Amanita phalloides (Fr.) Link in Willd. Death Cap, Amanite phalloide, Oronge ciquë vert, Grüner Knollenblätterpilz, Gyilkos galoca. Cap 6-15cm across, convex then flattened; variable in color but usually greenish or yellowish with an olivaceous disc and paler margin; also, paler and almost white caps do occur occasionally; smooth, slightly sticky when wet, with faint, radiating fibers often giving it a streaked appearance; occasionally white patches of volval remnants can be seen on cap. Gills free, close, broad; white. Stem 60-140 x 10-20mm, solid, sometimes becoming hollow, tapering slightly toward the top; white, sometimes flushed with cap color; smooth to slightly scaly; the ball-shaped basal bulb is encased in a large, white, lobed, saclike volva. Veil partial veil leaves skirt-like ring hanging near the top of the stem. Flesh firm, thicker on disc; white to pale yellowish green beneath cap cuticle. Odor sickly sweet becoming disagreeable. Spores broadly ellipsoid to subglobose, amyloid, 8-10.5 x 7-9µ. Deposit white. Habitat singly or in small groups on the ground in mixed coniferous and deciduous woods. Quite common in Europe, formerly rare in north America but seemingly spreading and becoming frequent, especially in northern California. Found in eastern North America, the Pacific Northwest, and California. Season August-November (November-January in California), Deadly poisonous. Comment This is the most deadly fungus known, and despite years of detailed research into the toxins it contains, no antidote exists against their effects on the human body. Poisoning by Amanita phalloides is characterized by a delay of between six and twenty-four hours from the time of ingestion to the onset of symptoms, during which time the cells of the liver and kidneys are attacked. However, if a gastroirritant has also been consumed-e.g., as the result of eating a mixed collection of mushrooms-gastric upset may occur without the characteristic delay, masking this vital diagnostic evidence. The next stage is one of prolonged and violent vomiting and diarrhea accompanied by severe abdominal pains, lasting for a day or more. Typically this is followed by an apparent recovery, when the victim may be released from the hospital or think his ordeal over. Yet within a few days death may result from kidney and liver failure. Although Amanita phalloides contains many poisonous compounds, it is believed that only the group known as amatoxins are responsible for human poisoning; the others (phallotoxins) are thought to be rendered harmless by being neutralized by other compounds or not being absorbed from the intestinal tract, by being present in very low concentrations, or by being so unstable as to be destroyed by cooking or digestive juices. The amatoxins, however, are fully active orally. The main constituent of this group is a-amanitin, which through its effect on nuclear RNA in liver cells causes the end of protein synthesis, leading to cell death. When filtered through the kidneys, it attacks the convoluted tubules and instead of entering the urine is reabsorbed into the bloodstream and recirculated, causing repeated liver and kidney damage. As with any hepatic disease, treatment relies on the monitoring of blood chemistries, urine output, and so on, and the maintenance of fluid and electrolyte balance. In cases of amatoxin poisoning, mortality is 50 to 90 percent, and any chance of survival depends on early recognition.
Amanita phalloides var. alba (Vitt.) Gilbert. differs from the type in being entirely white throughout; like Amanita phalloides, it is also deadly poisonous.