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Amanita ocreata



Amanita ocreata
Western North American destroying angel

Conservation status
Secure
Scientific classification
Kingdom: Fungi
Division: Basidiomycota
Class: Homobasidiomycetes
Subclass: Hymenomycetes
Order: Agaricales
Family: Amanitaceae
Genus: Amanita
Section: Phalloideae
Species: A. ocreata
Binomial name
Amanita ocreata
Peck
Amanita ocreata
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

Error creating thumbnail:  

edibility: deadly

Amanita ocreata, commonly known as the death angel, destroying angel or more precisely Western North American destroying angel, is a poisonous basidiomycete fungus, one of many in the genus Amanita. Occurring in North America's Pacific Northwest, A. ocreata associates with oak trees. The large fruiting bodies (the mushrooms) generally appear in spring; the cap may be white or ochre and often develops a brownish centre, while the stipe, ring, gill and volva are all white.

Amanita ocreata resemble several edible species commonly consumed by humans, increasing the risk of accidental poisoning. Mature fruiting bodies can be confused with the edible A. velosa, A. lanei or Volvariella speciosa, while immature specimens may be difficult to distinguish from edible Agaricus mushrooms or puffballs. Similar in toxicity to the death cap (A. phalloides) and destroying angels of Europe (A. virosa) and eastern North America (A. bisporiga), it is one of the most poisonous of all known toadstools and is responsible for a number of poisonings in California.[1] Its principal toxic constituent, α-amanitin, damages the liver and kidneys, often fatally, and has no known antidote.[2] The initial symptoms are gastrointestinal and include colicky abdominal pain, diarrhea and vomiting. These subside temporarily after 2–3 days, though ongoing damage to internal organs during this time is common; symptoms of jaundice, diarrhea, delirium, seizures, and coma may follow with death from liver failure 6–16 days post ingestion.

Additional recommended knowledge

Contents

Taxonomy and naming

Amanita ocreata was first described by American mycologist Charles Horton Peck in 1909 from material collected by a C. F. Baker in Claremont, California.[3] The specific epithet is derived from the Latin ocrěātus 'wearing greaves' from ocrea 'greave'.[4] Amanita bivolvata is a botanical synonym. It belongs to the section Phalloideae within the genus Amanita, which contains several deadly poisonous fungi including the death cap (A. phalloides) and several all-white species of Amanita also known as "destroying angels": Amanita bisporiga of eastern North America, and the European A. virosa. "Death angel" is used as an alternate common name.[5]

Description

A. ocreata is generally stouter than the other fungi termed destroying angels. It first appears as a white egg-shaped object covered with a universal veil. As it grows, the mushroom breaks free, though there may rarely be ragged patches of veil left at the cap edges. The cap is initially hemispherical, before becoming more convex and flattening, sometimes irregularly. This may result in undulations in the cap, which may reach up to 12 cm (5 in) in diameter. The colour varies from white, through yellowish-white to shades of ochre, sometimes with a brownish centre. Occasionally parts of the fruiting bodies may have pinkish tones. The crowded, free to narrowly adnate gills are white, as is the stipe and the thin, smooth sac-like volva. The stipe is 8–20 cm (3–8 in) high and 1.5–2 cm (½–⅔ in) thick at the apex, and bears a thin white membranous ring. The spore print is white, and the ovate to subelliptic amyloid spores are 9–14 x 7–10 μm viewed under a microscope.[1] The toadstool typically has no smell, but may have a slight odour, described as that of bleach or chlorine, dead fish or iodine. Like other destroying angels, the flesh stains yellow when treated with potassium hydroxide (KOH).[6]

This fungus 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, so those collecting immature fungi run the risk of confusing the varieties. It also resembles and grows in the same areas as the edible and prized Amanita velosa, which can be distinguished from A. ocreata by its lack of ring, striate cap margin and thick universal veil remnants comprising the veil.[5] The edible Amanita lanei lacks a ring and is more likely to have veil patches remaining on its cap, which is generally darker. Volvariella speciosa has pink spores and no ring or volva.[7]

Distribution and habitat

Appearing from January to April, A. ocreata occurs later in the year than other amanitas except A. calyptroderma. It is found in mixed woodland on the Pacific coast of North America,[1] from Washington south through California to Baja California in Mexico.[6] It may feasibly occur on Vancouver Island in British Columbia though this has never been confirmed.[8] It forms ectomycorrhizal relationships and is found in association with Coast Live Oak (Quercus agrifolia),[9] as well as hazel (Corylus spp.).[6] In Oregon and Washington, it may also be associated with the Garry Oak (Quercus garryana).[8]

