Destroying angel | |
---|---|
Scientific classification | |
Domain: | Eukaryota |
Kingdom: | Fungi |
Division: | Basidiomycota |
Class: | Agaricomycetes |
Order: | Agaricales |
Family: | Amanitaceae |
Genus: | Amanita |
Species: | A. virosa |
Binomial name | |
Amanita virosa Bertill. (1866) | |
Synonyms | |
Agaricus virosus Fr. (1838) (nom. illegit.) |
Amanita virosa | |
---|---|
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 is a species of fungus in the class Agaricomycetes. In the UK, it has the recommended English name of destroying angel [1] and is known internationally as the European destroying angel. [2] Basidiocarps (fruit bodies) are agaricoid (mushroom-shaped) and pure white with a ring on the stem and a sack-like volva at the base. The species is deadly poisonous. It occurs in Europe and northern Asia. [3] Amanita virosa was formerly reported from North America, but research has shown that similar-looking American species, including Amanita bisporigera and A. ocreata , are distinct.
Amanita virosa was first described in 1838 by Swedish mycologist Elias Magnus Fries as Agaricus virosus, but this name is illegitimate since it had already been used for an earlier and different species. Amanita virosa was legitimately published by French mycologist Louis-Adolphe Bertillon in 1866.
The specific epithet is derived from the Latin adjective virōsus meaning 'toxic' [4] [5] (compare virus).
Amanita virosa first appears as a white, egg-shaped object covered with a universal veil. As it expands, the mushroom-shaped fruit body breaks free, though ragged patches of veil may persist at the cap edges. The cap is initially conical with inturned edges, before becoming hemispherical and flattening with a diameter up to 12 cm (4+3⁄4 in). The cap often has a distinctive boss; it is able to be peeled and is white, though the centre may be ivory. The crowded, free gills are white, as is the stipe and volva. The thin stipe is up to 15 cm (5.9 in) tall, with a hanging, grooved ring. The spore print is white and the spores are subglobose and 7–10 μm long. They are amyloid, staining purple with Melzer's reagent. The flesh is white, with a smell reminiscent of radishes, and turns bright yellow with sodium hydroxide. [6]
In Europe, the spring-fruiting Amanita verna is a similar all-white species, as is the autumn-fruiting, white form of Amanita phalloides (deathcap). Both are equally poisonous. In their immature, button-mushroom stage, all these poisonous species could be mistaken for young, white-capped, edible mushrooms ( Agaricus species), highlighting the danger of picking immature fruit bodies for food.
Amanita virosa is found in woodland in late summer and autumn, especially in association with beech and chestnut, but also with pine, spruce, and fir. [2] As with most Amanita species, it forms a mutually beneficial, ectomycorrhizal relationship with the roots of these trees. Amanita virosa was originally described from Sweden and is known throughout Europe, with additional confirmed records from northern Asia (China). The name was formerly used for similar-looking agarics in North America, but research has shown that these American species, including the eastern Amanita bisporigera , the western A. ocreata , and the northern Amanita amerivirosa , are distinct. [2]
Amanita virosa is highly toxic, and has been responsible for severe mushroom poisonings. [7] Eating just one cap of A. virosa is enough to kill an adult human. [7] The symptoms of poisoning generally come several hours after consumption, a delay which may make treatment more difficult.
Fruit bodies contain both amatoxins and phallotoxins.
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. [8] Of the amatoxins, α-Amanitin is the chief component and along with β-Amanitin is probably responsible for the toxic effects. [9] [10] 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 cease and the cell dies. [11] 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. [7]
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. [11] Furthermore, phalloidin is also found in the edible Amanita rubescens . [8] 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. [11]
It is unclear why this fungus, which closely resembles edible species, has been implicated in fewer deaths than the death cap, though its comparative rarity may contribute to this. [14] Some authorities strongly advise against putting fruit bodies in the same basket with those collected for the table and to avoid handling them. [15] [16]
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. [17]
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. [17] [18] 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. [17]
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, [19] and trials with cephalosporins show promise. [7] [20] 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. [21] [22] [23] N-acetylcysteine has shown promise in combination with other therapies. [24] Animal studies indicate the amatoxins deplete hepatic glutathione; [25] N-acetylcysteine serves as a glutathione precursor and may therefore prevent reduced glutathione levels and subsequent liver damage. [26] 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. [17] Repeated doses of activated carbon may be helpful by absorbing any toxins that are returned to the gastrointestinal tract following enterohepatic circulation. [27] Other methods of enhancing the elimination of the toxins have been trialed; techniques such as hemodialysis, [28] hemoperfusion, [29] plasmapheresis, [30] and peritoneal dialysis [31] have occasionally yielded success but overall do not appear to improve outcome. [11]
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. [32] [33] [34] This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant. [17] 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. [35] [36] [37] 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. [7] However, a follow-up study has shown that most survivors recover completely without any sequelae if treated within 36 hours of mushroom ingestion. [38]
Amanita virosa extract has antibacterial efficacy against Pseudomonas aeruginosa and Staphylococcus aureus in vitro . [39] It also has shown inhibitory activity on thrombin. [40]
Amanita phalloides, commonly known as the death cap, is a deadly poisonous basidiomycete fungus and mushroom, one of many in the genus Amanita. Originating in Europe, but later introduced to other parts of the world since the late twentieth century, A. phalloides forms ectomycorrhizas with various broadleaved trees. In some cases, the death cap has been introduced to new regions with the cultivation of non-native species of oak, chestnut, and pine. The large fruiting bodies (mushrooms) appear in summer and autumn; the caps are generally greenish in colour with a white stipe and gills. The cap colour is variable, including white forms, and is thus not a reliable identifier.
