Good mushroom-hunting practice

[Tsathoggua]

Herein you shall find a guide to good practise while hunting and IDing mushrooms.

The intent being to have fun, have a good meal/trip and not to shit your liver out in liquid form.

When hunting, harvest by digging up the mushroom using a knife or spoon, do not yank them up by the stem, or rip the caps alone off, the stem, and base of the stem are vital diagnostic characteristics for telling what you have. Is a volva (cup-like structure) present at the base of the stem? this is diagnostic of two families, Amanita, and Volvariella, which are unrelated (confusion of the edible straw mushroom popular with orientals, and often used in chinese food, Volvariella spp. with deathcaps of varying species such as Amanita phalloides, A.ocreata and some of the similar looking Amanita subsection Phalloidea members is a major cause of death amongst eastasian immigrant mushroom hunters coming to the states or europe who make a dangerous fuckup as they look quite similar)

Be very wary and careful of any mushroom with a volva, do not bag said mushrooms in the same container you are taking any harvest that will be eaten home in unless it is to be fed to an enemy.

Is a ring present on the stem? in some species this tends to disintegrate or fray with age, and in some others, it is moveable up and down the stem if you do so carefully, IIRC, the parasol mushroom, Lepiota procera, a large member of the Lepiota family, which unlike some,which are deadly poisonous, is edible, and indeed, one I rather like to eat, can have its ring slid/rolled up and down the stem if you do it carefully. A few fungi have double rings, but this isn't particularly common.

Pay close attention to the morphology of the cap, and stem. Does the cap have a peelable surface, if the species has a cap. Some do not. Some species one can peel it off, such as the slippery jack bolete (suillus luteus), the related larch bolete (also in the genus Suillus), as do the death cap (Amanita phalloides) and common button mushrooms bought in stores, of the genus Agaricus, most commonly A.bitorquis (ick!....I don't like store bought mushrooms at all, apart from shiitake, oysters etc.) Whilst others do not, for example Mycena spp. and a good few of the Coprinus species. Does the cap become viscid when wet? or is it permanently sticky/glutinous, or is it not so at all? Note texture and smell of the fruitbody, it can help to crush some to release any smell more.

Some fungi have very diagnostic odours, such as in certain Russulas, the smell of decaying shellfish for R.foetens, in R.fellea, there is a pronounced smell of geranium, or in the case of, for example, Russula queletii, the scent of fresh apples.

Check gill structure (gills decurrent, running down the stem? adnexed? adnate? detatched from the stem? texture and resilience of gills, are they waxy? firm? do they break easily? pores like a bolete? some fungi, including a few absolutely excellent edibles, the hedgehog fungi, have pointy spines pointing downwards from the underside of the cap) Some fungi have no true gills, but instead, raised, forking, ridge-like pseudogills forming the fertile area, and some, have no gills at all, such as the horn of plenty/black funnel of death, known to be a very sought after edible, meant to be particularly good in soup or stew, after being dried for storage like one can with porcini/cep/Boletus edulis, but I have never been lucky enough to find any

In some genera, SOME, mind you, but not all, taste is important. Russula, Lactarius, and to a lesser extent, Boletus and their relatives such as Suillus and Chalciporus (C.piperatus for example, the peppery bolete, I use as a spice, dried and ground, just like I use chillis or pepper, its hot and firey, but in a different way to either spice)

The procedure for tasting is to break off a small piece of cap, and nibble it between the teeth for a short time, make sure it gets on the tongue, is it sweet? acrid? or is there a specific taste of something? In particular with Russula and Lactarius species, this test is borderline vital, and in these two families, there are none that a mere taste will kill. Although actually eating a scant handful of Lactarius species has done so in the past, and Russula subnigricans, the blackening russula (not to be confused with R.nigricans or R.nigrescens) contains a potent myotoxin, cycloprop-2-ene-1-carboxylic acid, causing severe rhabdomyolysis and subsequent kidney failure, this species can be lethal, and most painfully, slowly so at that.

Taste, but do not swallow. Spit.

