Amanita virosa: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
←Blanked the page
ClueBot (talk | contribs)
1,596,818 edits
m Reverting possible vandalism by 204.39.176.40 to version by Prashanthns. False positive? Report it. Thanks, User:ClueBot. (333483) (Bot)
Line 1: Line 1:
{{Taxobox
| name=Destroying Angel
| status= secure
| image= Destroying Angel 02.jpg
| image_width=250px
| regnum=[[Fungus|Fungi]]
| divisio=[[Basidiomycota]]
| classis=[[Agaricomycetes]]
| subclassis=[[Hymenomycete]]s
| ordo=[[Agaricales]]
| familia=[[Amanitaceae]]
| genus=''[[Amanita]]''
| species='''''A. virosa'''''
| binomial=''Amanita virosa''
| binomial_authority=([[Elias Magnus Fries|Fr.]]) Bertillon
}}
{{mycomorphbox
| name=Amanita virosa
| whichGills=free
| capShape=convex
| capShape2=flat
| hymeniumType=gills
| stipeCharacter=ring and volva
| ecologicalType=mycorrhizal
| sporePrintColor=white
| howEdible=deadly
}}
'''''Amanita virosa''''', commonly known as the '''destroying angel''' or more precisely as '''European destroying angel''', is a poisonous [[basidiomycete]] [[fungus]], one of many in the genus ''[[Amanita]]''. Occurring in [[Europe]], ''A. virosa'' [[mycorrhiza|associates]] with various deciduous and coniferous trees. The large fruiting bodies (''i.e.'', the [[mushrooms]]) appear in summer and autumn; the [[Pileus (mycology)|caps]], [[stipe (mycology)|stipe]]s and [[Lamella (mycology)|gill]]s are all white in colour.

Immature specimens of ''A. virosa'' resemble several edible species commonly consumed by humans, increasing the risk of accidental [[poison]]ing. Along with its geographical namesakes, ''A. virosa'' is one of the most poisonous of all known toadstools; its principal toxic constituent [[alpha-amanitin|α-amanitin]] damages the liver and kidneys, often fatally. No antidote is known.

==Taxonomy and naming==
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 ''[[Amanita ocreata|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'' 'stinking' or 'foetid'.<ref>{{cite book | last = Simpson | first = D.P. | title = Cassell's Latin Dictionary | publisher = Cassell Ltd. | date = 1979 | edition = 5 | location = London | pages = 883 | id = ISBN 0-304-52257-0}}</ref>

''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==
''A. virosa'' first appears as a white egg-shaped object covered with a universal [[Veil (botany)|veil]]. As it grows, the mushroom breaks free, though there may be ragged patches of veil at the cap edges. The [[Pileus (mycology)|cap]] is initially conical with inturned edges, before becoming hemispherical and flattening with a diameter up to 12&nbsp;cm (4½&nbsp;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 [[Lamella (mycology)|gills]] are white, as is the stipe and [[Volva (mycology)|volva]]. The thin [[Stipe (mycology)|stipe]] is up to 15&nbsp;cm (6&nbsp;in) tall, with a hanging grooved ring. The [[spore print]] is white and the spores egg-shaped conical and 7-10&nbsp;[[micrometre|μm]] long. They stain blue with [[iodine]]. The flesh is white, with a taste reminiscent of radishes, and turns bright yellow with [[sodium hydroxide]].<ref name ="Zeitl">{{cite book|last=Zeitlmayr|first= Linus|year=1976|title=Wild Mushrooms:An Illustrated Handbook|pages=p. 62-63|publisher=Garden City Press|location=Hertfordshire|isbn= 0-584-10324-7}}</ref>

This fungus highlights the danger of picking immature fungi as it resembles the edible mushrooms ''[[Agaricus arvensis]]'' and ''[[Agaricus campestris|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.<ref name = "Ramsbottom53">{{cite book | author = Ramsbottom J | year = 1953 | title = Mushrooms & Toadstools |pages=p. 39 | publisher = Collins | id = ISBN 1870630092}}</ref>

==Distribution and habitat==
''A. virosa'' is found in mixed woodland, especially in association with [[beech]], on mossy ground in summer and autumn.<ref name ="Zeitl"/> All ''[[Amanita]]'' species form [[mycorrhiza|ectomycorrhizal]] relationships with the roots of certain trees.