Toxicity

  Amanita ocreata is highly toxic, and has been responsible for a number of mushroom poisonings in western North America, particularly in the spring. It contains highly toxic amatoxins, as well as phallotoxins, a feature shared with the closely related death cap (A. phalloides) and other species known as destroying angels.[1] There is some evidence it may be the most toxic of all the North American phalloideae, as a higher proportion of people consuming it had organ damage and 40% perished.[10] Dogs, too, have been known to consume this fungus in California with fatal results.[11]

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.[12] Of the amatoxins found in A. ocreata, α-amanitin is the most prevalent and along with β-amanitin is likely to be responsible for the toxic effects.[1][13][14] The 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 stop and the cell dies.[15] The liver is the principal organ affected, as it is the first organ encountered after absorption by the gastrointestinal tract, though other organs, especially the kidneys, are susceptible to the toxins.[16]

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,[17] they have since been found to have little input into the destroying angel's toxicity as they are not absorbed through the gut.[15] Furthermore, phalloidin is also found in the edible (and sought-after) Blusher (Amanita rubescens).[12] Another group of minor active peptides found in A. ocreata are the virotoxins, which consist of six similar monocyclic heptapeptides.[18] Like the phallotoxins they do not exert any acute toxicity after ingestion in humans.[15]

Symptoms

Symptoms of poisoning by A. ocreata are initially gastrointestinal in nature and include colicky abdominal pain, with watery diarrhea and vomiting which may lead to dehydration, and, in severe cases, hypotension, tachycardia, hypoglycemia, and acid-base disturbances.[19][20] The initial symptoms resolve two to three days after ingestion of the fungus. A more serious deterioration signifying liver involvement may then occur—jaundice, diarrhea, delirium, seizures, and coma due to fulminant hepatic failure and attendant hepatic encephalopathy caused by the accumulation of normally liver-removed substances in the blood.[21] Renal failure (either secondary to severe hepatitis[22][18] or caused by direct toxic renal damage[15]) and coagulopathy may appear during this stage. Life-threatening complications include increased intracranial pressure, intracranial hemorrhage, sepsis, pancreatitis, acute renal failure, and cardiac arrest.[19][20] Death generally occurs six to sixteen days after the poisoning.[23]

Treatment

Consumption of A. ocreata is a medical emergency that requires hospitalization. There are four main categories of therapy for poisoning: preliminary medical care, supportive measures, specific treatments, and liver transplantation.[2]

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 long after ingestion, potentially reducing the efficacy of these interventions.[2][24] 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.[2]

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,[25] and trials with cephalosporins show promise.[26][27] There is some evidence that intravenous silibinin, an extract from the blessed milk thistle (Silybum marianum), may be beneficial in reducing the effects of amatoxins, preventing their uptake by hepatocytes, thereby protecting undamaged hepatic tissue. It also stimulates DNA-dependent RNA polymerases, leading to an increase in RNA synthesis.[28][29][30] N-acetylcysteine has shown promise in combination with other therapies.[31] Animal studies indicate the amatoxins deplete hepatic glutathione;[32] N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage.[33] 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.[2] Repeated doses of activated carbon may be helpful in absorbing any toxins that are returned to the gastrointestinal tract following enterohepatic circulation.[34] Other methods of enhancing the elimination of the toxins have been trialled; techniques such as hemodialysis,[35] hemoperfusion,[36] plasmapheresis,[37] and peritoneal dialysis[38] have occasionally yielded successes but overall do not appear to improve outcome.[15]

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.[20][19][39] This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant.[2] As a result, 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.[40][41][42] 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.[43] However, a follow-up study has shown that most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion.[44]

