Amanita phalloides, commonly known as the death cap, is a poisonous basidiomycete fungus, one of many in the genus Amanita. Widely distributed across Europe, A. phalloides associates with various deciduous and coniferous trees. In some cases, death cap has been accidentally introduced to new regions with the cultivation of non-native species of oak, chestnut, and pine. The large fruiting bodies (i.e., the mushrooms) appear in summer and autumn; the caps are generally greenish in colour, with a white stipe and gills.

Coincidentally, these toxic mushrooms resemble several edible species (most notably the straw mushroom) commonly consumed by humans, increasing the risk of accidental poisoning. A. phalloides is one of the most poisonous of all known toadstools. It has been involved in the majority of human deaths from mushroom poisoning, possibly including the deaths of Roman Emperor Claudius and Holy Roman Emperor Charles VI. It has been the subject of much research, and many of its biologically active agents have been isolated. The principal toxic constituent is α-amanitin, which damages the liver and kidneys, often fatally. No antidote is known.

This is one of the most poisonous European toadstools (3). All parts of the fungus are deadly, and it should never be eaten (4). The cap is typically yellowish to olivaceous green, sometimes paling almost to white, usually with darker streaks radiating outwards (3) (4) (5). It is convex at first, but becomes flattened as it ages, and may develop a sickly sweet smell (2) (5). The gills underneath the cap are white, and the white stem has a distinct ring, although this may become damaged or lost (3) (4). The base of the stem bulges into a 'bulb', which is covered by a white sheath known as a volva (2). WARNING: Many species of fungus are poisonous or contain chemicals that can cause sickness. Never pick and eat any species of fungus that you cannot positively recognise or are unsure about. Some species are deadly poisonous and can cause death within a few hours if swallowed.

The tradition of picking and eating wild mushrooms is prominent in most Slavic countries such as Russia, Poland, Ukraine, Slovakia and the Czech Republic among others. Whole families often venture into the nearest forest after a heavy rain during mushroom season, picking bucketfuls of mushrooms, which are cooked and eaten for dinner upon return or alternatively dried or marinated for later consumption.

The ability to identify, collect, and prepare edible mushrooms is usually passed down through generations. Methods can be different from those used elsewhere: the Slavic way does not require identification to species, but relies more on experience and familiarity with varieties that have been collected before. Many people would not consider eating a species that they cannot positively identify using a field guide, but most Slavic collectors would view this attitude as overly paranoid. Some mushroom species listed as poisonous in Western literature are even listed as edible in Slavic literature; this may be because the majority of people do not have any adverse reaction, or because the reaction, when it occurs, is generally mild. (It must be noted that ALL mushroom species cause adverse reaction in a few individuals, even the common champignon.) The relative leniency toward potential health risks can be justified by the fact that only a handful of poisonous mushrooms lead to fatal poisonings and are reasonably easy to avoid, and that children usually learn to identify edible mushrooms quite reliably through live examples, rather than textual descriptions. Also, some species have been shown to contain different amounts of toxins when growing in the New World and the Old World. Additionally, the toxins of numerous mildly poisonous mushrooms can be broken down or eliminated with specific cooking or drying methods, and these are handed down together with collecting skills as part of the mushroom-consuming tradition.

Literature and picking guides also frequently offer reminders to always cut a mushroom with a blade, rather than pulling it out, and to never kick or otherwise destroy mushrooms one does not want, thus preserving the forest ecosystem.

A deadly poisonous fungus common to Europe and the West Coast of North America.

There is no type specimen for Amanita phalloides. For other specimens see 'specimen information', above.

The death cap was first described by French botanist Sébastien Vaillant in 1727, who gave a succinct phrase name "Fungus phalloides, annulatus, sordide virescens, et patulus", which is still recognizable as the fungus today (Vaillant 1727).Though the scientific name phalloides means "phallus-shaped", it is unclear whether it is named for its resemblance to a literal phallus or the stinkhorn mushrooms Phallus. In 1821, Elias Magnus Fries described it as Agaricus phalloides, but included all white Amanitas within its description (Fries 1821). Finally in 1833, Johann Heinrich Friedrich Link settled on the name Amanita phalloides (Link 1833), after Persoon had named it Amanita viridis thirty years earlier (Persoon 1797, Persoon 1801). Although Louis Secretan's use of the name Amanita phalloides predates Link's, it has been rejected for nomenclatural purposes because Secretan's works did not use binomial nomenclature consistently (Donk 1962, Demoulin 1974); some taxonomists have, however, disagreed with this opinion (Singer et al. 1962, Machol 1984).

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 Amanita virosa and A. bisporiga 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" (North 1967) and "deadly amanita" (Benjamin 1995).

A rarely appearing all-white form was initially described A. phalloides f. alba by Max Britzelmayr (Tulloss, Jordan et al. 2001), though its status has been unclear. It is often found growing amid normally coloured death caps. It has been described, in 2004, as a distinct variety and includes what was termed A. verna var. tarda.(Neville 2004) The true Amanita verna fruits in spring and turns yellow with KOH solution, whereas A. phalloides never does (Tulloss).

References

• Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.
• Demoulin, V. (November 1974). "Invalidity of Names Published in Secretan's Mycographie Suisse and Some Remarks on the Problem of Publication by Reference". Taxon 23 (5/6): 836–843. 
• Donk, M.A. (June 1962). "On Secretan's Fungus Names". Taxon 11 (5): 170–173. 
• Fries, Elias Magnus (1821). Systema Mycologicum I. Gryphiswaldiae: Ernesti Mauritii.
• Jordan Peter, Wheeler Steven. (2001). The Ultimate Mushroom Book. London: Hermes House.
• Link JHF (1833) Grundriss der Kraeuterkunde IV. Haude und Spenerschen Buchhandlung (S.J. Joseephy), Berlin
• Machol, Robert E. (August 1984). "Leave the Code Alone". Taxon 33 (3): 532–533. 
• Neville, Pierre; Serge Poumarat (2004). Amaniteae: Amanita, Limacella and Torrendia, Fungi Europaei (9).
• North, Pamela Mildred (1967). Poisonous plants and fungi in colour. London: Blandford Press. 
• Persoon, Christian Hendrik (1797). Tentamen Dispositionis Methodicae Fungorum. Lipsiae: P.P. Wolf,.
• Persoon, Christian Hendrik (1801). Synopsis Methodica Fungorum. GÖttingen: H. Dietrich.
• Singer, Rolf; Robert E. Machol (June 1962). "Are Secretan's Fungus Names Valid?". Taxon 26 (2/3): 251–255. 
• Tulloss, Rodham Amanita verna (Bull.: Fr.) Lam. Amanita Studies site. Retrieved on 2007-05-22.
• Tulloss, Rodham E. (Fr.:Fr.) Link. Amanita Studies site. Retrieved on 2007-05-22.
• Vaillant, Sébastien (1727). Botanicon Parisiense. Leide & Amsterdam: J. H. Verbeek and B. Lakeman. (Plate and Explication in the Biodiversity Heritage Library.)