==Toxicity==
[[Image:Amanita virosa 02.jpg|thumb|left|young fruiting bodies showing conical caps]]
''Amanita virosa'' is highly toxic, and has been responsible for severe [[mushroom poisoning]]s.<ref name="benjamin200">Benjamin.p200</ref> Like the closely related death cap (''[[Amanita phalloides|A. phalloides]]''), it contains the highly toxic [[amatoxin]]s, as well as [[phallotoxin]]s. Some authorities strongly advise against putting these fungi in the same basket with those collected for the table and to avoid touching them.<ref name="Jord99">Jordan & Wheeler. p99</ref><ref>{{cite book | author = Carluccio A | year = 2003 | title = The Complete Mushroom Book | publisher = Quadrille | location = London|pages = 224| id = ISBN 1-84400-040-0}}</ref>

Amatoxins consist of at least eight compounds with a similar structure, that of eight amino-acid rings; they were isolated in 1941 by [[Heinrich Otto Wieland|Heinrich O. Wieland]] and Rudolf Hallermayer of the [[Ludwig Maximilians University of Munich|University of Munich]].<ref name="Litten75">{{cite journal |last=Litten|first= W. |year=1975|month=March |title=The most poisonous mushrooms |journal=[[Scientific American]] |volume=232 |issue=3 |pages=90–101 |pmid=1114308}}</ref> Of the amatoxins, [[α-amanitin]] is the chief component and along with [[β-amanitin]] is likely responsible for the toxic effects.<ref name="Koppel">{{cite journal |author=Köppel C |title=Clinical symptomatology and management of mushroom poisoning |journal=Toxicon |volume=31 |issue=12 |pages=1513–40 |year=1993 |pmid=8146866 |doi=10.1016/0041-0101(93)90337-I}}</ref><ref name="dart">{{cite book |last=Dart| first= RC |chapter=Mushrooms |title=Medical toxicology |publisher=Williams & Wilkins| location=Philadelphia |year=2004|pages=1719–35| isbn=0-7817-2845-2}}</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 biosynthesis|protein synthesis]] and hence cell metabolism grind to a halt and the cell dies.<ref name=" Karlson-Stiber">{{cite journal |author=Karlson-Stiber C, Persson H |title=Cytotoxic fungi - an overview |journal=Toxicon |volume=42 |issue=4 |pages=339-49 |year=2003 |pmid=14505933|doi=10.1016/S0041-0101(03)00238-1}}</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 [[kidney]]s, are susceptible.<ref name="benjamin217">Benjamin.p217</ref>

The phallotoxins consist of at least seven compounds, all of which have seven similar peptide rings. [[Phalloidin]] was isolated in 1937 by [[Feodor Felix Konrad Lynen|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>{{cite journal |author=Wieland T, Govindan VM |title=Phallotoxins bind to actins |journal=FEBS Lett. |volume=46 |issue=1 |pages=351-3 |year=1974 |pmid=4429639|doi=10.1016/0014-5793(74)80404-7}}</ref> they have since been found to have little input into the destroying angel'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]] (''Amanita rubescens'').<ref name="Litten75"/> Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides.<ref name = "Vetter">{{cite journal|first=János| last=Vetter|year=1998| month=January| title=Toxins of ''Amanita phalloides''| journal=Toxicon| volume=36| issue=1 |pages=13–24|pmid=9604278| doi=10.1016/S0041-0101(97)00074-3}}</ref> Like the phallotoxins they do not exert any acute toxicity after ingestion in humans.<ref name=" Karlson-Stiber"/>

