Deathcap Amanita phalloides (Vaill. ex Fr.) Link (illustrated (a) 40% life size) Cap 4–12cm across, convex then flattened; variable in colour, but usually greenish or yellowish with an olivaceous flush, although paler, almost white caps do occur; smooth, with faint radiating fibres, often giving it a streaked appearance, slightly shiny when wet. Stem 50–130×10–18mm, thickening towards the large basal bulb; white, flushed with the cap colour and often faintly banded; sometimes becoming hollow, basal bulb encased in a large, white, saccate volva. Flesh white, with a faint yellowish flush below cap cuticle; smell sickly sweet, becoming noticeably stronger after collection. Gills free, crowded; white. Spores 8–10.5×7–8¼, broadly elliptical to subglobose, amyloid. Spore print white. Habitat in mixed deciduous woodlands, especially with oak; late summer to autumn. Common. Deadly poisonous. Note There is a white form, which differs from the type in being pure white throughout. Like A. phalloides, it is deadly poisonous. I have collected this form in western France.

This is the most deadly fungus in the British Isles, and despite years of detailed research into the toxins it contains, no antidote exists against their effects on the human body. Poisoning by Deathcap is characterized by a delay of 6 to 24 hours between ingestion and the onset of symptoms, during which time the cells of the liver and kidneys are attacked. However, if a gastroirritant has also been consumed, for example as the result of eating a mixed collection of mushrooms, the delay in gastric upset may not occur, and this vital diagnostic evidence will be masked. The next stage is one of prolonged and violent vomiting and diarrhoea 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 hospital or think their ordeal over, but death results from kidney and liver failure within a few days.

Although A. phalloides contains many poisonous compounds, it is believed that only those in the group known as amatoxins are responsible for human poisoning. The others, phallotoxins, are considered to be harmless because they are either neutralized by other compounds, present in very low concentrations, so unstable as to be destroyed by cooking or digestive juices, or not absorbed from the intestinal tract. The amatoxins, however, are fully active when ingested. The main constituent of this group is α-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 it is reabsorbed into the bloodstream and recirculated, causing repeated liver and kidney damage. As with any hepatic disease, treatment relies on the monitoring of factors such as blood chemistries and urine output, and the maintenance of fluid and electrolyte balance. Mortality in cases of amatoxin poisoning is still up to 90%, and any chance of survival depends on early recognition. The tropical fungus Galerina sulcipes has a higher α-amanitin content; it is cocasionally found in hothouses.