Amanita ocreata

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.

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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

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.