===Treatment===
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]].<ref name="Enjalbert">{{cite journal |author=Enjalbert F, Rapior S, Nouguier-Soulé J, Guillon S, Amouroux N, Cabot C |title=Treatment of amatoxin poisoning: 20-year retrospective analysis |journal=Journal of Toxicology - Clinical Toxicology |volume=40 |issue=6 |pages=715-57 |year=2002 |pmid=12475187}}</ref>

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.<ref name="Enjalbert"/><ref name="Vesconi">{{cite journal |author=Vesconi S, Langer M, Iapichino G, Costantino D, Busi C, Fiume L |title=Therapy of cytotoxic mushroom intoxication |journal=Critical care medicine |volume=13 |issue=5 |pages=402-6 |year=1985 |pmid=3987318}}</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 for amatoxin poisoning is available, but some specific treatments have been shown to improve survivability. High-dose continuous intravenous [[Penicillin#Benzylpenicillin .28penicillin G.29|penicillin G]] has been reported to be of benefit, though the exact mechanism is unknown,<ref name="Floer82">{{de icon}}{{cite journal| last=Floerscheim| first=G.L.| Coauthors=O. Weber, P. Tschumi & M. Ulbrich|year=1982|month=August|title=Die klinische knollenblatterpilzvergiftung (''Amanita Phalloides''): prognostische faktoren und therapeutische massnahmen (Clinical death-cap (Amanita phalloides) poisoning: prognostic factors and therapeutic measures.)| journal=Schweizerische medizinische Wochenschrift |volume=112 |issue=34 |pages=1164–1177 |pmid=6291147}}</ref> and trials with [[cephalosporin]]s show promise.<ref name="benjamin227">Benjamin.p227</ref><ref>{{de icon}}{{cite journal|author=Neftel, K. ''et al.''| year=1988| month=January|title=(Are cephalosporins more active than penicillin G in poisoning with the deadly ''Amanita''?)|journal=Schweizerische medizinische Wochenschrift|volume=118| issue=2|pages=49–51|pmid=3278370}}</ref> There is some evidence that intravenous [[silibinin]], an extract from the [[Silybum marianum|blessed milk thistle]] (''Silybum marianum''), may be beneficial in reducing the effects of death cap poisoning. Silibinin prevents the uptake of amatoxins by [[hepatocyte]]s, thereby protecting undamaged hepatic tissue; it also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.<ref>{{cite journal |author=Hruby K, Csomos G, Fuhrmann M, Thaler H |title=Chemotherapy of Amanita phalloides poisoning with intravenous silibinin |journal=Human toxicology |volume=2 |issue=2 |pages=183-95 |year=1983 |pmid=6862461}}</ref><ref>{{it icon}} {{cite journal|author=Carducci, R. ''et al.''| year=1996| month=May| title=[[Silibinin and acute poisoning with ''Amanita phalloides'']]|journal=Minerva Anestesiologica|volume=62 |issue=5 |pages=187–93|pmid=8937042}}</ref><ref>{{cite book| last=Jahn| first=W.| coauthors=|year=1980|chapter=Pharmacokinetics of {3H}-methyl-dehydroxymethyl-amanitin in the isolated perfused rat liver, and the influence of several drugs| editor=Helmuth Faulstich, B. Kommerell & Theodore Wieland| title=Amanita toxins and poisoning|publisher=Witzstrock| location=Baden-Baden|pages=80–85|isbn=3-87921-132-9}}</ref> [[Acetylcysteine|N-acetylcysteine]] has shown promise in combination with other therapies.<ref>{{cite journal |author=Montanini S, Sinardi D, Praticò C, Sinardi A, Trimarchi G |title=Use of acetylcysteine as the life-saving antidote in Amanita phalloides (death cap) poisoning. Case report on 11 patients |journal=Arzneimittel-Forschung |volume=49 |issue=12 |pages=1044–7 |year=1999 |pmid=10635453}}</ref> Animal studies indicate the amatoxins deplete hepatic [[glutathione]];<ref>{{cite journal |author=Kawaji A, Sone T, Natsuki R, Isobe M, Takabatake E, Yamaura Y |title=In vitro toxicity test of poisonous mushroom extracts with isolated rat hepatocytes |journal=The Journal of toxicological sciences |volume=15 |issue=3 |pages=145-56 |year=1990 |pmid=2243367}}</ref> N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage.<ref>{{cite journal |author=Chyka P, Butler A, Holliman B, Herman M |title=Utility of acetylcysteine in treating poisonings and adverse drug reactions |journal=Drug safety |volume=22 |issue=2 |pages=123-48 |year=2000 |pmid=10672895}}</ref> None of the antidotes used have undergone prospective, [[randomized clinical trial]]s, 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 that are returned to the gastrointestinal tract following [[enterohepatic circulation]].<ref> {{cite journal |author=Busi C, Fiume L, Costantino D, Langer M, Vesconi F |title=Amanita toxins in gastroduodenal fluid of patients poisoned by the mushroom, Amanita phalloides |journal=New England Journal of Medicine |volume=300 |issue=14 |pages=800 |year=1979 |pmid=423916}'''''Bold text''how fast will this be fixed?'''