Amanita phalloides: Difference between revisions
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1. ↑ Benjamin DR. (1995) Amatoxin syndrome. ''Mushrooms: poisons and panaceas -- a handbook for naturalists, mycologists and physicians.'' New York: W H Freeman and Company: 198-241 | 1. ↑ Benjamin DR. (1995) Amatoxin syndrome. ''Mushrooms: poisons and panaceas -- a handbook for naturalists, mycologists and physicians.'' New York: W H Freeman and Company: 198-241 | ||
2. ↑ Cetto B (1970). I funghi dal vero, vol. 1. Saturnia, Trento (Italy), 690 pp. ISBN 88-85013-01-5 | |||
3. ↑ Gerhardt E. (2005) Guida ai finghi. Zanichelli, Bologna (Italy), 720 pp. Translated from German to Italian by Bernicchia A. ISBN 88-08-19068-4 | |||
4. ↑ Trim GM ''et. al.''(1999). Poisoning by ''Amanita phalloides'' ("deathcap") mushrooms in the Australian Capital Territory. ''Medical Journal of Australia.'' '''171''':247-249 |
Revision as of 18:40, 22 April 2009
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Scientific classification | ||||||||||||||||
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Amanita phalloides (Vaill. ex Fr.) Secr. |
Amanita phalloides (also known as 'Death cap') is a poisonous mushroom, commonly found in woods of hilly to middle mountain regions of all continents except Antarctica. It is renowned as one of the most toxic of all fungi, having been responsible for the majority of deaths from eating poisonous mushrooms[1]. Its dangerousness is heightened by its similarity to some widely eaten species, for instance the straw mushroom. A. Phalloides produces the most poisonous mushroom toxins.Most of mushroom poisonings are caused by A. Phalloides. This mushroom affects both humans and animals, and just half a cap can actually kill a human.
Description[2][3]
Macroscopic features
A. phalloides has a large and distinctive fungal fruiting body composed of a stalk with ring and volva and a cap with gills.
- Cap: usually 5-15 cm across, convex, yellowish, greenish or brown but always with a green tinge which is one of the most diagnostic features. However, some completely white forms (A. phalloides var. alba) are also rarely found. Young fruiting bodies are enclosed in a partial veil. The cap of adult specimens have thin whitish radial fibrils. The gills are free, white and dense.
- Stem: 4-18 cm long and 1-3 cm thick, bulbous, initially full, then void, white and decorated with silky shagreens. It brings a large pendant white ring and a semi-free volva at the base.
- Flesh: White, fibrous especially in the stalk; old specimens have a unpleasant smell.
Microscopic features
- Spores: amiloid, elliptical to subglobose, 8-10 X 7-9 mm.
Smell
The smell is said to be weak and not so strong at first and honey-sweet but eventually becomes very strong, intense and a very unpleasant, intolerable smell.
Similar species
In Europe, A. phalloides is often mistaken with Macrolepiota procera (the 'Parasol mushroom') or other edible species of the same genus. All species of the genus Macrolepiota, however, do not have volva, have a mobile ring, are generally bigger, and have evident scales on a cap that never show the typical green tinge of A. phalloides. Confusion sometimes arisen with mushrooms of the Agaricus campestris group (the 'champignons')[2]. All Agaricus can be distinguished from A. phalloides because of the pink or brown gills, the brown, purple or black spore print and the absence of the volva. Asian immigrants in North America, Europe and Australia have often mistaken A. phalloides for Volvariella volvacea ('paddy straw mushroom'), edible, due to their similarity in appearance[4]. This is a leading cause of mushroom poisoning in the United States. All Volvariella have pink spore print and never bring a ring.
Other similar species are A. subjunquillea in eastern Asia and A. arocheae with a range extending from Andean Colombia to central Mexico (at least). White forms are very similar to A. verna. The cap of Tricholoma sejectum has a color identical to typical A. phalloides, but lacks ring and volva. Some edible mushrooms of the genus Russula (e.g., R. virescens) also have a similar color, but lack ring and volva and have an overall different (more robust) bringing.