Original Description

Fries EM 1821 Systema Mycologicum I. sumtibus Ernesti Mauritii, Gryphiswaldiae (Digital image at Libri Fungorum)

The combination Amanita phalloides was proposed in:

Link DHF (1833) Grundriss der Kraeuterkunde IV. Haude und Spenerschen Buchhandlung (S.J. Joseephy), Berlin

Good specimen information from Europe can be found at Global Biodiversity Information Facility (GBIF); otherwise, large herbaria with online databases include the New York Botanical Garden and the University of Michigan. Note that early collections from North America may be species misidentified as A. phalloides.

Found throughout much of Europe, where its status is variable, but is more common towards the south. It occurs in New Zealand, and also North America and South Africa, with oak trees imported from Europe (4).

A preliminary map of the native range of Amanita phalloides, as well as regions where A. phalloides has been introduced.

Reference

Pringle, A., E. C. Vellinga. 2006. Last chance to know? Using literature to explore the biogeography of and invasion biology of the death cap mushroom Amanita phalloides (Vaill. Ex Fr. :Fr) Link. Biological Invasions 8:1131-1144.

Distribution in the United Kingdom (compiled from forays taken by the British Mycological Society)

Amanita phalloides was originally described from Europe. In Europe in occurs with beech (Fagus), oak (Quercus), pine (Pinus), chestnut (Castanea), horse chestnut (Aesculus), birch (Betula), filbert and hazelnuts (Corylus maxima), iron wood or hornbeam (Carpinus), and spruce (Picea). In the northern hemisphere the present species when transplanted can spread to local trees of the same genera in addition to Canadian hemlock (Tsuga). It is reported under Leptospermum in New Zealand and under Eucalyptus and leguminous trees in Tanzania. Importation in the western hemisphere has occurred from Canada to Argentina. 

This species is easily exported with its symbionts (oaks, pines, nut trees, etc.). As a consequence, it has been introduced in many countries in which European trees of its symbionts have been planted. It can then be exported from those countries it has colonized. It would appear that it and A. muscaria (L.:Fr.) Lam. subsp. muscaria have been the most commonly exported species of Amanita.

Everywhere it has been imported, it is a major cause of life-threatening mushroom poisonings. See also, A. arocheae Tulloss, Ovrebo & Halling, A. fuliginea Hongo, A. marmorata Cleland & E.-J. Gilbert, and A. subjunquillea S. Imai. The reader may want to examine the recently revised key to the taxa of sect. Phalloideae in North America.

The Deathcap is common in many Canberra suburbs and can be found in most autumns near oak trees, with which it forms a symbiotic association. It is also well-established in several Melbourne suburbs and in some Victorian country towns.

It is not native to Australia, but has been accidentally introduced from the northern hemisphere.

There is some evidence of it associating with eucalypts in Canberra, but this needs further study. It has been reported from eucalypt and acacia plantations in east Africa, and eucalypt plantations in Morocco.

The Deathcap is one of the FUNGIMAP target species and this link [http://www.rbg.vic.gov.au/fungimap/fsp/sp053.html] will take you to the Fungimap entry (and a map showing you where this fungus has been found in Australia).

The death cap is native to Europe, where it is widespread (Lange 1974). It is found from the southern coastal regions of Scandinavia in the north, to Ireland in the west, east to Poland and western Russia (Neville & Poumarat 2004), and south throughout the Balkans, in Italy and Spain, and in Morocco and Algeria in north Africa (Malençon & Bertault 1973). There are records from further east into Asia but these have yet to be confirmed as A. phalloides (Pringle & Vellinga 2006).

It is ectomycorrhizally associated with a number of tree species. In Europe, these include a large number of 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 (Tullos 2007). In other areas, A. phalloides may also be associated with these trees or only with some species but not others. In coastal California, for example, A. phalloides is associated with coast live oak but not with the various coastal pine species, such as Monterey pine (Arora 1986). In countries where it has been introduced it has been restricted to those exotic trees it would associate with in its natural range. There is, however, evidence of A. phalloides associating with hemlock and with genera of the Myrtaceae: Eucalyptus in Tanzania (Pegler 1977) and Algeria (Malençon & Bertault 1973), and Leptospermum and Kunzea in New Zealand (Ridley 1991; Tullos 2007). This suggests the species may have invasive potential (Pringle & Vellinga 2006).

By the end of the 19th century, Charles Horton Peck had reported A. phalloides in North America (Peck 1897). However, in 1918, samples from the Eastern United States were identified as being a distinct though similar species, A. brunnescens, by G. F. Atkinson of Cornell University.[29] By the 1970s it had become clear that A. phalloides actually does occur in the United States, apparently having been introduced from Europe alongside chestnuts, with populations on the West and East Coasts (Litten 1975; Benjamin 1995). A more recent historical review concluded that the East Coast populations were introduced but that the origins of the West Coast population remain unclear, due to the scantness of historical records (Pringle & Vellinga 2006).

