California FungiConocybe filaris

(Photo: Fred Stevens) Conocybe filaris (Fries) Khner Le Genera Galera, 139. 1935. Common Name: none Synonym: Pholiotina filaris (Fries) Singer Pileus Cap 1-2.5 cm broad, obtuse-conic to convex, expanding to nearly plane, sometimes with a slight umbo; margin decurved, plane to slightly upturned in age; surface glabrous to faintly wrinkled, striate when moist, otherwise obscurely so, butterscotch-brown to dull

tawny-brown, the margin paler, fading when dry (hygrophanous) to cream-buff; context thin, 1-1.5 mm thick, cream-buff to tan-buff, unchanging or darkening only slightly when exposed; odor and taste mild.

Lamellae Gills adnexed to notched, thin, close, moderately broad; at first cream-buff, becoming dingy light-brown, finally tinged dull rustybrown from spores; lamellae up to 3-seried; gill edges lighter than the faces, fimbriate when young (use hand lens). Stipe Stipe 1.5-5 cm long, 1-3 mm thick, more or less equal, straight to slightly flexuous, fragile, hollow at maturity, surface fibrillose-striate, above and below, occasionally lustrous, apex pruinose, with gill edges sometimes evident; surface colored like the young cap, becoming darker in age, except for a pallid apex; partial veil fibrillosemembranous, cream-buff, separating early from the cap margin, upper surface striate-grooved, sometimes drab rusty-brown from spores, loosely attached, forming a superior ring that may shrivel and disappear with age. Spores Spores 7.5-9.5 x 5-5.5 m, ellipsoid, moderately thick-walled, smooth, with an apical germ pore; spore print dull rusty-brown. Habitat Scattered, gregarious, to clustered on soil, often near woody debris; fruiting from late fall to mid-winter. Edibility Contains deadly amanitoxins.

Comments This uncommon little brown mushroom (LBM) is characterized by a tawny-brown, striate-margined cap which fades to buff-brown, minutely fringed gill edges, and a striate-grooved annulus. Though seemingly distinctive, it belongs to species complex, members of which are distinguished largely by microscopic characters. The above description is based on a small number of local collections. References Hausknecht, A. (2009). A monograph of the genera Conocybe Fayod & Pholiotina Fayod in Europe. Edizioni Candusso: Alassio, Italy. 968 p. Noordeloos, M.E., Kuyper, T.W. & Vellinga, E.C. (2005). Flora Agaricina

NeerlandicaCritical monographs on the families of agarics and boleti occurring in the Netherlands. Volume 6. Coprinaceae & Bolbitiaceae. Taylor & Francis: Boca Raton, FL. 227 p. Watling, R. (1982). British Fungus Flora: Agarics and Boleti. Vol 3. Bolbitiaceae: Agrocybe, Bolbitius, & Conocybe. Royal Botanic Garden: Edinburgh, Scotland. 139 p. Other Descriptions and Photos o Fred Stevens: Conocybe filaris (CP) o Boleslaw Kuznik -- Hunting for Mushrooms: Conocybe filaris (CP) o Mushroom Observer: Conocybe filaris (CP) o Arora (1986): p. 471 (D) o Ammirati et al.: p. 94 (D), fig. 23 (I), fig. 38 (CP) o Breitenbach & Krnzlin (vol. 4): sp. 401 (D, I, & CP) o Lincoff: p. 559 (D), plate 81 (CP) o Phillips: p. 185 (D & CP) o Smith & Weber: sp. 214 (D & CP) o Watling (1982): p. 92 (D), figs. 221 & 222 (I)

CONOCYBE (CONOCYBE)

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Conocybe mushrooms grow commonly in Nova Scotia in pastures or other open, grassy areas. They are often gathered by individuals mistaking them for Psilocybespecies. Like many fungi, they rapidly lose moisture and dry out, appearing like any other little brown mushroom. Conocybe filaris (Deadly Conocybe) is common in Nova Scotia and contains deadly amanitins (cyclopeptides) like those found in the Destroying Angel (Amanita spp.) and can be lethal if consumed. Although there are a few species of Conocybe that contain psychoactive compounds, most dont occur in Nova Scotia. The chances that local species can be mistaken for the deadly Conocybe, or may also be poisonous, are high. Refrain from eating any little brown mushrooms, the consequences from a mistaken identification can be unpleasant at best and deadly in the worst case scenario.

POISON LOCATION

All parts of Conocybe filaris, and probably other species, contain toxins. Poison concentration varies within mushrooms and among geographical locations where they are found. Cooking or processing toxic mushrooms will not destroy the toxins in most cases.

POISON TYPE Amanitins, a group of cyclic peptides, are among the most lethal organic compounds in the world. Tiny amounts have deadly results in humans, though squirrels and rabbits seem to be able to nibble these fungi without suffering amanitin poisoning (although few people have likely followed these animals for the 6-24 hours that it typically takes for the symptoms to develop).

TYPICAL POISONING SCENARIO Since most little brown mushrooms (LBMs) all look very similar this sort of poisoning usually occurs when inexperienced mushroom gatherers accidentally collect them as food, or inadvertently collect them along with those containing psychoactive compounds. Sadly, because the effects of cyclic peptides are delayed by their chemistry, the poisoning is often discovered too late to prevent major organ damage, or death, of the victim. It is not true that mushrooms nibbled by wildlife are safe for human consumption. There are only a very few choice, edible fungi native to Nova Scotia, so it is best to learn which are safe to eat from an expert and avoid eating all others. When collecting wild mushrooms, always retain an uncooked specimen for later study should you fall ill from eating your harvest. Your only chance in the event of poisoning is prompt, accurate identification of the fungus and its toxin, so that treatment and monitoring can be more effective.