}</ref> Other methods of enhancing the elimination of the toxins have been trialed; techniques such as [[hemodialysis]],<ref> {{cite journal |author=Sabeel AI, Kurkus J, Lindholm T |title=Intensive hemodialysis and hemoperfusion treatment of Amanita mushroom poisoning |journal=Mycopathologia |volume=131 |issue=2 |pages=107-14 |year=1995 |pmid=8532053}}</ref> [[hemoperfusion]],<ref>{{cite journal |author=Wauters JP, Rossel C, Farquet JJ |title=Amanita phalloides poisoning treated by early charcoal haemoperfusion |journal=British medical journal |volume=2 |issue=6150 |pages=1465 |year=1978 |pmid=719466}}</ref> [[plasmapheresis]],<ref> {{cite journal |author=Jander S, Bischoff J, Woodcock BG |title=Plasmapheresis in the treatment of Amanita phalloides poisoning: II. A review and recommendations |journal=Therapeutic apheresis |volume=4 |issue=4 |pages=308-12 |year=2000 |pmid=10975479| doi=10.1046/j.1526-0968.2000.004004303.x}}</ref> and [[peritoneal dialysis]]<ref> {{cite journal |author=Langer M, Vesconi S, Iapichino G, Costantino D, Radrizzani D |title=The early removal of amatoxins in the treatment of amanita phalloides poisoning |language=German |journal=Klinische Wochenschrift |volume=58 |issue=3 |pages=117-23 |year=1980 |pmid=7366125}}</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="klein">{{cite journal|author= Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW |year=1989| month=February|title= ''Amanita'' poisoning: treatment and the role of liver transplantation|journal=American Journal of Medicine| volume=86| issue=2| pages=187–93|pmid=2643869|doi=10.1016/0002-9343(89)90267-2}}</ref><ref name="pinson">{{cite journal|author=Pinson CW, Daya MR, Benner KG, Norton RL, Deveney KE, Ascher NL, Roberts JP, Lake JR, Kurkchubasche AG, Ragsdale JW |year=1990|month=May| title=Liver transplantation for severe ''Amanita phalloides'' mushroom poisoning| journal=American Journal of Surgery|volume=159|issue=5|pages=493–9|pmid=2334013|doi=10.1016/S0002-9610(05)81254-1}}</ref><ref>{{cite journal |author=Ganzert M, Felgenhauer N, Zilker T |title=Indication of liver transplantation following amatoxin intoxication |journal=Journal of Hepatology |volume=42 |issue=2 |pages=202-9 |year=2005 |pmid=15664245|doi=10.1016/j.jhep.2004.10.023}}</ref> This is a complicated issue, however, as transplants themselves may have significant [[Complication (medicine)|complications]] and mortality; patients require long-term [[immunosuppression]] to maintain the transplant.<ref name="Enjalbert"/> That being the case, there has been a reassessment of criteria such as onset of symptoms, [[prothrombin time]] (PTT), serum [[bilirubin]], and presence of [[hepatic encephalopathy|encephalopathy]] for determining at what point a transplant becomes necessary for survival.<ref>{{cite journal|last=O'grady| first=John G.| coauthors=Graeme J.M. Alexander, Karen M. Hayllar & Roger Williams|title=Early indicators of prognosis in fulminant hepatic failure| month=august| year=1989| journal=Gastroenterology|volume=97| issue=2| pages=439–445|pmid=2490426}}</ref><ref>{{cite journal| last=Panaro| first=Fabrizio| coauthors=Enzo Andorno, Nicola Morelli, Marco Casaccia, Giuliano Bottino, Ferruccio Ravazzoni, Monica Centanaro, Sara Ornis & Umberto Valente|year=2006| month=April| title=Letter to the editor: Liver transplantation represents the optimal treatment for fulminant hepatic failure from ''Amanita phalloides'' poisoning| journal= Transplant International|volume=19 |issue=4 |pages=344-5| pmid=16573553|doi=10.1111/j.1432-2277.2006.00275.x}}</ref><ref>{{cite journal |author=Escudié L, Francoz C, Vinel JP, Moucari R, Cournot M, Paradis V, Sauvanet A, Belghiti J, Valla D, Bernuau J, Durand F |title=Amanita phalloides poisoning: reassessment of prognostic factors and indications for emergency liver transplantation |journal=J. Hepatol. |volume=46 |issue=3 |pages=466-73 |year=2007 |pmid=17188393 |doi=10.1016/j.jhep.2006.10.013}}</ref> 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.<ref name="benjamin231">Benjamin.p231–232</ref> However, a follow-up study has shown that most survivors recover completely without any [[sequelae]] if treated within 36 hours of mushroom ingestion.<ref>{{cite journal |author=Giannini L, Vannacci A, Missanelli A, Mastroianni R, Mannaioni PF, Moroni F, Masini E |title=Amatoxin poisoning: A 15-year retrospective analysis and follow-up evaluation of 105 patients |journal=Clinical toxicology (Philadelphia, Pa.) |volume=45 |issue=5 |pages=539-42 |year=2007 |pmid=17503263 |doi=10.1080/15563650701365834}}</ref>

