are being severely, sometimes irreparably, damaged—makes them particularly dangerous. Initially, symptoms are gastrointestinal in nature and include colicky abdominal pain, with watery diarrhea, nausea, and vomiting, which may lead to dehydration if left untreated, and, in severe cases, hypotension, tachycardia, hypoglycemia, and acid–base disturbances.<ref name="pinson"/><ref name="klein"/> These first symptoms resolve two to three days after the ingestion. A more serious deterioration signifying liver involvement may then occur—jaundice, diarrhea, delirium, seizures, and coma due to fulminant liver failure and attendant hepatic encephalopathy caused by the accumulation of normally liver-removed substances in the blood.<ref name="North67">Template:Cite book</ref> Kidney failure (either secondary to severe hepatitis<ref name="Vetter">Template:Cite journal</ref><ref>Template:Cite journal</ref> or caused by direct toxic kidney damage<ref name=" Karlson-Stiber"/>) and coagulopathy may appear during this stage. Life-threatening complications include increased intracranial pressure, intracranial bleeding, pancreatic inflammation, acute kidney failure, and cardiac arrest.<ref name="pinson"/><ref name="klein"/> Death generally occurs six to sixteen days after the poisoning.<ref>Template:Cite journal</ref>
It is noticed that after up to 24 hours have passed, the symptoms seem to disappear and the person might feel fine for up to 72 hours. Symptoms of liver and kidney damage start 3 to 6 days after the mushrooms were eaten, with the considerable increase of the transaminases.<ref>Template:Cite web</ref>
Mushroom poisoning is more common in Europe than in North America.<ref>Template:Cite web</ref> Up to the mid-20th century, the mortality rate was around 60–70%, but this has been greatly reduced with advances in medical care. A review of death cap poisoning throughout Europe from 1971 to 1980 found the overall mortality rate to be 22.4% (51.3% in children under ten and 16.5% in those older than ten).<ref name="Floer82">Template:Cite journal</ref> This was revised to around 10–15% in surveys reviewed in 1995.<ref name="benjamin215">Benjamin, p.215</ref>
Treatment
Consumption of the death cap is a medical emergency requiring hospitalization. The four main categories of therapy for poisoning are preliminary medical care, supportive measures, specific treatments, and liver transplantation.<ref name="Enjalbert">Template:Cite journal</ref>
Preliminary care consists of gastric decontamination with either activated carbon or gastric lavage; due to the delay between ingestion and the first symptoms of poisoning, it is common for patients to arrive for treatment many hours after ingestion, potentially reducing the efficacy of these interventions.<ref name="Enjalbert"/><ref name="Vesconi">Template:Cite journal</ref> 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.<ref name="Enjalbert"/>
No definitive antidote 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,<ref name="Floer82"/> and trials with cephalosporins show promise.<ref name="benjamin227">Benjamin, p.227</ref><ref>Template:Cite journal</ref> Some evidence indicates intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of death cap poisoning. A long-term clinical trial of intravenous silibinin began in the US in 2010.<ref>Template:Cite web</ref> Silibinin prevents the uptake of amatoxins by liver cells, thereby protecting undamaged liver tissue; it also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite book</ref> According to one report<ref>Template:Cite journal</ref> based on a treatment of 60 patients with silibinin, patients who started the drug within 96 hours of ingesting the mushroom and who still had intact kidney function all survived. As of February 2014 supporting research has not yet been published.