Amanita phalloides has been conveyed to new countries across the southern hemisphere with the importation of hardwoods and conifers. Introduced oaks appear to have been the vector to Australia and South America; populations under oaks have been recorded from Melbourne and Canberra (Reid 1980; Cole 1993), as well as Uruguay (Herter 1934). It has been recorded under other introduced trees in Argentina (Hunzinker 1983) and Chile (Valenzuella et al. 1992). Pine plantations are associated with the fungus in Tanzania (Pegler 1977) and South Africa, where it is also found under oaks and poplars (Reid & Eicker 1991).

References

• Arora, David (1986). Mushrooms demystified : a comprehensive guide to the fleshy fungi. Berkeley, California: Ten Speed Press.
• Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.
• Cole, F.M. (June 1993). "Amanita phalloides in Victoria". Medical Journal of Australia 158 (12): 849–850.
• Herter, W.G. (1934). "La aparición del hongo venenoso Amanita phalloides en Sudamérica.". Revista Sudamericana de Botánica 1: 111–119.
• Hunzinker, A.T. (1983). "Amanita phalloides en las Sierras de Córdoba". Kurtziana 16: 157–160.
• Lange, Lene (1974). "The distribution of macromycetes in Europe". Dansk Botanisk Arkiv 30: 5–105.
• Litten, W. (March 1975). "The most poisonous mushrooms". Scientific American 232 (3): 90–101.
• Malençon, Georges; R. Bertault (1970). Flore des Champignons Supérieurs du Maroc I, Travaux de l'Institut scientifique chérifien et de la Faculté des sciences. Série botanique et biologie végétale (32). Rabat: Faculté des Sciences.
• Neville, Pierre; Serge Poumarat (2004). Amaniteae: Amanita, Limacella and Torrendia, Fungi Europaei (9).
• Peck, Charles H. (1897). Annual report of the state botanist. Albany: University of the State of New York
• Pegler (1977). A preliminary agaric flora of East Africa, Kew Bulletin Additional Series (6). Royal Botanic Gardens, Kew.
• Pringle, Anne; Else C. Vellinga (July 2006). "Last chance to know? Using literature to explore the biogeography of and invasion biology of the death cap mushroom Amanita phalloides. (Vaill. ex Fr. :Fr) Link". Biological Invasions 8 (5): 1131–1144.
• Reid, D.A. (1980). "A monograph of the Australian species of Amanita Pers. ex Hook (Fungi)". Australian Journal of Botany Supplementary Series 8: 1–96
• Reid, D.A.; A. Eicker (1991). "South African fungi: the genus Amanita". Mycological Research 95 (1): 80–95.
• Ridley, G.S. (1991). "The New Zealand Species of Amanita (Fungi: Agaricales)". Australian Systematic Botany 4 (2): 325–354.
• Tulloss, Rodham E.. (Fr.:Fr.) Link. Amanita Studies site. Retrieved on 2007-05-22.
• Valenzuella, E.; G. Moreno & M. Jeria (1992). "Amanita phalloides en bosques de Pinus radiata de la IX Region de Chile: taxonomia, toxinas, metodos de dedection, intoxicacion faloidiana". Boletín Micológico 7: 17–21.

The mushrooms in Amanita include some of the world's most famous (and most deadly) fungi. Amanita species are recognized by their (usually) pale gills, which are free from the stem; their white spore prints; the presence of a universal veil that often creates a volva or other distinctive features on the stem; and their more or less dry caps (as opposed to the slimy caps in Limacella). Many species of Amanita have warts or patches on their caps, and most have a ring on the stem.

Although there are some edible mushrooms in the genus, no amanita should be eaten. The genus contains lethal mushrooms that are quite similar to the "edible" ones. See Mushroom Toxins and The Meixner Test for information on the poisons present in the most dangerous amanitas.

The cap of Amanita phalloides is (40±) 65 - 152 (-300±) mm wide, with pigment arranged in narrow bands of variously colored spots giving the illusion of multicolored radially arranged imbedded fibers. Among the colors involved are pale to dark variance of olive-green, yellow green to yellow, gray, and brown. Often described as dark fibers on a greenish or yellowish ground color; however, this is an optical illusion. Sometimes the center of the cap may be entirely of the darkest tints while sometimes the center of the cap may appear bleached. The cap is often palest at the margin (for example white or extremely pale yellow or extremely pale yellow green). The cap is subovoid to hemispheric with incurved margin at first, becoming convex, eventually subplanar with decurved margin, smooth, wet and sticky when moist, shiny when dry, sometimes faintly pruinose particularly over the center, with a nonstriate and nonappendiculate margin. The volva is absent or occasionally present as membranous patch, white to sordid white to pale beige. The flesh is white except for a  yellow line below the cap skin, however the yellow tint disappears with age, with such a line disappearing in age, unchanging when cut or bruised, 4.5- - 7.5+ mm thick over the stem, thinning evenly to margin. 

The gills are free to narrowly adnate, crowded, white to cream in mass, white to cream to faintly pinkish cream to sordid cream to cream with slight yellow-greenish tinge in side view, unchanging when cut or bruised, 6 - 9 mm broad, with or without decurrent line on stipe apex. The short gills are truncate to excavate truncate to subtruncate, unevenly distributed, of diverse lengths, common, and occasionally arising at the stem as well as at the cap margin.

The stem is (35±) 54+ - 135 (-300±) × 8 - 17.5 (-20+) mm, largely white to pale yellow below the ring, sometimes more strongly yellow near the stem base, sometimes with faint yellowish white areas above the ring, narrowing upward, slightly flaring at the top in age, decorated with fine raised concolorous fibrils that darken from handling sometimes forming the "flame" pattern especially in the lowest third of stem. The bulb is 20 - 35+ × 16 - 50 mm, globose to subglobose, sometimes slightly compressed vertically, white, and very soft. The ring is in the upper part of the stem, membranous, up to 30± mm from the stem to its edge, white to pale yellow with fine radial striations on the upper side, somewhat felted and ranging from white to containing one or more of the cap colors (which may be in irregular patterns) on the under side. The limbate volva is white on outer surface, white to yellow or with other tints from the cap (sometimes similarly unevenly pigmented) on the inner surface, membranous, persistent, opening somewhat irregularly, with top of limb up 26- - 65 mm from the base of the bulb, with the limb more or less the same height as the bulb vertical thickness. 