Some fungi take time for a taste to develop, others start one way, then turn another, such as starting mild, but with a rapid, or slow development of an intense acrid burning sensation in the case of some of the Lactarius (milk caps).

In the case of this family, milk cap, comes from their bleeding a milky liquid substance when injured. Cause this to happen if you think you may have one from this genus, observe the consistency and color of the 'milk', some change color on exposure to air after a few minutes, blotting some milk onto white, absorbent paper such as a tissue, or bit of blotting paper can aid the development of the change. There are some good edibles to be had here, one or two species, such as L.torminosus, the wooly milk-cap may be fatal if eaten, but most likely will just cause severe GI irritation and accompanying miserable symptoms for a day or two. The toxins are most likely in most cases to be sesquiterpene compounds, as are those in many of the acrid Russulas (brittlegills). The Russulas, are, with the exception of the myotoxin-bearing R.subnigricans, not fatal, barring some freak ill luck, and besides, are so acrid in many cases for the toxic ones (in fact almost all toxic russilas, bar that species have a hot, burning taste. With very few exceptions, all burning russulas are for the chuck, and some consider it a general rule that all mild ones are edible, I do not rely on rules of thumb though to be exact, not when it comes to potential toxicity, but its very unlikely that you will be poisoned by a mild-tasting Russula.

There are some genera that you simply do not taste. Amanitas, don't do it. Inocybes, don't do it-there aren't any worth eating, and quite possibly none safe to eat either. The entire genus is chock-full of muscarine, with a few exceptions. Most are incredibly hard to ID, and impossible to do so without a microscope to check the spores, gill microstructure and hyphae out. Fun to pick for the challenge of an ID, but certainly not for eating. One mycologist became so ill after tasting a tiny piece of Amanita xanthocephala, an unusual species, not amatoxic, but most virulent nevertheless, that he broke his toes trying to get to the bathroom he was in such a hurry. And tasting a small piece of what turned out to be Podostroma cornu-damae, an oriental club fungus/coral type bugger would at the least burn and blister like mustard gas, and quite possibly prove fatal, although fungi of such extreme toxicity are the exception rather than the rule, and tasting even an amatoxic species by accident is very unlikely to kill you, although may nevertheless make you severely ill and cause liver damage to some degree.

Eat no mushroom that displays bioluminescence. All of them I am aware of that do phosphoresce in the dark, such as Lampteromyces japonicus, and Omphalotus species (the jack'o'lantern fungi) are poisonous. Interestingly the latter family produce their phosphorescence in the same way that fireflies do, the reaction between luciferin and luciferase. Eat something that glows in the dark, and you will regret it. Won't kill you, but will cause very severe GI upset.

Don't taste any Lepiota species either, many contain the same deadly amatoxins that the Amanita (subsection Phalloidea) do. Likewise for Galerina, and Conocybe, there are psilocybin-bearing members of both, but likewise amatoxin carrying ones, avoid tasting or eating these families in their entirety, its not worth repeatedly squirting your liver and kidneys down the inside of your trouser leg in a cloud of blood and cholera-esque chunky fecal soup until you shrivel up, turn yellow, and die over several weeks.

More on toxicity later, I'll give a breakdown of the main groups of toxic compounds, and the species (not totally comprehensive, its a bit too much to expect of me to know and to remember to name every single species in every family containing a given toxin or toxins, but I will give a wide range, of both the common ones, and a fair few more unusual and little nown nasties, where they are found and how they work)

Take note also of the habitat-is it growing on wood, if so, if you can tell, what kind of wood? growing on turds? or near, but not ON shit. In lawns/grassland? woodland? many fungi are what is called mycorrhizal, meaning they form an intimate composite structure between plant roots and the mushroom mycelium. If growing in association with plants, take samples of the nearby (for a few meters) trees and shrubs, most commonly a mycorrhizal fungus will form an association between a tree or woody shrub, macrofungi growing in association with herbs are much less common, and in the case of ergots, take at least one entire grass plant, leaving sclerotia in the seedhead for ID, as the host species often defines the parasite, C.purpurea excepted, which is unusual amongst the Clavicipitacea in being a bit of a whore really, where as others such as C.fusiformis are more picky, there is even one species specialising in bamboo.

