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Common Name: Destroying Angel, Death angel,  - The common names are  mixed metaphors for a pallid, angelic beauty whose virulent toxins are usually characterized as 'deadly poisonous' in field guides.


Scientific Name: Amanita bisporigera - The generic name is taken directly from the Greek word amanitai, which may refer to Mount Amanus in northern Syria; the use of  Amanita is attributed to Claudius Galenus (better known as Galen), the noted Greek physician, who, according to Charles McIlvane in 1,000 American Fungi, used the term to describe 'esculent fungi.' The specific name indicates that it  has only  two spores on each of its basidia in contrast to the standard four spores of the basidiomycete. Virtually indistinguishable from Amanita virosa and Amanita verna.


The Destroying Angel is one of few fungi that is more universally known by its common name rather than its scientific name. Three distinct characteristic features define the archetype. First and foremost is the volva, a cuplike structure at the base of  and surrounding the stalk or stipe; the volva is frequently hypogeal and can then only be detected by removing the soil to allow inspection. The volva is the bottom part of the universal veil, which is an ovate membrane that envelops the mushroom during the subterranean growth phase. With the epigeal extension of the stipe to expose the cap and gills of the  fruiting body for spore dispersal, the universal veil tears around its circumference. The volva is the lower part of the "egg-shell" that remains attached to the bottom of the stipe.  The second most important feature is the absolute whiteness of the pileus or cap, the stipe and the gills. The whiteness is described by Bill Russell in his Field Guide to Wild Mushrooms of Pennsylvania and the Mid-Atlantic as having a "strange luminous aura that draws the eye" that is "easily visible from one hundred feet away with its serene, sinister, angelic radiance." The last  feature is less prominent but serves to confirm the identification through a more detailed,  closer examination. The cap is completely smooth, usually described as 'glabrous' and 'viscid when wet' in field guides. This is to distinguish it from most of the other species in the Amanita genus that have warty patches of the universal veil on the cap.


The species that fit the Destroying Angel description are A. bisporigera, A. virosa and A. verna in eastern North America and A. ocreata in western North America.  The three eastern variants are distinguished according to  the nature of their spores, their reaction  to potassium hydroxide (KOH), and/or their subtle nuances in terms of  size and time of fruiting. Most basidiomycete or gilled mushrooms produce four reproductive basidiospores on the their namesake structure, the basidium. While it is certainly true that only A. bisporigera differs from this is having only two basidiospores, Amanita expert Rod Tulloss has evinced that  there is a noted tendency for two-spored basidia to become four-spored over the course of a single growing season. So even if you could do a spore count, which requires high magnification equipment in a workbench environment, it would not necessarily be conclusive. In general,  A. bisporigera is somewhat smaller and A. verna is somewhat more slender than A. virosa and that both appear earlier in the season. It may be reasonably concluded that distinguishing the three eastern variants according to their physical and temporal appearance is not practical.


The confusion of the three eastern Destroying Angel species is due to a number of factors, of which the mischaracterization of A. verna is the most notable.  A. verna is sometimes called Spring Destroying Angel because it is purported to fruit earlier in the year. The species name verna is from the Latin vernus, meaning 'belonging to the spring' to reflect this association. It is also known as Fool's Mushroom, perhaps because spring is noted for lighthearted vernal foolery; however, it is more likely that the association is another way of characterizing the deceptive appearance that fools the unwitting mycophagist into eating a deadly toadstool. A. verna was first described in France and is primarily a European species. It is not unlikely that an early French colonist found a similar mushroom in North America and came to the incorrect conclusion that it was A. verna.  The most conclusive species test is the application of  potassium hydroxide (KOH), as A. verna is different from the other two species in that it purportedly does not turn yellow. However, studies carried out in France by a number of different mycologists  found that all of the A. verna specimens collected stained yellow, just like A. virosa and A. bisporigera. It is probable that all of the North American Destroying Angel mushrooms variants are actually A. bisporigera. Those misidentified as A. verna are due to the original confusion with the European species. Those misidentified as A. virosa are  due to the observed transition of the two-spored A. bisporigera into a four-spored A. bisporigera and not a new species. The variation in yellow staining due to the KOH reaction is therefore likely a matter of variance in the chemicals in the mushroom that produce the color and not in a species difference.


The reason that it is important to know and recognize the taxonomy of the Destroying Angel is that it is one of the most deadly mushrooms known, or, as eloquently stated by Nicholas Money in Mr. Bloomfield's Garden "misused as a cooking ingredient, its alabaster flesh has wiped out whole families."  The toxic  chemicals  are called  amatoxins (from the generic name Amanita), which are small protein molecules  made up of eight amino acids in a ring called a cyclopeptide with a molecular weight of about 900. There are at least eight amatoxins identified; α-amanitin is the one with fatal result. The destructive mechanism involves RNA polymerase, which is necessary for the production of messenger RNA, the key to protein synthesis as it carries the code from the DNA. The ultimate result is a cessation of cell metabolism and cell death. As the process involves the inability of the cells to grow, it is the cells that have high turnover rates that are most affected by the poison: the gastrointestinal mucosa cells of the stomach; the hepatocytes of the liver; and the renal tubular cells of the kidneys. The liver is most at risk because the hepatocytes that absorb  α-amanitins are excreted with the bile and then reabsorbed.


The initial stages of poisoning can start anywhere from 6 to 24 (average 10) hours after ingestion and consist of the usual gastrointestinal distress symptoms of nausea, vomiting, diarrhea, stomach cramps with a severity indicated by hematuria (blood in the urine). This is likely the reaction of the gastrointestinal mucosa cells.  There follows a period 12 to 48 hours after the initial ingestion of apparent recovery, although liver and kidney disturbances can be clinically detected. This is probably after the stomach cells are recovering and before the onset of the slower hepatic and renal processes. The third and final stage occurs about 72 hours after ingestion and consists of a progressive series of  organ failures that begin with the liver and kidneys and end in convulsions, coma and death. The people who fall victim to amanitin poisoning are for the most part amateur mushroom gatherers who mistake the Destroying Angel (or its close relative A. phalloides, the Death Cap) for a known edible such as Agaricus campestris, the meadow mushroom. Not atypically, they are foreigners who mistake the delectable looking Amanitas for a native edible. Michael Beug, writing in Fungi Magazine (Summer 2008) reports that the North American Mycological Association (NAMA) received a total of 126 reports of Amanita poisoning over 30 years, or about 4 per year. Traditionally, about 30 percent of the victims have eventually died due to liver and/or kidney failure, but this number has improved recently to about 5 percent  due to a better understanding of the physiology of the amanitin and aggressive therapy. The basic tenet of the treatment is to reduce the concentration of the amatoxins in the blood serum as rapidly as possible. Gastric lavation is used if the ingestion was recent enough and is followed by a thorough purging using emetics to induce vomiting and cathartics to induce evacuation of the bowels.  Perhaps the most important therapy is the administration of  activated charcoal, as amatoxins have a high affinity for adsorption on its surface. Although there is no proven antidote for amanitin poisoning, intravenous injections of penicillin have been used with some apparent benefit. The most promising treatment is silibinin, an extract of the blessed milk thistle (Silybum marianum), which has recently been offered commercially by a German pharmaceutical company as Legalon´┐ŻSIL. Liver transplant was once considered the last resort for amatoxin poisoning, but it has fallen into disfavor due to its concomitant iatrogenic effects.

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