The odor is sometimes absent in early development, eventually sickeningly sweet or cloying like a "sweet ester."

The spores measure (7.5-) 8.0 - 10.1 (-13.5) x (5.5-) 6.1 - 8.0 (-10.5) µm and are subglobose to broadly ellipsoid to ellipsoid and amyloid. Clamps are not found at bases of basidia.

Major features:

Smooth, yellowish-green to olive-brown cap; white gills; white stem; membranous skirt on stem; cup-like structure around the base of the stem.

A more detailed description:

Cap: The young caps are close to hemispherical in shape but then flatten as they expand. When fully open they are gently curved and smooth. The colour is usually yellowish green, but may sometimes be olive to light brown. The fully open caps are commonly 10-15 centimetres in diameter. However, you can find fully mature Deathcaps with caps under 10 centimetres across, occasionally even as little as 5 centimetres. Much depends on what the weather has been doing. The cap is slightly sticky in wet weather but dry and shiny in dry weather.

Gills: White. The gills don’t reach the stem.

Stem: The stem is white and from 5 to 15 centimetres long and 1 to 2 centimetres in diameter. The base of the stem is bulbous (up to 4 centimetres in diameter) and is contained within a cup-like structure (called a volva). Sometimes the bulbous base and the volva will be partially buried in the soil or hidden by grasses and leaf litter. Occasionally the volva is poorly developed.

There is usually a loose, white, skirt-like membrane (called a ring) around the upper part of the stem, but it’s not too hard to rub off this ring if you handle the mushroom roughly. At an earlier stage that membrane would have stretched from the stem to the edge of the cap and covered the young gills.

Flesh: White

Spore print: White

Universal veil: When the Deathcap is still fairly small, it is wrapped up in a smooth, white skin - called a universal veil. As the stem lengthens and the cap expands, the Deathcap breaks through that veil. The cup-like volva at the base of the stem is a remnant of that universal veil. For a short time a part of the universal veil may stay on the cap as a white patch, but this soon disappears. The photos show such patches on some of the smaller mushrooms that have not yet fully developed.

Pileus

Cap 3.5-15 cm broad, convex, expanding to nearly plane, at maturity the disc sometimes slightly raised or depressed; margin entire, seldom striate, or if so, obscurely so; surface subviscid when moist, smooth, occasionally with a faint, appressed, white universal veil patch; color: olive, olive-brown, to yellowish-brown, rarely white, typically with innate, darker streaks, the margin paler, fading overall to dull tan in age; flesh soft, white, moderately thick at the disc, unchanging, at times yellowish-brown just below the cuticle; odor slightly pungent; taste mild.

Lamellae

Gills free, close, moderately broad, white becoming cream, staining pink to vinaceous with concentrated sulfuric acid.

Stipe

Stipe 4-18 cm long, 1-3 cm thick, equal to tapering to an enlarged, sometimes bulbous base, usually solid but the apex sometimes stuffed; surface finely striate at the apex, otherwise smooth or with scattered, flattened small scales, white to pale yellowish; flesh white, firm, unchanging; partial veil membranous, cream-colored to tinged like the cap, the upper surface striate, lower surface slightly pubescent, forming a pendulous, superior annulus; volva membranous, thin, white, sac-like, usually erect from the stipe.

Spores

Spores 7-12 x 6-10 µm, ovoid to elliptical, amyloid; spore print white.

This fungus grows in deciduous woodlands, particularly under beech and oak trees, and shows a slight preference for acidic soils (4) (5). In mountainous areas it occurs in coniferous forests, and is also found in pastures on the edge of woodlands (4).

California

Solitary, scattered, to gregarious under Coast Liveoak (Quercus agrifolia), occasionally with other oaks and ornamental hardwoods; fruiting sporadically during the summer months in watered areas or from fog drip along the coast; common from early to mid-winter.

Amanita phalloides is a symbiont of trees and grows in temperate forests.

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

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

In Great Britain and/or Ireland:
Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita citrina is ectomycorrhizal with live root of Fagus
Remarks: Other: uncertain
Other: major host/prey

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita citrina is ectomycorrhizal with live root of Betula
Remarks: Other: uncertain
Other: major host/prey

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita citrina is ectomycorrhizal with live root of Quercus
Remarks: Other: uncertain
Other: major host/prey

Foodplant / mycorrhiza / ectomycorrhiza
fruitbody of Amanita citrina is ectomycorrhizal with live root of Pinopsida
Remarks: Other: uncertain
Other: minor host/prey

Fungus / parasite
sporangium of Syzygites megalocarpus parasitises fruitbody of Amanita citrina

Mushrooms that are mycorrhizal are involved in a symbiotic (mutually beneficial) relationship with the tiny rootlets of plants--usually trees. The cells of the mushroom's mycelium surround the tree rootlets with a sheath, and the mushroom helps the tree absorb water and nutrients while the tree provides sugars and amino acids to the mushroom. The organisms may need each other to survive. It is estimated that about 85% of plants depend on mycorrhizal relationships with fungi (Kirk et al., 2001; Dictionary of the Fungi). Many mushrooms are mycorrhizal with plants, including most Amanitas and Russulas.

Ectomycorrhizal fungi are likely to cycle both carbon and nitrogen through an ecosystem.

A mycorrhiza (Greek for fungus roots; typically seen in the plural forms mycorrhizae or mycorrhizas) is a symbiotic (occasionally weakly pathogenic) association between a fungus and the roots of a plant (Kirk et al. 2001). In a mycorrhizal association the fungus may colonize the roots of a host plant either intracellularly or extracellularly.