==References==
{{Reflist}}
==Sources==
*{{cite book |last=Benjamin| first= Denis R. |title=Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians |publisher=WH Freeman and Company| location=New York |year=1995| isbn=0-7167-2600-9}}
*{{cite book | author=Jordan Peter, Wheeler Steven. | year=2001 | title=The Ultimate Mushroom Book | location=London | publisher=Hermes House | isbn = 1-85967-092-X}}

[[Category:Amanita]]
[[Category:Basidiomycota]]
[[Category:Deadly fungi]]
[[Category:Poisonous mushrooms]]

Revision as of 14:01, 22 April 2008

Destroying Angel
Secure
Scientific classification
Kingdom:
Fungi
Division:
Basidiomycota
Class:
Agaricomycetes
Subclass:
Hymenomycetes
Order:
Agaricales
Family:
Amanitaceae
Genus:
Amanita
Species:
A. virosa
Binomial name
Amanita virosa
(Fr.) Bertillon
Amanita virosa
View the Mycomorphbox template that generates the following list
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 is deadly

Amanita virosa, commonly known as the destroying angel or more precisely as European destroying angel, is a 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 toadstools; its principal toxic constituent α-amanitin damages the liver and kidneys, often fatally. No antidote is known.

Taxonomy and naming

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 'stinking' or 'foetid'.[1]

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

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.[2]

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.[3]

Distribution and habitat

A. virosa is found in mixed woodland, especially in association with beech, on mossy ground in summer and autumn.[2] All Amanita species form ectomycorrhizal relationships with the roots of certain trees.