The name destroying angel applies to several similar, closely related species of deadly all-white mushrooms in the genus Amanita. They are Amanita virosa in Europe and A. bisporigera and A. ocreata in eastern and western North America, respectively. Another European species of Amanita referred to as the destroying angel, Amanita verna—also referred to as the "Fool's mushroom"—was first described in France in 1780.
The genus Amanita contains about 600 species of agarics, including some of the most toxic known mushrooms found worldwide, as well as some well-regarded edible species. The genus is responsible for approximately 95% of fatalities resulting from mushroom poisoning, with the death cap accounting for about 50% on its own. The most potent toxin present in these mushrooms is α-Amanitin.
α-Amanitin (alpha-Amanitin) is a cyclic peptide of eight amino acids. It is possibly the most deadly of all the amatoxins, toxins found in several species of the mushroom genus Amanita, one being the death cap as well as the destroying angel, a complex of similar species, principally A. virosa and A. bisporigera. It is also found in the mushrooms Galerina marginata, Lepiota subincarnata and Conocybe filaris. The oral LD50 of amanitin is 100 μg/kg for rats.
Mushroom poisoning is poisoning resulting from the ingestion of mushrooms that contain toxic substances. Symptoms can vary from slight gastrointestinal discomfort to death in about 10 days. Mushroom toxins are secondary metabolites produced by the fungus.
Amatoxin is the collective name of a subgroup of at least nine related cyclic peptide toxins found in three genera of deadly poisonous mushrooms and one species of the genus Pholiotina. Amatoxins are very potent, as little as half a mushroom cap can cause severe liver injury if swallowed.
Amanita verna, commonly known as the fool's mushroom or the spring destroying angel, is a deadly poisonous basidiomycete fungus, one of many in the genus Amanita. Occurring in Europe in spring, A. verna associates with various deciduous and coniferous trees. The caps, stipes and gills are all white in colour.
Galerina marginata, known colloquially as funeral bell, deadly skullcap, autumn skullcap or deadly galerina, is a species of extremely poisonous mushroom-forming fungus in the family Hymenogastraceae of the order Agaricales. It contains the same deadly amatoxins found in the death cap. Ingestion in toxic amounts causes severe liver damage with vomiting, diarrhea, hypothermia, and eventual death if not treated rapidly. About ten poisonings have been attributed to the species now grouped as G. marginata over the last century.
Amanita ocreata, commonly known as the death angel, destroying angel, angel of death or more precisely western North American destroying angel, is a deadly poisonous basidiomycete fungus, one of many in the genus Amanita. The large fruiting bodies 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. A. ocreata resembles 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 Volvopluteus gloiocephalus, while immature specimens may be difficult to distinguish from edible Agaricus mushrooms or puffballs.
β-Amanitin (beta-Amanitin) is a cyclic peptide comprising eight amino acids. It is part of a group of toxins called amatoxins, which can be found in several mushrooms belonging to the genus Amanita. Some examples are the death cap and members of the destroying angel complex, which includes A. virosa and A. bisporigera. Due to the presence of α-Amanitin, β-Amanitin, γ-Amanitin and epsilon-Amanitin these mushrooms are highly lethal to human beings.
γ-Amanitin (gamma-Amanitin) is a cyclic peptide of eight amino acids. It is an amatoxin, a group of toxins isolated from and found in several members of the mushroom genus Amanita, one being the death cap as well as the destroying angel, a complex of similar species, principally A. virosa and A. bisporigera. The compound is highly toxic, inhibits RNA polymerase II, disrupts synthesis of mRNA, and can be fatal.
The phallotoxins consist of at least seven compounds, all of which are bicyclic heptapeptides, isolated from the death cap mushroom (Amanita phalloides). They differ from the closely related amatoxins by being one residue smaller, both in the final product and the precursor protein.