SYMPTOMS Amanitin poisoning is not a pleasant experience. The onset of symptoms does not normally begin for about 10 hours, long enough for the victim to forget about a mushroom meal. When the toxin finally affects the victim, it causes severe abdominal upset, cramps, violent vomiting and diarrhea, followed by liver and kidney failure. Additionally, there is typically a short remission of symptoms 1-2 days after consumption, which complicates diagnosis and may give a false impression of recovery. Although treatment is possible if the correct diagnosis of amanitin poisoning is made early (1-2 hours after consumption), there is no known antidote; and the damage to liver, kidneys and other systems is severe enough to cause a painful death.

CONOCYBE POISON INFORMATION

Proteins and Amino Acids Proteins and amino acids are complex chemicals necessary to all living cells; most are highly beneficial, not harmful. Chains of amino acids form proteins; if more than two are joined, they are called peptides, rings of amino acids joined together make cyclopeptides like amanitins, some of which are the most deadly poisons known.

http://museum.gov.ns.ca/poison/?section=species&id=132

Amanitina
The compound -amanitina alpha-amanitina or is Peptide not eight cyclical Ribosomal of Amino acids probably one of Toxins of the groupmore lethal Amatoxinas, found in several species of the sort of hongo+s phalloides Amanitas in particular oronja green or Amanita and Amanita virosa . The compound also is in the fungi marginata Galerina and Conocybe filaris . lethal dose for 50% of the test individuals is approximately 0. The -amanitina is an inhibiter of ARN polymerase II, which causes that he is so lethal ponsoa in animal. Penicillin competes with the amanitinas in the system of cellular entrance of the membrane of the hepatocito, reason why is a cash Antidote against the effects of the envenenamiento by these toxics Amino acids

Structure
The chemical structure of the -amanitina is the one of little typical Polypeptide, due to the ramifications of the chain of amino acids. Two amino acids of Triptofano and one modified Cistena allow to the formation of a second internal cyclical bow, as it is observed in the image of his chemical structure. The most external bow is formed by the normal peptide connection between the ends carboxilo and amino terminals of the chain.

Besides the -amanitina, octapptidos structurally related, called exist other cyclical -amanitina and -amanitina, all resistant to the baking and hepatotoxic, cariolticos and highly hipoglucemiantes .

Clinical picture
The -amanitina has a strong and specific attraction, outside the usual thing, by Enzyme ARN polymerase II. When the compound interferes, one to the enzyme, being caused effective Citolisis of cells of the liver . Few effects in the first 10 hours have been reported only, in fact, it is not outside the common thing that the effects ofimportance do not even appear but until 24 hours after the ingestion of the compound. This delay in the appearance of the mortal symptoms causes that it is more difficult to diagnose the emponzoamiento. For whenthey appear the symptoms, the gastric washing has become useless. The first symptoms are Diarrhea and Clicos but these yields, giving a false impression of recovery. Generally, the quarter or fifth day, the toxins begin to haveeffect on the liver and kidneys, entailing to an insufficiency of both organs. The death happens approximately one week after the ingestion of the toxin. Near a 15% of the poisoned patients they will soon die to the 10 days happening through a state comatos and hepatic Insufficiency, hepatic comma, respiratory Insufficiency and finally the death. Those that recovers still have the risk of a hepatic insufficiency.

Mechanism of action
With the crystal structure it is by Bushnell ET to., knows that to the amanitina polymerase II interacts with the helix of the ARN. This interaction interferes with the traslocacin of the ARN and the DNA necessary to leave the site of action of the free enzyme for the following cycle in the ARN synthesis. The union of the -amanitina can only diminish it rates of traslocacin of the ARN polymerase II at a speed of several Nucleotides per minute, although it has little effect in the affinity of the polymerase by the nucleoside triphosphate, so that still theconnections can be formed to fosfodiester. The helix at issue has evolved so that he is flexible and their conformacionales

movements are required for the traslocacin of polymerase II of the chain of the DNA. The onethat one the -amanitina, occurs sufficient rigidity him to the molecule, that is what it prevents the traslocacin him, reducing the speed of synthesis of ARN molecules.
http://www.myetymology.com/encyclopedia/Amanitina.html

Effects of the Deadly Amanitin Toxin From the Poisonous Amanita phalloidesMushroom
Alpha amanitin is a molecule made from the death cap mushroom and is a known potent inhibitor RNA polymerase. One single mushroom could very easily lead to a fast death in 10 days.

The mechanism of action is that alpha amanitin inhibits RNA polymerase at both the initiation and elongation states of transcription. The binding site for the inhibitor is the cleft between Rpb1 and Rpb2 in RNA polymerase. The cleft formed between these two subunits is connected to a helix bridge. The alpha amanitin toxin binds just beneath the bridge restricting the movement of the bridge by interactions between amanitin and residues 726, 767, 768, 769, and 822 of Rpb1 and by hydrogen bonding to residue 763 and 765 of Rbp2 (Bushnell, et al, 2002).