Take spore prints, this is a very important step if you are uncertain of the identification. A microscope is helpful too, for some genera, it is vital if you are to ID down to species level, such as the genus Inocybe in particular (not that any of these are ones you want to eat, although a few contain psilocybin and psilocin, I.aeruginescens contains a novel tryptamine, the trimethyltryptammonium quat of psilocybin, although this will not pass the BBB, and is a POTENT 5HT6 agonist, which will make you feel very, very, very severely nauseated and cause quite spectacular vomiting, if its active in vivo at all, compare with ondansetron etc. the antinauseant drugs. The tryptamine bearing Inocybes in many cases contain very low concentrations of actives, avoid them IMO, as most species are full of the cholinergic neurotoxin muscarine, in many cases in large quantities, in some, enough to prove fatal) Pretty much all Inocybes are small to moderate sized LBMs (little brown mushrooms) with fibrous cap surfaces and very hard to ID.

Note spore color, and miscroscopic characteristics if you have a microscope. I need a new one :/

Next-Colorimetric reactions and reagent testing.


Testing fungi with chemicals is a very useful diagnostic tool, this can be done in the field in many cases.

First and foremost-the Meixner test. This isn't a test for species ID, but rather, for the presence of a specific group of toxins, the deadly cytotoxic amatoxins, on which, more information later on in my guide. It is sensitive to 2mcg of amatoxin (calc. as amatoxin-a, alpha-amanitin), a typical Amanita phalloides fruitbody of medium size contains between 4-7mg of total amatoxins, maybe a little more, maybe a little less, fungi are very variable as to chemotype, A.ocreata may contain even more. 10mg/fruitbody-1mg-gram wet tissue on average, or slightly more. 0.1mg/kg is more than enough to kill.

Take a small sample of mushroom cap, or if somebody has eaten the mushroom and an amatoxic species is suspected or even wondered about but only bits of stem or other waste is available, use that, and a slip of paper, this must be high in lignin, or the test will fail to work, or at best will work very poorly, indeed this has failed before, with the result of the direst consequences for the poor bastard the test had been done on behalf of when lab filter paper was used. Newspaper is an excellent type to use.

Mash the sample up good onto the paper, after drawing a pencil circle to tell you where the spot is going to appear if the test is positive, around the area. Work the sample in there, and get it saturated with mushroom juice, really work it in there well. The more amatoxin is present the more there is to react and the better the test will perform in the event of a positive result.

Now add a couple of drops of concentrated hydrochloric acid solution (aq).

If the sample contains amatoxins, then a bluey-lilac-ish halo will appear around the sampled area, sometimes this can take several minutes, I would leave it to develop for 15 minutes at the absolute minimum, preferably double that for a good reliability, unless a result is shown earlier than this. If it does-THROW AWAY ANY AND ALL OF THE REST OF YOUR HARVEST! its not something I would like to do, would be pretty gutted if I had to toss the entire lot of a meal out. I have however once kept a batch of P.cyanescens, after a rust brown sporeprint developed (indicative of the possibility but by no means certainty of the presence of a Galerina, of which some are amatoxic, however this was a single, small mushroom (couple of centimeters wide post drying) amidst an entire large harvest of several hundred grams of definite cyans, and was weeded out. In fact believe I still have that mushroom somewhere actually)

Just a point!!! The amatoxin cyclopeptide core structure contains several rather unusual aminoacids, in a cyclic ring structure, linked to a center heterocyclic nucleus in the middle, the core is an indole molecule in the center. The Meixner test displays  cross-reactivity with tryptamines, I.E psilocybin fungi. 100% crossreactivity for psilocin!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

I have wanted to test this for some time but have not been able due to the lack of an amatoxic mushroom to test with. Next time I find a deadly Lepiota or Amanita I shall have to bust out the lab. Oh, and take controls, people! Although i shouldn't have to tell anybody here that. IIRC the greenyblue-lilac-purplish color produced by a positive amatoxic substrate does not do this, whereas newspaper can go pink after a time in the sunlight, UV being responsible. Do the Meixner test out of bright sunlight if at all possible, and there is no reason it should not.