Toxicity

young fruiting bodies showing conical caps

Amanita virosa is highly toxic, and has been responsible for severe mushroom poisonings.[4] 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.[5][6]

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.[7] Of the amatoxins, α-amanitin is the chief component and along with β-amanitin is likely responsible for the toxic effects.[8][9] 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.[10] 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.[11]

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,[12] they have since been found to have little input into the destroying angel's toxicity as they are not absorbed through the gut.[10] Furthermore, phalloidin is also found in the edible (and sought-after) Blusher (Amanita rubescens).[7] Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides.[13] Like the phallotoxins they do not exert any acute toxicity after ingestion in humans.[10]

Treatment

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.[14]

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.[14][15] 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.[14]

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,[16] and trials with cephalosporins show promise.[17][18] 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.[19][20][21] N-acetylcysteine has shown promise in combination with other therapies.[22] Animal studies indicate the amatoxins deplete hepatic glutathione;[23] N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage.[24] 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.[14] Repeated doses of activated carbon may be helpful by absorbing any toxins that are returned to the gastrointestinal tract following enterohepatic circulation.[25] Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis,[26] hemoperfusion,[27] plasmapheresis,[28] and peritoneal dialysis[29] have occasionally yielded success but overall do not appear to improve outcome.[10]

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.[30][31][32] This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant.[14] 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.[33][34][35] 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.[36] However, a follow-up study has shown that most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion.[37]