This mutualistic association provides the fungus with relatively constant and direct access to mono- or dimeric carbohydrates, such as glucose and sucrose produced by the plant in photosynthesis (Harrison 2005). The carbohydrates are translocated from their source location (usually leaves) to the root tissues and then to the fungal partners. In return, the plant gains the use of the mycelium's very large surface area to absorb water and mineral nutrients from the soil, thus improving the mineral absorption capabilities of the plant roots (Selosse et al. 2006). Plant roots alone may be incapable of taking up phosphate ions that are immobilized, for example, in soils with an basic pH. The mycelium of the mycorrhizal fungus can however access these phosphorus sources, and make them available to the plants they colonize (Li et al. 2006). The mechanisms of increased absorption are both physical and chemical. Mycorrhizal mycelia are much smaller in diameter than the smallest root, and can explore a greater volume of soil, providing a larger surface area for absorption. Also, the cell membrane chemistry of fungi is different from that of plants. Mycorrhizae are especially beneficial for the plant partner in nutrient-poor soils.

Mycorrhizal plants are often more resistant to diseases, such as those caused by microbial soil-borne pathogens, and are also more resistant to the effects of drought. These effects are perhaps due to the improved water and mineral uptake in mycorrhizal plants.

Mycorrhizae form a mutualistic relationship with the roots of most plant species (although only a small proportion of all species have been examined, 95% of all plant families are predominantly mycorrhizal) (Trappe 1987).

Plants grown in sterile soils and growth media often perform poorly without the addition of spores or hyphae of mycorrhizal fungi to colonise the plant roots and aid in the uptake of soil mineral nutrients. The absence of mycorrhizal fungi can also slow plant growth in early succession or on degraded landscapes (Jeffries et al. 2003).

References

• Harrison MJ (2005). Signaling in the arbuscular mycorrhizal symbiosis. Annu Rev Microbiol. 59: 19-42.
• Jeffries, P; Gianinazzi, S; Perotto, S; Turnau, K; Barea, J-M (2003). "The contribution of arbuscular mycorrhizal fungi in sustainable maintenance of plant health and soil fertility". Biol. Fertility Soils 37: 1-16.
• Kirk, P.M., P.F. Cannon, J.C. David & J. Stalpers 2001. Ainsworth and Bisby’s Dictionary of the Fungi. 9th ed. CAB International, Wallingford, UK.
• Li H, Smith SE, Holloway RE, Zhu Y, Smith FA. (2006). Arbuscular mycorrhizal fungi contribute to phosphorus uptake by wheat grown in a phosphorus-fixing soil even in the absence of positive growth responses. New Phytol. 172: 536-543.
• Selosse MA, Richard F, He X, Simard SW (2006). Mycorrhizal networks: des liaisons dangereuses?. Trends Ecol Evol. 21: 621-628.
• Trappe, J. M. 1987. Phylogenetic and ecologic aspects of mycotrophy in the angiosperms from an evolutionary standpoint. Ecophysiology of VA Mycorrhizal Plants, G.R. Safir (EDS), CRC Press, Florida

Fungi are not able to ingest their food like animals do, nor can they manufacture their own food the way plants do. Instead, fungi feed by absorption of nutrients from the environment around them. They accomplish this by growing through and within the substrate on which they are feeding. Numerous hyphae network through the wood, cheese, soil, or flesh from which they are growing. The hyphae secrete digestive enzymes which break down the substrate, making it easier for the fungus to absorb the nutrients which the substrate contains.

This filamentous growth means that the fungus is in intimate contact with its surroundings; it has a very large surface area compared to its volume. While this makes diffusion of nutrients into the hyphae easier, it also makes the fungus susceptible to dessication and ion imbalance. But usually this is not a problem, since the fungus is growing within a moist substrate.

Most fungi are saprophytes, feeding on dead or decaying material. This helps to remove leaf litter and other debris that would otherwise accumulate on the ground. Nutrients absorbed by the fungus then become available for other organisms which may eat fungi. A very few fungi actively capture prey, such as Arthrobotrys which snares nematodes on which it feeds. Many fungi are parastitic, feeding on living organisms without killing them. Ergot, corn smut, Dutch elm disease, and ringworm are all diseases caused by parasitic fungi.

Fungi and plants are sessile (immobile). Unlike animals, they cannot walk or fly to new habitats. Their immobility generally leaves only two ways for fungi and plants to extend their range: they can grow into an adjoining area, or disperse spores or seeds. Most fungal spores are single cells. They can travel beyond the physical limits of their parent into more distant territory. 

An organism's physical growth for a single season usually limits yearly dispersal by growth to short distances. The maximum outward growth rate of fairy rings in the soil is only 8 inches (20 cm) per year. In plants, outward growth is also slow. Aspen clones, for example, are created by the roots of the parent trees sending up new stems on the edge of the clone. This type of growth results in a dome-shaped cluster of trees because the older trees in the center are taller. Fairy rings and aspen clones can become enormous, but it takes hundreds to many thousands of years. An aspen clone in Utah covers 17.2 acres (43 hectares) and is estimated to be one million years old.

Many plant seeds depend upon wind to increase the range of dispersal. Some seeds are modified to increase the chances of long range dispersal. If the seeds are heavy, or the wind light, the seeds will land close to the parent. Seeds with "wings" (maples) or "parachutes" (milkweed) will stay aloft longer and be dispersed farther from the parent.

The spores of fungi are smaller and lighter than all plant seeds, but fungi encounter more barriers than plants do in achieving successful dispersal. A major problem is that many fungi do not grow tall enough to clear the "boundary layer" of still air next to the ground. Most plants grow through the boundary layer. Fungi have adapted to the problem posed by the boundary layer by either shooting their spores through it, or evading it entirely by utilizing vectors (animals or water or wind) for dispersal. Once spores are caught by the wind they can be carried very long distances. Spores of a wheat rust have been reported to have been dispersed 1,243 miles (2000 km) by the wind.

Spore dispersal is a two-step process. The first step is spore discharge or release. The second step is dispersal away from the parent. Fungi have evolved a number of different mechanisms for spore discharge and dispersal.

Solutions for dispersal can be grouped into passive and active mechanisms.

Although very little is known about life history strategies in fungi, all filamentous fungi (including Amanita phalloides) grow as a combination of hyphae and spores. The spores of Amanita phalloides are sexual. Other species may make both sexual and asexual spores.

There are no known fossils of Amanita phalloides. In fact very little is known about the paleobiology of mushrooms.

Amanita phalloides (Vaill. ex Fr.) Link, Handbuck zur Erkennung der Nutzbarsten und am Häufigsten Vorkommenden Gewächse 3: 272 (1833)

Sanctioning author:
Fr.

