![Amanita phalloides ( Death Cap ) [ Original photo copyright © Pam Catcheside ]](images/other_life/PMPT00011.jpg)
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Phylum: Basidiomycota
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Class: Basidiomycetes
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Order: Agaricales
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Family: Pluteaceae
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Genus: Amanita
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Species: phalloides
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Common Names: Death Cap , Green Death Cap
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Countries
Australia, New Zealand, United States of America
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Biology
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Habitat
Gregarious on ground under trees (mainly deciduous, sometimes coniferous), Fruiting in summer and early autumn.
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Description
PILEUS (cap) 4-15 cm diameter. Ovoid to hemispherical at first, then plane and uplifted with age. Disc at maturity sometimes slightly raised or depressed. Surface smooth to finely radially fibrillose, slightly viscid in wet weather, dry and shiny in dry weather. Colour variable: pale olive, olive-brown, olive green to yellowish-brown, occasionally white, typically with innate, darker streaks, occasionally with faint, white universal veil patch. Margin paler, entire, not striate.
LAMELLAE (gills) free, white, becoming cream, sometimes with greenish shades, close, unequal, moderately broad (6-12 mm wide).
STIPE (stem) 4-18 cm in height, 1-3 cm thick. Equal to tapering with an enlarged base (up to 4 cm in diameter). White, often with flattened small green to brownish scales, scales sometimes in faint bands near base. Solid when young, pithy to hollow with age.
VOLVA (basal sac) membranous, thin, white, sac-like, usually erect from the stipe, fragile, sometimes disintegrating, often partially buried in soil.
ANNULUS (ring) membranous, loose, cream to white, skirt-like, pendulous, superior, disintegrating easily. Upper surface striate, lower surface slightly pubescent.
FLESH soft, white, moderately thick at disc, unchanging on cutting or bruising, at times yellowish-brown below cap cuticle. Taste mild, nutty. Smell mild at first becoming nauseating, sickly sweet.
SPORE PRINT white.
MICROSCOPIC DETAILS
Spores 7-12 x 6-9 μm, subglobose to broadly ellipsoid, smooth, colourless, amyloid.
Basidia 50-62 x 12-15 μm, clavate, 4-spored, basal clamp connection absent.
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First Aid
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Description: First aid for poisoning by plants or mushrooms where no agreed first aid method is currently available.
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Details
In the absence of research or clinical data about first aid for poisoning caused by this species, no first aid method can currently be recommended. Seek Medical Advice without delay.
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Clinical Effects & Treatment
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Dangerousness
Deadly poisonous
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Toxin Classification
GROUP 1 Amatoxins, delayed, cellular destruction
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Toxins
The total toxin content is 7-9 mg/g dry weight, about one third of this contains amatoxins.
Amatoxins (cyclic octapeptides); alpha-amanitin, beta-amanitin mainly (90%), gamma amanitin (<10%.) Inhibitors of RNA polymerase II, causing cell death. Target organs:Mucous membranes in intestine, liver, kidneys.
Varying amounts of these amatoxins are present in the death cap
alpha-Amanitin
beta-Amanitin
gamma-Amanitin
epsilon-Amanitin
Amanin
Amanullin
Amanullinic acid
Proamanullin
Amatoxins are bicyclic octapeptides with an indole-(R)-sulphoxide bridge.
Amatoxins are colourless, crystalline substances, soluble only in polar solvents such as water and methanol. They remain stable on boiling and in the presence of enzymes.
Phallotoxins are bicyclic heptapeptides with an indole/thio-etherbridge. Phallotoxins do not cause poisoning when administered orally, but when introduced to the blood stream they are about one tenth as toxic as amatoxins.
Virotoxins are heptapeptides have a monocyclic structure, this includes 2-methylsulphonyltryptophan or 2-methylsulphoxytryptophan and dihydroxyproline. Virotoxins exhibit a comparable activity on actin.
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Clinical Effects Overview
Poisoning by consumption of Amatoxin containing mushrooms is associated with the highest level of potential morbidity and mortality for any group of mushroom poisons. Numerous deaths still occur every year as a result of eating this type of mushroom.
Levels of Amatoxin vary between species of mushrooms, so the quantity of mushrooms that need to be eaten to cause toxicity vary, but the underlying clinical effects are the same. For some species, consumption of just one mushroom can deliver a lethal dose.