Do bear in mind also, that not all amatoxic species, all of the time, react. You are very unlikely, ever, ever to get a false positive, but some amatoxic species occasionally fruit a few that contain either extremely little, or perhaps even no amatoxin! particularly, I read, in the case of Amanita virosa, the destroying (or death) angel. (the species epithet coming from the latin 'virosus' meaning poisonous, same as the root origin of the words 'virulent' and 'virus')

Can anyone get the full text of this paper, I wont post it as a request in the request thread for it is far more appropriate if it is put here.

http://www.jstor.org/pss/3759568

Now onto the colorimetric species diagnostic reagent tests, families applicable in particular, are Amanita, Russula and Lactarius, although reagent tests are valuable in many more instances.

I will give the reagent, its preparation if needs be, and both the practical use of it, and a couple of representative color changes and the species they occur in.

HCl-concentrated HCl solution can be dropped into various fungi, its used for one, in the aforementioned Meixner test, or a mixture of HCl and para-DMAB (dimethylaminobenzaldehyde) will give a rapid blue/violet color change with a tryptamine containing mushroom. Again, due to that damnable indolic moiety in the cyclopeptide amatoxins/phallotoxins/virotoxins I need to see if this will crossreact with a known amatoxic species.

This is a variation on erlich's reagent/van urk, and these likewise can be used. There are quite a few variations on the erlichs/van urk reagent theme actually, involving H2SO4, ferrous sulfate (this alone reacts with some fungi bear in mind) and ferric chloride (again, quite probably so does this)

KOH or NaOH as moderately concentrated (10-15%) solutions are very common, very easily available reagents and can be kept in vials in a kit for field-testing specimens.


For instance its capable of differentiating Amanita virosa from its very, very close lookalike, although somewhat rarer, A.verna, both lethal amatoxin-packing species, both pure ghost-white, with white spores, a large ring and pronounced volva. The flesh (cap in particular) of A.virosa stains yellow when treated with KOH or NaOH whereas that of A.verna does not. A.ocreata does, whereas the white form of the deathcap sensu stricto, A.phalloides var.alba does not.

A particularly striking KOH/NaOH reaction is that of Hapilopilus rutilans, or H.nidulans, the purple dye polypores, these are dangerous poisonous species to eat (they turn woody and totally uneatable physically as they age, but when younger are softer), these cause a delayed neurotoxic encepalopathy if eaten, but are used to make dye, by reaction with the hydroxides, on which they turn a shocking purple.

Gives a dark ink-black, blacker than the heart of condoleeza rice, although a little less corrosive, when applied to the cap of certain Cortinarius species (webcaps, some of which contain a particularly insidious, very, very slowly acting nephrotoxin structurally related to paraquat)

Iron salts, particularly the ferrous sulfate and ferric chloride are of use IDing boletes (which have spongy, squishy pores, rather than gills), and Russula or Lactarius spp. giving in various cases, no change, or a change to various blues, greens, pinkish-reds, purples, yellow/yellowish greens depending on species.

Phenol as a 3-4% solution gives color changes, IIRC yellow in the case of certain Agaricus. Not too well up on the use of phenol for colorimetric testing of fungi.


With all these, test various parts, stem, cap, cut open stem/cap, gills.

A very important and useful reagent, although it will take a bit of work, is Melzer's, which is used on spores, rather than cap or stem, although quite possibly in some species, I don't know for sure would work on gill pieces.

The formula is, to make up 100ml, which will last a long time

dH2O: 100ml
Chloral hydrate: 100g
Iodine crystals: 2.5g
KI: 7.5g


This is used on spore print material, scraped onto glass (it can react with paper)
Reactions can be either none, amyloid, or dextrinoid.

Amyloid reaction is a dark violet-black. Same color as potato treated with tincture of iodine, dextrinoid is a rufous reddish-brown color.