Basionym:
Agaricus phalloides Vaill. ex Fr. 1821

Citations in published lists:
Saccardo's Syll. fung. V: 9; XII: 906; XIX: 54; XXIII: 5. Page Image in Published List

Position in classification:
Pluteaceae, Agaricales, Agaricomycetidae, Agaricomycetes, Basidiomycota, Fungi

Synonymy:
Agaricus phalloides Vaill. ex Fr., Syst. mycol. (Lundae) 1: 13 (1821)
Amanita viridis Pers., Tent. disp. meth. Fung.: 67 (1797)
Amanitina phalloides (Vaill. ex Fr.) E.-J. Gilbert, Iconographia Mycologica 27(Suppl. 1): 78 (1941)
Fungus phalloides Vaill., Parerga lichenol. (Breslau): tab. 14, fig. 5 (1859)

Synonymy Contributor(s):
Kew Mycology (2005); IMI

Index Fungorum LSID: urn:lsid:indexfungorum.org:names:178962

Index Fungorum Record Details

An emerging consensus of fungal classification can be found on the Tree of Life pages.

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 (Litten 1975). Of the amatoxins, α-amanitin is the chief component and along with β-amanitin is likely responsible for the toxic effects (Köppel 1993; Dart 2004). 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 (Karlson-Stiber & Persson 2003). 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 (Benjamin 1995). The RNA polymerase of Amanita phalloides is insensitive to the effects of amatoxins; as such, the mushroom does not poison itself (Horgen et al. 1978).

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 (Wieland & Govindan 1974), they have since been found to have little input into the death cap's toxicity as they are not absorbed through the gut (Karlson-Stiber & Persson 2003). Furthermore, phalloidin is also found in the edible (and sought-after) Blusher (Amanita rubescens) (Litten 1975). Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides (Vetter 1998). Like the phallotoxins they do not exert any acute toxicity after ingestion in humans(Karlson-Stiber & Persson 2003).

References

• Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.
• Dart, RC (2004). "Mushrooms", Medical toxicology. Philadelphia: Williams & Wilkins, 1719–35.
• Horgen, Paul A.; Allan C. Vaisius and Joseph F. Ammirati (1978). "The insensitivity of mushroom nuclear RNA polymerase activity to inhibition by amatoxins". Archives of Microbiology 118 (3): 317–9.
• Karlson-Stiber C, Persson H (2003). "Cytotoxic fungi - an overview". Toxicon 42 (4): 339-49.
• Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40.
• Litten, W. (March 1975). "The most poisonous mushrooms". Scientific American 232 (3): 90–101.
• Vetter, János (January 1998). "Toxins of Amanita phalloides". Toxicon 36 (1): 13–24.
• Wieland T, Govindan VM (1974). "Phallotoxins bind to actins". FEBS Lett. 46 (1): 351-3.

The ITS molecular marker is minimally variable within the species. Molecular data can be found in GenBank; as of 12/17/07, there were 34 matches to Amanita phalloides in the database.

The Amanita Genome Project focuses on a closely related species.

Amanita phalloides is not a threatened species, but has been introduced from Europe to other parts of the world and may pose a threat to native fungal or plant species.

The status of this widespread species is variable in Europe (2).

This species is not threatened.

There is no research on the management of Amanita phalloides in areas where it has been introduced.

Amanita phalloides cannot be cultured.

Conservation action has not been targeted at this species.

Several historical figures may have died from Amanita phalloides poisoning (or other similar, toxic Amanitas). These were either accidental poisonings or assassination plots. Alleged victims of this kind of poisoning include Roman Emperor Claudius, Pope Clement VII, Tsaritsa Natalia Naryshkina, and Holy Roman Emperor Charles VI.

R. Gordon Wasson recounted the details of these deaths, noting the likelihood of Amanita poisoning. In the case of Clement VII, the illness that led to his death lasted some five months, making the case clearly inconsistent with amatoxin poisoning. Natalia Naryshkina is said to have consumed a large quantity of pickled mushrooms prior to her death. However, it is unclear whether the mushrooms themselves were poisonous or whether she succumbed to food poisoning.

Charles VI experienced indigestion after eating a dish of sautéed mushrooms. This led to an illness from which he died ten days later — symptomology consistent with amatoxin poisoning. Charles' death led to the War of Austrian Succession. Noted Voltaire, "this dish of mushrooms changed the destiny of Europe."

The case of the Claudius poisoning is more complex. It is known that Claudius was 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. However, ancient authors such as Tacitus and Suetonius are unanimous about there having been poison added to the mushroom dish, rather than the dish having been prepared from poisonous mushrooms. Wasson speculates that the poison used to kill Claudius was derived from death caps, with a fatal dose of colocynth being administered later during his illness.

References

• Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.
• Wasson, Robert Gordon (1972). "The death of Claudius, or mushrooms for murderers". Botanical Museum Leaflets, Harvard University 23 (3): 101–128.

The milk thistle Silybum marianum is used to treat Amanita phalloides poisonings.

Reference

• http://www.etnobotanica.us/

Although Amanita phalloides may have killed both a Roman Emperor and the Holy Roman Emperor Charles VI (Benjamin 1995), the species has not been widely researched by ethnobotanists. However, it does feature prominently in popular culture.

Mushroom poisoning is caused by the consumption of raw or cooked fruiting bodies (mushrooms, toadstools) of a number of species of higher fungi. The term toadstool (from the German Todesstuhl, death's stool) is commonly given to poisonous mushrooms, but for individuals who are not experts in mushroom identification there are generally no easily recognizable differences between poisonous and nonpoisonous species. Old wives' tales notwithstanding, there is no general rule of thumb for distinguishing edible mushrooms and poisonous toadstools. The toxins involved in mushroom poisoning are produced naturally by the fungi themselves, and each individual specimen of a toxic species should be considered equally poisonous. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing. Thus, the only way to avoid poisoning is to avoid consumption of the toxic species. Poisonings in the United States occur most commonly when hunters of wild mushrooms (especially novices) misidentify and consume a toxic species, when recent immigrants collect and consume a poisonous American species that closely resembles an edible wild mushroom from their native land, or when mushrooms that contain psychoactive compounds are intentionally consumed by persons who desire these effects.