SLCO1B3 has been identified as the human hepatic uptake transporter for amatoxins; moreover, substrates and inhibitors of that protein—among others rifampicin, penicillin, silibinin, antamanide, paclitaxel, ciclosporin and prednisolone—may be useful for the treatment of human amatoxin poisoning.<ref>Template:Cite journal</ref>
N-acetylcysteine has shown promise in combination with other therapies.<ref>Template:Cite journal</ref> Animal studies indicate the amatoxins deplete hepatic glutathione;<ref>Template:Cite journal</ref> N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage.<ref>Template:Cite journal</ref> 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.<ref name="Enjalbert"/> Repeated doses of activated carbon may be helpful by absorbing any toxins returned to the gastrointestinal tract following enterohepatic circulation.<ref>Template:Cite journal</ref> Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis,<ref>Template:Cite journal</ref> hemoperfusion,<ref>Template:Cite journal</ref> plasmapheresis,<ref>Template:Cite journal</ref> and peritoneal dialysis<ref>Template:Cite journal</ref> have occasionally yielded success, but overall do not appear to improve outcome.<ref name=" Karlson-Stiber"/>
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.<ref name="pinson">Template:Cite journal</ref><ref name="klein">Template:Cite journal</ref><ref>Template:Cite journal</ref> This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant.<ref name="Enjalbert"/> That being the case, the criteria have been reassessed, such as onset of symptoms, prothrombin time (PT), serum bilirubin, and presence of encephalopathy, for determining at what point a transplant becomes necessary for survival.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> Evidence suggests, 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.<ref name="benjamin231">Benjamin, pp.231–232</ref> A follow-up study has shown most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion.<ref>Template:Cite journal</ref>
Notable victims
Several historical figures may have died from A. phalloides poisoning (or other similar toxic Amanita species). These were either accidental poisonings or assassination plots. Alleged victims of this kind of poisoning include Roman Emperor Claudius, Pope Clement VII, the Russian tsaritsa Natalia Naryshkina, and Holy Roman Emperor Charles VI.<ref name="wasson">Template:Cite journal</ref>
R. Gordon Wasson recounted the details of these deaths, noting the likelihood of Amanita poisoning.<ref name="wasson" /> In the case of Clement VII, the illness that led to his death lasted five months, making the case inconsistent with amatoxin poisoning. Natalya Naryshkina is said to have consumed a large quantity of pickled mushrooms prior to her death. It is unclear whether the mushrooms themselves were poisonous or if she succumbed to food poisoning.
Charles VI, Holy Roman Emperor experienced indigestion after eating a dish of sautéed mushrooms in October 1740. This led to an illness from which he died 10 days later—symptomatology consistent with amatoxin poisoning. His death caused the end of the agnatic line of the House of Habsburg and led to the War of the Austrian Succession. Noted Voltaire, "this mushroom dish has changed the destiny of Europe."<ref name="wasson"/><ref name="benjamin35">Benjamin, p.35</ref>
The case of Claudius's poisoning is more complex. Claudius was known to have been very fond of eating Caesar's mushroom. Following his death, many sources have attributed it to his being fed a meal of death caps instead of Caesar's mushrooms. Ancient authors, such as Tacitus and Suetonius, are unanimous about poison having been added to the mushroom dish, rather than the dish having been prepared from poisonous mushrooms. Wasson speculated the poison used to kill Claudius was derived from death caps, with a fatal dose of an unknown poison (possibly a variety of nightshade) being administered later during his illness.<ref name="wasson"/><ref name="benjamin33">Benjamin, pp.33–34</ref> Other historians have speculated that Claudius may have died of natural causes.
In the 2023 Leongatha mushroom murders, Australian woman Erin Patterson was found guilty of three murders and one attempted murder of members of her estranged husband's family by serving them beef Wellingtons that contained A. phalloides. Three of the four guests died within days of the meal, while one survived after a liver transplant and weeks in a coma.<ref>Template:Cite news</ref><ref>Template:Cite news</ref>
See also
- List of Amanita species
- List of deadly fungi
- Template:Anl, known for expertise in treating mushroom poisoning
References
Cited texts
External links
Template:Spoken Wikipedia Template:Commons
- UK Telegraph Newspaper (September 2008) - One woman dead, another critically ill after eating Death Cap fungi
- AmericanMushrooms.com - The Death Cap Mushroom Amanita phalloides
- Amanita phalloides: the death cap
- Amanita phalloides: Invasion of the Death Cap
- Key to species of Amanita Section Phalloideae from North and Central America - Amanita studies website
- California Fungi—Amanita phalloides
- Death cap in Australia - ANBG website
- On the Trail of the Death Cap Mushroom from National Public Radio
- Template:EOL
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