Eastern North American destroying angel

Appearance

The mushroom has a smooth white cap that can reach up to 10 cm across, and a stipe, up to 14 cm long by 1.8 cm thick, that has a delicate white skirt-like ring near the top. The bulbous stipe base is covered with a membranous sac-like volva. The white gills are free from attachment to the stalk and crowded closely together. As the species name suggests, ''A. bisporigera'' typically bears two spores on the basidia, although this characteristic is not as immutable as was once thought.

Naming

''Amanita bisporigera'' was described as a new species in 1906. It is classified in the section ''Phalloideae'' of the genus ''Amanita'' together with other amatoxin-containing species. Amatoxins are cyclic peptides which inhibit the enzyme RNA polymerase II and interfere with various cellular functions. The first symptoms of poisoning appear 6 to 24 hours after consumption, followed by a period of apparent improvement, then by symptoms of liver and kidney failure, and death after four days or more. ''Amanita bisporigera'' closely resembles a few other white amanitas, including the equally deadly ''A. virosa'' and ''A. verna''. These species, difficult to distinguish from ''A. bisporigera'' based on visible field characteristics, do not have two-spored basidia, and do not stain yellow when a dilute solution of potassium hydroxide is applied. The DNA of ''A. bisporigera'' has been partially sequenced, and the genes responsible for the production of amatoxins have been determined.

Distribution

The fruit bodies are found on the ground in mixed coniferous and deciduous forests of eastern North America south to Mexico, but are rare in western North America; the fungus has also been found in pine plantations in Colombia.

Habitat

Like most other ''Amanita'' species, ''A. bisporigera'' is thought to form mycorrhizal relationships with trees. This is a mutually beneficial relationship where the hyphae of the fungus grow around the roots of trees, enabling the fungus to receive moisture, protection and nutritive byproducts of the tree, and giving the tree greater access to soil nutrients. Fruit bodies of ''Amanita bisporigera'' are found on the ground growing either solitarily, scattered, or in groups in mixed coniferous and deciduous forests; they tend to appear during summer and early fall. The fruit bodies are commonly found near oak, but have been reported in birch-aspen areas in the west. It is most commonly found in eastern North America, and rare in western North America. It is widely distributed in Canada, and its range extends south to Mexico. The species has also been found in Colombia, where it may have been introduced from trees exported for use in pine plantations.

Defense

''Amanita bisporigera'' is considered the most toxic North American ''Amanita'' mushroom, with little variation in toxin content between different fruit bodies. Three subtypes of amatoxin have been described: α-, β, and γ-amanitin. The principal amatoxin, α-amanitin, is readily absorbed across the intestine, and 60% of the absorbed toxin is excreted into bile and undergoes enterohepatic circulation; the kidneys clear the remaining 40%. The toxin inhibits the enzyme RNA polymerase II, thereby interfering with DNA transcription, which suppresses RNA production and protein synthesis. This causes cellular necrosis, especially in cells which are initially exposed and have rapid rates of protein synthesis. This process results in severe acute liver dysfunction and, ultimately, liver failure. Amatoxins are not broken down by boiling, freezing, or drying. Roughly 0.2 to 0.4 milligrams of α-amanitin is present in 1 gram of ''A. bisporigera''; the lethal dose in humans is less than 0.1 mg/kg body weight. One mature fruit body can contain 10–12 mg of α-amanitin, enough for a lethal dose. The α-amanitin concentration in the spores is about 17% that of the fruit body tissues. ''A. bisporigera'' also contains the phallotoxin phallacidin, structurally related to the amatoxins but considered less poisonous because of poor absorption. Poisonings have also been reported in domestic animals, including dogs, cats, and cows.

The first reported poisonings resulting in death from the consumption of ''A. bisporigera'' were from near San Antonio, Mexico, in 1957, where a rancher, his wife, and three children consumed the fungus; only the man survived. ''Amanita'' poisoning is characterized by the following distinct stages: the ''incubation stage'' is an asymptomatic period which ranges from 6 to 12 hours after ingestion. In the ''gastrointestinal stage'', about 6 to 16 hours after ingestion, there is onset of abdominal pain, explosive vomiting, and diarrhea for up to 24 hours, which may lead to dehydration, severe electrolyte imbalances, and shock. These early symptoms may be related to other toxins such as phalloidin. In the cytotoxic stage, 24 to 48 hours after ingestion, clinical and biochemical signs of liver damage are observed, but the patient is typically free of gastrointestinal symptoms. The signs of liver dysfunction such as jaundice, hypoglycemia, acidosis, and hemorrhage appear. Later, there is an increase in the levels of prothrombin and blood levels of ammonia, and the signs of hepatic encephalopathy and/or kidney failure appear. The risk factors for mortality that have been reported are age younger than 10 years, short latency period between ingestion and onset of symptoms, severe coagulopathy , severe hyperbilirubinemia , and rising serum creatinine levels.