Nature of Disease

Mushroom poisonings are generally acute and are manifested by a variety of symptoms and prognoses, depending on the amount and species consumed. Because the chemistry of many of the mushroom toxins (especially the less deadly ones) is still unknown and positive identification of the mushrooms is often difficult or impossible, mushroom poisonings are generally categorized by their physiological effects. There are four categories of mushroom toxins: protoplasmic poisons (poisons that result in generalized destruction of cells, followed by organ failure); neurotoxins (compounds that cause neurological symptoms such as profuse sweating, coma, convulsions, hallucinations, excitement, depression, spastic colon); gastrointestinal irritants (compounds that produce rapid, transient nausea, vomiting, abdominal cramping, and diarrhea); and disulfiram-like toxins. Mushrooms in this last category are generally nontoxic and produce no symptoms unless alcohol is consumed within 72 hours after eating them, in which case a short-lived acute toxic syndrome is produced.

Diagnosis of Human Illness

A clinical testing procedure is currently available only for the most serious types of mushroom toxins, the amanitins. The commercially available method uses a 3H-radioimmunoassay (RIA) test kit and can detect sub-nanogram levels of toxin in urine and plasma. Unfortunately, it requires a 2-hour incubation period, and this is an excruciating delay in a type of poisoning which the clinician generally does not see until a day or two has passed. A 125I-based kit which overcomes this problem has recently been reported, but has not yet reached the clinic. A sensitive and rapid HPLC technique has been reported in the literature even more recently, but it has not yet seen clinical application. Since most clinical laboratories in this country do not use even the older RIA technique, diagnosis is based entirely on symptomology and recent dietary history. Despite the fact that cases of mushroom poisoning may be broken down into a relatively small number of categories based on symptomatology, positive botanical identification of the mushroom species consumed remains the only means of unequivocally determining the particular type of intoxication involved, and it is still vitally important to obtain such accurate identification as quickly as possible. Cases involving ingestion of more than one toxic species in which one set of symptoms masks or mimics another set are among many reasons for needing this information. Unfortunately, a number of factors (not discussed here) often make identification of the causative mushroom impossible. In such cases, diagnosis must be based on symptoms alone. In order to rule out other types of food poisoning and to conclude that the mushrooms eaten were the cause of the poisoning, it must be established that everyone who ate the suspect mushrooms became ill and that no one who did not eat the mushrooms became ill. Wild mushrooms eaten raw, cooked, or processed should always be regarded as prime suspects. After ruling out other sources of food poisoning and positively implicating mushrooms as the cause of the illness, diagnosis may proceed in two steps. The first step, outlined in Table 1, provides an early indication of the seriousness of the disease and its prognosis.

As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged.

Associated Foods

Mushroom poisonings are almost always caused by ingestion of wild mushrooms that have been collected by nonspecialists (although specialists have also been poisoned). Most cases occur when toxic species are confused with edible species, and a useful question to ask of the victims or their mushroom-picking benefactors is the identity of the mushroom they thought they were picking. In the absence of a well- preserved specimen, the answer to this question could narrow the possible suspects considerably. Intoxication has also occurred when reliance was placed on some folk method of distinguishing poisonous and safe species. Outbreaks have occurred after ingestion of fresh, raw mushrooms, stir-fried mushrooms, home-canned mushrooms, mushrooms cooked in tomato sauce (which rendered the sauce itself toxic, even when no mushrooms were consumed), and mushrooms that were blanched and frozen at home. Cases of poisoning by home-canned and frozen mushrooms are especially insidious because a single outbreak may easily become a multiple outbreak when the preserved toadstools are carried to another location and consumed at another time.

Specific cases of mistaken mushroom identity appears frequently. The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra. Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta. The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3. Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus, Lactarius, Russula, Tricholoma, Coprinus, Pluteus, and others. The Inky Cap Mushroom (Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned. Some other members of the genus Coprinus (Shaggy Mane, C. comatus; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided.

Most of the psychotropic mushrooms (Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom (Psilocybe cubensis) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible. Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom (Marasmius oreades) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom (Gymnopilus spectabilis), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A. pantherina varieties are the Yellow Blusher (Amanita flavorubens). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom (Armillariella mellea). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs.

Relative Frequency of Disease

Accurate figures on the relative frequency of mushroom poisonings are difficult to obtain. For the 5-year period between 1976 and 1981, 16 outbreaks involving 44 cases were reported to the Centers for Disease Control in Atlanta (Rattanvilay et al. MMWR 31(21): 287-288, 1982). The number of unreported cases is, of course, unknown. Cases are sporadic and large outbreaks are rare. Poisonings tend to be grouped in the spring and fall when most mushroom species are at the height of their fruiting stage. While the actual incidence appears to be very low, the potential exists for grave problems. Poisonous mushrooms are not limited in distribution as are other poisonous organisms (such as dinoflagellates). Intoxications may occur at any time and place, with dangerous species occurring in habitats ranging from urban lawns to deep woods. As Americans become more adventurous in their mushroom collection and consumption, poisonings are likely to increase.

Course of Disease and Complications

The normal course of the disease varies with the dose and the mushroom species eaten. Each poisonous species contains one or more toxic compounds which are unique to few other species. Therefore, cases of mushroom poisonings generally do not resembles each other unless they are caused by the same or very closely related mushroom species. Almost all mushroom poisonings may be grouped in one of the categories outlined above.

PROTOPLASMIC POISON

Amatoxins

Several mushroom species, including the Death Cap or Destroying Angel (Amanita phalloides, A. virosa), the Fool's Mushroom (A. verna) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins. Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver. Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney.

