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Amanita ocreata, commonly known as the death angel, destroying angel, angel of death or more precisely western North American destroying angel, is a deadly basidiomycete fungus, one of many in the genus Amanita. The large fruiting bodies (the ) 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 Amanita velosa (springtime amanita), Amanita lanei or Volvopluteus gloiocephalus, while immature specimens may be difficult to distinguish from edible Agaricus mushrooms or puffballs.
The species occurs in the Pacific Northwest and California Floristic Provinces of North America, mycorrhiza with oak trees. Similar in toxicity to the death cap ( A. phalloides) and destroying angels of Europe ( Amanita virosa) and eastern North America ( A. bisporigera), it is a potentially deadly fungus responsible for several poisonings in California. Its principal toxic constituent, , damages the liver and , often fatally, and has no known antidote, though silybin and show promise. The initial symptoms are gastrointestinal and include 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.
The stipe ranges from in height and is about thick, bearing a thin white membranous ring until old age. The volva is thin, smooth and sac-like, although may be quite extensive and contain almost half the stipe. The spore print is white, and the to to , amyloid spores are 9–14 x 7–10 μm viewed under a microscope. There is typically no smell, though some fruiting bodies 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.Thiers HD. (1982). The Agaricales (Gilled Fungi) of California 1: Amanitaceae. Eureka, CA: Mad River Press. .
Amatoxins consist of at least eight compounds with a similar structure, that of eight amino-acid rings; of those found in A. ocreata, α-Amanitin is the most prevalent and along with β-Amanitin is likely to be responsible for the toxic effects. 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. 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 , are susceptible to the toxins.Benjamin, Mushrooms: poisons and panaceas, p. 217
The phallotoxins consist of at least seven compounds, all of which have seven similar peptide rings. Although they are highly toxic to liver cells, phallotoxins have since been found to have little input into the destroying angel's toxicity as they are not absorbed through the gut. Furthermore, one phallotoxin, phalloidin, is also found in the edible (and sought-after) blusher ( Amanita rubescens).
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. 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.
No definitive antidote for amatoxin poisoning is available, but some specific treatments such as intravenous Benzylpenicillin have been shown to improve survival. There is some evidence that intravenous silibinin, an extract from the Silybum marianum ( Silybum marianum), may be beneficial in reducing the effects of amatoxins, preventing their uptake by , thereby protecting undamaged hepatic tissue. 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. This is a complicated issue, however, as transplants themselves may have significant complications and mortality; patients require long-term immunosuppression to maintain the transplant. 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.Benjamin, Mushrooms: poisons and panaceas, pp. 231–232 However, a follow-up study has shown that most survivors recover completely without any sequelae if treated within 36 hours of the mushrooms ingestion.
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