Phallolysin is a protein found the Amanita phalloides species of the Amanita genus of mushrooms, the species commonly known as the death cap mushroom. The protein is toxic and causes cytolysis in many cells found in animals and is noted for its hemolytic properties. It was one of the first toxins discovered in Amanita phalloides when the various toxins in the species where first being researched. The protein itself is observed to come in 3 variations, with observed differences in isoelectric point. Cytolysis can be best described as being the destruction of cells, likely due to exposure from an external source such as pathogens and toxins. Hemolysis then follows a similar destructive pathway, but instead focuses specifically on the destruction of red blood cells. Phallolysin is known to be thermolabile, meaning that it is destroyed at high temperatures, and acid labile, meaning that it is easily broken down in acidic environments.
Lepiota brunneoincarnata, the deadly dapperling, is a gilled mushroom of the genus Lepiota in the order Agaricales. Widely distributed in Europe and temperate regions of Asia as far east as China, it grows in grassy areas such as fields, parks and gardens, and is often mistaken for edible mushrooms. The mushroom has a brown scaled cap up to 4 cm wide with a pinkish brown stem and white gills. It is highly toxic, with several deaths having been recorded as it resembles the edible grey knight and fairy ring champignon.
Galerina sulciceps is a dangerously toxic species of fungus in the family Strophariaceae, of the order Agaricales. It is distributed in tropical Indonesia and India, but has reportedly been found fruiting in European greenhouses on occasion. More toxic than the deathcap, G. sulciceps has been shown to contain the toxins alpha- (α-), beta- (β-) and gamma- (γ-) amanitin; a series of poisonings in Indonesia in the 1930s resulted in 14 deaths from the consumption of this species. It has a typical "little brown mushroom" appearance, with few obvious external characteristics to help distinguish it from many other similar nondescript brown species. The fruit bodies of the fungus are tawny to ochre, deepening to reddish-brown at the base of the stem. The gills are well-separated, and there is no ring present on the stem.
Amanita bisporigera is a deadly poisonous species of fungus in the family Amanitaceae. It is commonly known as the eastern destroying angel amanita, the eastern North American destroying angel or just as the destroying angel, although the fungus shares this latter name with three other lethal white Amanita species, A. ocreata, A. verna and A. virosa. The mushroom has a smooth white cap that can reach up to 10 centimetres across and a stipe up to 14 cm tall with a white skirt-like ring near the top. The bulbous stipe base is covered with a membranous sac-like volva. The white gills are free from attachment to the stalk and crowded closely together. As the species name suggests, A. bisporigera typically bears two spores on the basidia, although this characteristic is not immutable. A. bisporigera closely resembles a few other white amanitas, including the equally deadly A. virosa and A. verna.
Amanita exitialis, also known as the Guangzhou destroying angel, is a mushroom of the large genus Amanita. It is distributed in eastern Asia, and probably also in India where it has been misidentified as A. verna. Deadly poisonous, it is a member of section Phalloideae and related to the death cap A. phalloides. The fruit bodies (mushrooms) are white, small to medium-sized with caps up to 7 cm (2.8 in) in diameter, a somewhat friable ring and a firm volva. Unlike most agaric mushrooms which typically have four-spored basidia, the basidia of A. exitialis are almost entirely two-spored. Eight people were fatally poisoned in China after consuming the mushroom in 2000, and another 20 have been fatally poisoned since that incident. Molecular analysis shows that the species has a close phylogenetic relationship with three other toxic white Amanitas: A. subjunquillea var. alba, A. virosa and A. bisporigera.
Amanita sphaerobulbosa, commonly known as the Asian abrupt-bulbed Lepidella, is a species of agaric fungus in the family Amanitaceae. First described by mycologist Tsuguo Hongo in 1969, it is found in Southern Asia.
Virotoxins are monocyclic peptides formed by at least five different compounds: alaviroidin, viroisin, deoxoviroisin, viroidin, and deoxoviroidin. The structure and biological activity of virotoxins are similar to that of phallotoxins, thus suggesting that virotoxins are biosynthetically derived from phallotoxins or share common precursor pathways. As with phallotoxins, virotoxins are not considered to have significant toxic effects after oral exposure. At the molecular level, like phallotoxins, they interact with actin, stabilizing the bonds between actin monomers and preventing microfilaments depolymerization. However, the ultraviolet-spectra of interaction between actin and virotoxins is different from that of actin-phallotoxins, suggesting a different molecular interaction. Virotoxins have a more flexible structure when compared with phallotoxins and the presence of two additional hydroxyl groups may provide different reactivity. The intraperitoneal LD50 of virotoxins in mice ranges from 1.0 to 5.1 mg/kg and their main toxicological feature is hemorrhagic hepatic necrosis caused by an interaction of the virotoxins with outer surface of the hepatocyte through unknown mechanisms. At this point, the role of virotoxins in human toxicity remains unclear, although due to its poor oral absorption, little clinical importance is given to this class of toxins.
Amanita hygroscopia, also known as the pink-gilled destroying angel is a deadly poisonous fungus, one of many in the genus Amanita.