References

  1. ^ Simpson, D.P. (1979). Cassell's Latin Dictionary (5 ed.). London: Cassell Ltd. p. 883. ISBN 0-304-52257-0.
  2. ^ a b Zeitlmayr, Linus (1976). Wild Mushrooms:An Illustrated Handbook. Hertfordshire: Garden City Press. pp. p. 62-63. ISBN 0-584-10324-7. {{cite book}}: |pages= has extra text (help)
  3. ^ Ramsbottom J (1953). Mushrooms & Toadstools. Collins. pp. p. 39. ISBN 1870630092. {{cite book}}: |pages= has extra text (help)
  4. ^ Benjamin.p200
  5. ^ Jordan & Wheeler. p99
  6. ^ Carluccio A (2003). The Complete Mushroom Book. London: Quadrille. p. 224. ISBN 1-84400-040-0.
  7. ^ a b Litten, W. (1975). "The most poisonous mushrooms". Scientific American. 232 (3): 90–101. PMID 1114308. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ 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.
  9. ^ Dart, RC (2004). "Mushrooms". Medical toxicology. Philadelphia: Williams & Wilkins. pp. 1719–35. ISBN 0-7817-2845-2.
  10. ^ 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.
  11. ^ Benjamin.p217
  12. ^ Wieland T, Govindan VM (1974). "Phallotoxins bind to actins". FEBS Lett. 46 (1): 351–3. doi:10.1016/0014-5793(74)80404-7. PMID 4429639.
  13. ^ Vetter, János (1998). "Toxins of Amanita phalloides". Toxicon. 36 (1): 13–24. doi:10.1016/S0041-0101(97)00074-3. PMID 9604278. {{cite journal}}: Unknown parameter |month= ignored (help)
  14. ^ 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. PMID 12475187.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ 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. PMID 3987318.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Template:De iconFloerscheim, G.L. (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. 112 (34): 1164–1177. PMID 6291147. {{cite journal}}: Unknown parameter |Coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  17. ^ Benjamin.p227
  18. ^ Template:De iconNeftel, K.; et al. (1988). "(Are cephalosporins more active than penicillin G in poisoning with the deadly Amanita?)". Schweizerische medizinische Wochenschrift. 118 (2): 49–51. PMID 3278370. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)
  19. ^ Hruby K, Csomos G, Fuhrmann M, Thaler H (1983). "Chemotherapy of Amanita phalloides poisoning with intravenous silibinin". Human toxicology. 2 (2): 183–95. PMID 6862461.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  20. ^ Template:It icon Carducci, R.; et al. (1996). "Silibinin and acute poisoning with ''Amanita phalloides''". Minerva Anestesiologica. 62 (5): 187–93. PMID 8937042. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)
  21. ^ 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 (ed.). Amanita toxins and poisoning. Baden-Baden: Witzstrock. pp. 80–85. ISBN 3-87921-132-9. {{cite book}}: Cite has empty unknown parameter: |coauthors= (help)
  22. ^ 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. PMID 10635453.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ 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. PMID 2243367.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Chyka P, Butler A, Holliman B, Herman M (2000). "Utility of acetylcysteine in treating poisonings and adverse drug reactions". Drug safety. 22 (2): 123–48. PMID 10672895.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ {{cite journal |author=Busi C, Fiume L, Costantino D, Langer M, Vesconi F |title=Amanita toxins in gastroduodenal fluid of patients poisoned by the mushroom, Amanita phalloides |journal=New England Journal of Medicine |volume=300 |issue=14 |pages=800 |year=1979 |pmid=423916}Bold texthow fast will this be fixed?}
  26. ^ Sabeel AI, Kurkus J, Lindholm T (1995). "Intensive hemodialysis and hemoperfusion treatment of Amanita mushroom poisoning". Mycopathologia. 131 (2): 107–14. PMID 8532053.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Wauters JP, Rossel C, Farquet JJ (1978). "Amanita phalloides poisoning treated by early charcoal haemoperfusion". British medical journal. 2 (6150): 1465. PMID 719466.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Jander S, Bischoff J, Woodcock BG (2000). "Plasmapheresis in the treatment of Amanita phalloides poisoning: II. A review and recommendations". Therapeutic apheresis. 4 (4): 308–12. doi:10.1046/j.1526-0968.2000.004004303.x. PMID 10975479.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. ^ Langer M, Vesconi S, Iapichino G, Costantino D, Radrizzani D (1980). "The early removal of amatoxins in the treatment of amanita phalloides poisoning". Klinische Wochenschrift (in German). 58 (3): 117–23. PMID 7366125.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW (1989). "Amanita poisoning: treatment and the role of liver transplantation". American Journal of Medicine. 86 (2): 187–93. doi:10.1016/0002-9343(89)90267-2. PMID 2643869. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  31. ^ Pinson CW, Daya MR, Benner KG, Norton RL, Deveney KE, Ascher NL, Roberts JP, Lake JR, Kurkchubasche AG, Ragsdale JW (1990). "Liver transplantation for severe Amanita phalloides mushroom poisoning". American Journal of Surgery. 159 (5): 493–9. doi:10.1016/S0002-9610(05)81254-1. PMID 2334013. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  32. ^ Ganzert M, Felgenhauer N, Zilker T (2005). "Indication of liver transplantation following amatoxin intoxication". Journal of Hepatology. 42 (2): 202–9. doi:10.1016/j.jhep.2004.10.023. PMID 15664245.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  33. ^ O'grady, John G. (1989). "Early indicators of prognosis in fulminant hepatic failure". Gastroenterology. 97 (2): 439–445. PMID 2490426. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  34. ^ Panaro, Fabrizio (2006). "Letter to the editor: Liver transplantation represents the optimal treatment for fulminant hepatic failure from Amanita phalloides poisoning". Transplant International. 19 (4): 344–5. doi:10.1111/j.1432-2277.2006.00275.x. PMID 16573553. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  35. ^ Escudié L, Francoz C, Vinel JP, Moucari R, Cournot M, Paradis V, Sauvanet A, Belghiti J, Valla D, Bernuau J, Durand F (2007). "Amanita phalloides poisoning: reassessment of prognostic factors and indications for emergency liver transplantation". J. Hepatol. 46 (3): 466–73. doi:10.1016/j.jhep.2006.10.013. PMID 17188393.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Benjamin.p231–232
  37. ^ Giannini L, Vannacci A, Missanelli A, Mastroianni R, Mannaioni PF, Moroni F, Masini E (2007). "Amatoxin poisoning: A 15-year retrospective analysis and follow-up evaluation of 105 patients". Clinical toxicology (Philadelphia, Pa.). 45 (5): 539–42. doi:10.1080/15563650701365834. PMID 17503263.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Sources

  • 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.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Amanita_virosa&oldid=207358784"