Target Populations

All humans are susceptible to mushroom toxins. The poisonous species are ubiquitous, and geographical restrictions on types of poisoning that may occur in one location do not exist (except for some of the hallucinogenic LBMs, which occur primarily in the American southwest and southeast). Individual specimens of poisonous mushrooms are also characterized by individual variations in toxin content based on genetics, geographic location, and growing conditions. Intoxications may thus be more or less serious, depending not on the number of mushrooms consumed, but on the dose of toxin delivered. In addition, although most cases of poisoning by higher plants occur in children, toxic mushrooms are consumed most often by adults. Occasional accidental mushroom poisonings of children and pets have been reported, but adults are more likely to actively search for and consume wild mushrooms for culinary purposes. Children are more seriously affected by the normally nonlethal toxins than are adults and are more likely to suffer very serious consequences from ingestion of relatively smaller doses. Adults who consume mushrooms are also more likely to recall what was eaten and when, and are able to describe their symptoms more accurately than are children. Very old, very young, and debilitated persons of both sexes are more likely to become seriously ill from all types of mushroom poisoning, even those types which are generally considered to be mild.

Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected.

Food Analysis

The mushroom toxins can with difficulty be recovered from poisonous fungi, cooking water, stomach contents, serum, and urine. Procedures for extraction and quantitation are generally elaborate and time-consuming, and the patient will in most cases have recovered by the time an analysis is made on the basis of toxin chemistry. The exact chemical natures of most of the toxins that produce milder symptoms are unknown. Chromatographic techniques (TLC, GLC, HPLC) exist for the amanitins, orellanine, muscimol/ibotenic acid, psilocybin, muscarine, and the gyromitrins. The amanitins may also be determined by commercially available 3H-RIA kits. The most reliable means of diagnosing a mushroom poisoning remains botanical identification of the fungus that was eaten. An accurate pre-ingestion determination of species will also prevent accidental poisoning in 100% of cases. Accurate post-ingestion analyses for specific toxins when no botanical identification is possible may be essential only in cases of suspected poisoning by the deadly Amanitas, since prompt and aggressive therapy (including lavage, activated charcoal, and plasmapheresis) can greatly reduce the mortality rate.

Selected Outbreaks

Isolated cases of mushroom poisoning have occurred throughout the continental United States.

The popular interest in gathering and eating uncultivated mushrooms has been associated with an increase in incidents of serious mushroom-related poisonings. From December 28, 1996, through January 6, 1997, nine persons in northern California required hospitalization after eating Amanita phalloides (i.e., "death cap") mushrooms; two of these persons died. Risks associated with eating these mushrooms result from a potent hepatotoxin. This report describes four cases of A. phalloides poisoning in patients admitted to a regional referral hospital in northern California during January 1997 and underscores that wild mushrooms should not be eaten unless identified as nonpoisonous by a mushroom expert.

Another one occurred in Oregon in October,1988, and involved the intoxication of five people who consumed stir-fried Amanita phalloides. The poisonings were severe, and at this writing three of the five people had undergone liver transplants for treatment of amanitin-induced liver failure.

Other cases have included the July, 1986, poisoning of a family in Philadelphia, by Chlorophyllum molybdites; the September, 1987, intoxication of seven men in Bucks County, PA, by spaghetti sauce which contained Jack O'Lantern mushroom (Omphalotus illudens); and of 14 teenage campers in Maryland by the same species (July, 1987). A report of a North Carolina outbreak of poisoning by False Morel (Gyromitra spp.) appeared in 1986. A 1985 report details a case of Chlorophyllum molybdites which occurred in Arkansas; a fatal poisoning case caused by an amanitin containing Lepiota was described in 1986.

In 1981, two Berks County, PA, people were poisoned (one fatally) after ingesting Amanita phalloides, while in the same year, seven Laotian refugees living in California were poisoned by Russula spp.

In separate 1981 incidents, several people from New York State were poisoned by Omphalotus illudens, Amanita muscaria, Entoloma lividum, and Amanita virosa.

An outbreak of gastroenterititis during a banquet for 482 people in Vancouver, British Columbia, was reported by the Vancouver Health Department in June, 1991. Seventy-seven of the guests reported symptoms consisting of early onset nausea (15-30 min), diarrhea (20 min-13 h), vomiting (20-60 min), cramps and bloated feeling. Other symptoms included feeling warm, clamminess, numbness of the tongue and extreme thirst along with two cases of hive-like rash with onset of 3-7 days. Bacteriological tests were negative. This intoxication merits special attention because it involved consumption of species normally considered not only edible but choice. The fungi involved were the morels Morchella esculenta and M. elata (M. angusticeps), which were prepared in a marinade and consumed raw. The symptoms were severe but not life threatening. Scattered reports of intoxications by these species and M. conica have appeared in anecodotal reports for many years.

Numerous other cases exist; however, the cases that appear in the literature tend to be the serious poisonings such as those causing more severe gastrointestinal symptoms, psychotropic reactions, and severe organ damage (deadly Amanita). Mild intoxications are probably grossly underreported, because of the lack of severity of symptoms and the unlikeliness of a hospital admission.

Deadly poisonous! A. phalloides contains both phallotoxins and amanitins. It is the amanitins that are responsible for the poisonings in humans. Amanitins are cyclic octapeptides that stop protein synthesis in the cells they encounter. All human organs are effected, but damage to the liver is most severe and liver failure is primarily responsible for the death of A. phalloides victims. Symptoms usually appear 8-12 hours after ingestion. Death occurs in 7-10 days in 10-15% of patients.

• Farlow Library and Herbarium of Cryptogamic Botany exhibit on Amanita phalloides
• MushroomExpert.com
• Tree of Life web project
• New Zealand Fungi: Amanita phalloides Taxanomic Details
• Virtual Mycota: NZ Fundal Identification
• Fungal Guide
  
• Wikipedia: Amanita phalloides page
• Wikipedia: WikiProject Fungi
• The WWW Virtual Library: Mycology

Mushroom Toxins and Toxicity

• Health A to Z: Mushroom Poisoning
• Patient Plus: Mushrooms and Toadstool Toxicology
• Mushroom Poisoning Case Registry: North American Mycological Association
• FDA: Mushroom Toxins

• Fungal Tree of Life
• 'Barcodes' for other species in the genus Amanita

• Rodham E. Tulloss
• Heather E. Hallen
• Anne Pringle