References

  1. ^ a b c d e Ammirati JF, Thiers HD, Horgen PA (1977). "Amatoxin containing mushrooms:Amanita ocreata and Amanita phalloides in California". Mycologia 69 (6): 1095–1108. doi:10.2307/3758932.
  2. ^ a b c d e f 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.
  3. ^ Peck CH (1909). "New species of fungi.". Bull. Torrey Bot. Club 36: 329–39.
  4. ^ Simpson, D.P. (1979). Cassell's Latin Dictionary, 5, London: Cassell Ltd., 883. ISBN 0-304-52257-0. 
  5. ^ a b Arora D. (1986). Mushrooms Demystified (2nd ed). Ten Speed Press: Berkeley, CA. ISBN 0-89815-169-4
  6. ^ a b c Tulloss RE (2005). Amanita ocreata Peck "Western American Destroying Angel". Studies in the Genus Amanita Pers.(Agaricales, Fungi). Tulloss RE. Retrieved on 2007-11-13.
  7. ^ Wood M, Stevens F (1998-2007). California fungi:Amanita ocreata. Mykoweb - The Fungi of California. Wood M. Retrieved on 2007-11-13.
  8. ^ a b Birch, Shannon (April 2006). "Is Amanita ocreata on Vancouver Island?" (PDF). Fungifama:The Newsletter of the South Vancouver Island Mycological Society: 5. Retrieved on 2007-12-11.
  9. ^ Benjamin, p. 205
  10. ^ Beug, Michael (April 2006). "Reflections on Mushroom Poisoning – Part I" (PDF). Fungifama:The Newsletter of the South Vancouver Island Mycological Society: 3–5. Retrieved on 2007-12-11.
  11. ^ Tegzes JH, Puschner B (2002). "Amanita mushroom poisoning: efficacy of aggressive treatment of two dogs.". Vet Hum Toxicol. 44 (2): 96–99. PMID 11931514.
  12. ^ a b Litten, W. (March 1975). "The most poisonous mushrooms". Scientific American 232 (3): 90–101. PMID 1114308.
  13. ^ 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.
  14. ^ Dart, RC (2004). "Mushrooms", Medical toxicology. Philadelphia: Williams & Wilkins, 1719–35. ISBN 0-7817-2845-2. 
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  16. ^ Benjamin.p217
  17. ^ 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.
  18. ^ a b Vetter, János (January 1998). "Toxins of Amanita phalloides". Toxicon 36 (1): 13–24. doi:10.1016/S0041-0101(97)00074-3. PMID 9604278.
  19. ^ a b c Pinson CW, Daya MR, Benner KG, Norton RL, Deveney KE, Ascher NL, Roberts JP, Lake JR, Kurkchubasche AG, Ragsdale JW (May 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.
  20. ^ a b c Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW (February 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.
  21. ^ North, Pamela Mildred (1967). Poisonous plants and fungi in colour. London: Blandford Press. OCLC 955264. 
  22. ^ Nicholls DW, Hyne BE, Buchanan P (1995). "Death cap mushroom poisoning". The New Zealand Medical Journal 108 (1001): 234. PMID 7603660.
  23. ^ Fineschi V, Di Paolo M, Centini F (1996). "Histological criteria for diagnosis of Amanita phalloides poisoning". J. Forensic Sci. 41 (3): 429–32. PMID 8656182.
  24. ^ 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.
  25. ^ (German)Floerscheim, G.L. (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 112 (34): 1164–1177. PMID 6291147.
  26. ^ Benjamin.p227
  27. ^ (German)Neftel, K. et al. (January 1988). "(Are cephalosporins more active than penicillin G in poisoning with the deadly Amanita?)". Schweizerische medizinische Wochenschrift 118 (2): 49–51. PMID 3278370.
  28. ^ 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.
  29. ^ (Italian) Carducci, R. et al. (May 1996). "[[Silibinin and acute poisoning with Amanita phalloides]]". Minerva Anestesiologica 62 (5): 187–93. PMID 8937042.
  30. ^ 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, 80–85. ISBN 3-87921-132-9. 
  31. ^ 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.
  32. ^ 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.
  33. ^ 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.
  34. ^ Busi C, Fiume L, Costantino D, Langer M, Vesconi F (1979). "Amanita toxins in gastroduodenal fluid of patients poisoned by the mushroom, Amanita phalloides". New England Journal of Medicine 300 (14): 800. PMID 423916.
  35. ^ Sabeel AI, Kurkus J, Lindholm T (1995). "Intensive hemodialysis and hemoperfusion treatment of Amanita mushroom poisoning". Mycopathologia 131 (2): 107–14. PMID 8532053.
  36. ^ Wauters JP, Rossel C, Farquet JJ (1978). "Amanita phalloides poisoning treated by early charcoal haemoperfusion". British medical journal 2 (6150): 1465. PMID 719466.
  37. ^ 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.
  38. ^ Langer M, Vesconi S, Iapichino G, Costantino D, Radrizzani D (1980). "The early removal of amatoxins in the treatment of Amanita phalloides poisoning" (in German). Klinische Wochenschrift 58 (3): 117–23. PMID 7366125.
  39. ^ 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.
  40. ^ O'grady, John G.; Graeme J.M. Alexander, Karen M. Hayllar & Roger Williams (august 1989). "Early indicators of prognosis in fulminant hepatic failure". Gastroenterology 97 (2): 439–445. PMID 2490426.
  41. ^ Panaro, Fabrizio; Enzo Andorno, Nicola Morelli, Marco Casaccia, Giuliano Bottino, Ferruccio Ravazzoni, Monica Centanaro, Sara Ornis & Umberto Valente (April 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.
  42. ^ 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.
  43. ^ Benjamin.p231–232
  44. ^ 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.

Bibliography

  • 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. 
 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Amanita_ocreata". A list of authors is available in Wikipedia.
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