Distribution
It is found primarily and originally in Europe but now is also in North America, southeastern Australia[5][6], South America, Asia, and Africa. A. phalloides is easily exported with conifers and hardwoods[7].
Ecology and Habitat
A. phalloides is mycorrhizal. It grows typically in low-middle altitude woods under oaks, beeches, nut trees, chestnut trees, other hardwoods and some conifers (for example, pines), usually from summer to early winter depending on the location.
Toxicity
Since A. phalloides is responsible of several deadly poisonings, its toxicity has been studied deeply. The toxins of this mushroom are phallotoxins (phalloidin, phalloin, phallisin, phallicidin) and amatoxins (amanitin, amanin, amanullin). The toxin most responsible for the deadly effects of A. phalloides is alpha-amanitin. A mid-sized mushroom is enough to kill a healthy adult[3]; preparations as prolonged cooking or maceration under salt do not diminish dangerousness.
Biochemsitry
A. Phalloides’ toxic agents are cyclopeptides, which has two different groups of toxins: the amatoxins and the phallotoxins.
Amatoxins- α-amanitin and β-amanitin are the reason and are what cause the toxic effects. The manner in which these toxins work, prevents RNA polymerase II. The RNA polymerase of A. Phalloides has no effect whatsoever of the amatoxins, meaning A. Phalloides does not poison itself. The amatoxins inhibit transcription by interacting with the enzyme.
Phallotoxins- Since 1938, the toxicity of phalloidin has been thoroughly researched.
It has been proven that phallotoxins are very toxic to liver cells yet they are not soaked up in gut so it is understood that they have very little to do with the toxicity of the mushroom.
Symptoms
Poisoning by A. phalloides has only long term symptoms, the toxins particularly affect the liver and kidneys. After 6-12 hours from the assumption of the mushroom, the patient is subject to stomach ache, diarrhea, vomiting. These symptoms may ease after 24 hours, but then diarrhea and vomiting returns. If untreated, the patient goes into coma and dies of liver failure.
Treatment
Poisoning can be treated by intravenous injection of silibinin dihydrogen disuccinate disodium. Frequently the only treatment for death cap poisoning is liver transplant.
References
1. ↑ Benjamin DR. (1995) Amatoxin syndrome. Mushrooms: poisons and panaceas -- a handbook for naturalists, mycologists and physicians. New York: W H Freeman and Company: 198-241 2. ↑ Cetto B (1970). I funghi dal vero, vol. 1. Saturnia, Trento (Italy), 690 pp. ISBN 88-85013-01-5 3. ↑ Gerhardt E. (2005) Guida ai finghi. Zanichelli, Bologna (Italy), 720 pp. Translated from German to Italian by Bernicchia A. ISBN 88-08-19068-4 4. ↑ Trim GM et. al.(1999). Poisoning by Amanita phalloides ("deathcap") mushrooms in the Australian Capital Territory. Medical Journal of Australia. 171:247-249
- ↑ Benjamin DR. (1995)Amatoxin syndrome. Mushrooms: poisons and panaceas -- a handbook for naturalists, mycologists and physicians. New York: W H Freeman and Company: 198-241
- ↑ 2.0 2.1 Cetto B (1970). I funghi dal vero, vol. 1. Saturnia, Trento (Italy), 690 pp. ISBN 88-85013-01-5
- ↑ 3.0 3.1 Gerhardt E. (2005) Guida ai funghi. Zanichelli, Bologna (Italy), 720 pp. Translated from German to Italian by Bernicchia A. ISBN 88-08-19068-4
- ↑ Trim GM et. al.(1999).Poisoning by Amanita phalloides ("deathcap") mushrooms in the Australian Capital Territory. Medical Journal of Australia.171: 247-249
- ↑ Reid DA. (1980) A monograph of the Australian species of Amanita Pers. ex Hook (Fungi). Australian Journal of Botany - Supplementary Series No. 8: 48
- ↑ Cole FM. (1993) Amanita phalloides in Victoria. Medical Journal of Australia; 158: 849-850
- ↑ Kuo, M. (2001, September). Amanita phalloides: The death cap. Retrieved from the MushroomExpert.Com Web site: http://www.mushroomexpert.com/amanita_phalloides.html