Amatoxins are cyclopeptides that cause widespread cellular injury and death, but the principal organ affected in humans, responsible for major morbidity and mortality, is the liver. The Amatoxins cause fatty degeneration of the liver, with centrilobular necrosis. Amatoxins are rapidly absorbed through the gut, though may remain in gastric aspirate for several days, as a result of biliary excretion. They are rapidly excreted through the kidneys and have an elimination half life of around 22 hours.
These mushrooms can be mistaken for edible species and so a number may be consumed in a meal, with potentially all who ate the meal at risk. Thus simultaneous presentation of multiple cases is common.
The first effects are not seen immediately after eating the mushrooms, but are commonly delayed, with onset at around 10-14hrs post-meal of often severe gastrointestinal (GIT) symptoms. These can include nausea, vomiting, that may be severe and recurrent, diarrhoea, and significant GIT fluid loss. The severity of the GIT effects can cause significant illness in their own right and require urgent medical support, but the danger lies in the subsequent course of the illness.
As the GIT effects resolve, the patient or treating doctor may consider this a simple and resolving GIT poisoning, but during a brief period of apparent remission, the more insidious cellular toxin effects are occurring.
Within the next 1-2+ days the patient may develop generalised pains, jaundice, bleeding as coagulation factor production in the liver ceases, renal failure, then progressive effects of widespread organ failure, with convulsions, hepatic coma and death.
In less severe cases the liver damage may be recoverable, with only mild coagulopathy, but in cases with major poisoning, complete irreversible liver failure will make death inevitable, the only hope of survival being a full liver transplant, a treatment that may be unavailable or untenable in many cases.
A schema for progress of toxicity has been suggested by Faulstich and Zilker:
Day 1: Mushroom meal and symptom free interval (6-12 hours).
Day 2: Gastrointestinal phase with vomiting, abdominal pain, diarrhoea.
Day 3: Apparent symptomatic remission, but laboratory evidence of developing liver damage.
Day 4: Coagulopathy develops and gastrointestinal bleeding commences.
Day 5: Onset of hepatic encephalopathy, onset of hepatic coma.
Day 6: Renal failure
Day 7: Death
The same authors have suggested a clinical grading for Amatoxin poisoning:
Grade 1: Patients with typical GIT symptoms following ingestion of Amatoxin-containg mushrooms, but never develop liver or kidney dysfunction on laboratory testing.
Grade 2: Patients with typical GIT symptoms following ingestion of Amatoxin-containg mushrooms, plus a mild elevation in transaminases (< 500U/L), no clotting dysfunction, no renal damage.
Grade 3: Patients with typical GIT symptoms following ingestion of Amatoxin-containg mushrooms, plus severe liver damage (transaminase > 500 U/L; coagulopathy).
Subgroup 3a: Bilirubinaemia mild or absent.
Subgroup 3b: Bilirubinaemia shows continuous and steep rise.
Grade 4: Patients with typical GIT symptoms following ingestion of Amatoxin-containg mushrooms, plus severe liver damage, steep rise in transaminases, steep fall in clotting factors, steep rise in bilirubin, onset of kidney dysfunction.
Grade 1 and 2 patients should survive with symptomatic treatment, while Grade 3 and 4 patients are at major risk, with Grade 3b of special concern, and Grade 4 unlikely to survive, despite treatment.
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Primary Clinical Effect
Cytotoxicity, principally hepatotoxicity leading to fulminant liver failure and its sequelae.
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Treatment Overview
If the patient is seen early, before even the gastrointestinal phase of poisoning (in the first 4 hours post-meal) then decontamination by clearance of gut contents may be justified, but thereafter only activated charcoal is indicated (within 36 hours of the meal).
Elimination of the toxins has proved difficult. plasmapheresis and haemoperfusion have not demonstrated efficacy. A molecular absorbent recirculating system (MARS) has been proposed, with albumin dialysate and there is growing clinical experience suggesting its effectiveness.
Supportive care is appropriate. In the early gastrointestinal phase, where fluid loss may be significant, fluid and electrolyte replacement IV is appropriate.
In addition, in the later liver failure stage, IV glucose may be helpful, and if there is active bleeding, FFP and vitamin K.
For fulminant liver failure, only full liver transplant will be life saving in the view of most authors. However, increasing experience using MARS suggests this may be an alternative to transplant in at least some cases.
There are no full antidotes for Amatoxins, but Silibinin (20-40mg/kg/day in divided doses) and Pencillin G (300,000 to 1 million U/kg/day). (see section on antidotes for more detail)
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![Amanita phalloides ( Death Cap ) [ Original photo copyright © Pam Catcheside ]](images/other_life/PMP00011.jpg)