One other thing, which I have been meaning to do, but haven't found time, is test things. ID species, test other chemicals on them. Plenty of books give a characteristic rxn or two, but not a comprehensive be-all-end-all-fuck-your-granny-in-the-process guide to the fungal anonymity apocalypse.

[Tsathoggua]

                                 

  On the subject of the toxic principles found in macrofungi

This is the section of my guide, where we explore the various toxic substances found in certain macrofungi, both the commonly known and imfamous ones, such as the amanitins, methylhydrazines, and orellanine, and some lesser known, but equally nasty ones.
I intend to cover the principle families of fungi, down to genus subsection level where applicable where these toxic principles are found, their structure, biological mode of action, and chemical antidotal agents, if such exist, although frequently they do not.



                                     

   Section I: The poisonous principles of the genus Amanita

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Amanita family toxins act I: The amatoxin complex

Within the genus Amanita, principally in the subsection Phalloidea there are found a number of potent hepatotoxins of a delayed-acting nature, the amatoxins, and their related compounds the phallotoxins and virotoxins.

The main important ones are the amatoxins, for the phallotoxins and virotoxins penetrate intact, living cell walls very poorly, and are thought not to contribute significant, if any toxicity in oral ingestions. Extremely toxic via injection though, which of course is not going to be applicable to human ingestions, short of pest control. Indeed the sought after Amanita rubescens, the blusher contains quantities of phallotoxins, so I believe.

The amatoxins are bicyclic octapeptides, the phallotoxins are hepapeptides, and the virotoxins are monocyclic heptapeptides, all based on a central hydroxyindole core, surrounded by a highl complex, branched cyclic ring structure of aminoacids. All these toxins target RNA polymerase II, halting protein synthesis in affected cells, and having specific, and extremely high degree of cytotoxicity towards the liver, and also damaging the kidneys. The amatoxins undergo extensive enterohepatic recirculation, being reabsorbed in the intestine, after doing damage, sent back where they came from, and re-excreted in the bile, only for it to happen again, and again, and again and then some, continuously being recycled and going back round for a fresh cycle of liver-rape.

Typical symptoms start with an uneasy feeling, approximately 6-8 hours after ingestion, by which time damage is already being done, and lots of it. Followed by violent gastroenteritis, of a most severe nature. Severe vomiting, diarrhea, GI pain, prostration.

Followed by apparent improvement after a day, quite often, or two, only to relapse after or on the second or third day, presenting as fulminant hepatorenal failure, with extensive fatty degeneration of the liver, and damage to the renal tubules. Electrolyte balances get disturbed, creatinine kinase values increase, as well as altered liver enzyme levels and hypoglycaemia. there can be a marked acidosis, and in severe cases, hepatic encephalopathy can ensue, resulting in seizure, and there can be, if the shit really hits the fan, not that it can be sprayed over many more fans than it already is, then fucking up of the blood clotting can result in the medical apocalypse known as disseminated intravascular coagulation, the horsemen of which being  Impaired blood clotting, followed by blood leaking out through blood vessels into the tissues, and counterintuitively, blood starting to clot, and clot everywhere, clogging up the circulatory system, causing emboli left right and center.

That is three horsemen, they were looking for a fourth, but nobody replied to the job ad I guess, so they borrowed one from traditional eschatology, War had gotten into a fight and got banged up inside, Famine said he got hungry and went to dinner, paid for by a few thousand ethiopians, and Pestilence was off sick.

Only one left, so by default, he got the job. Bit of a skinny fella though.

Treatment must be started early, and in a large part is supportive, correction of the acidosis with bicarb infusions, maintaining electrolyte balance, rehydration to correct the profuse emesis and diarrhea, antinauseant medication, and repeated infiltration of activated charcoal into the digestive tract, to hopefully, bind a bit more toxin each time it goes round for another swing at one's liver.

Very high dose penicillin G has been tried with some success, although the doses used, seeing as it has to be used as the sodium or potassium salt cause dangers of their own due to salt overdosing. Glutathione precursors appear helpful as the amatoxins deplete glutathione. N-acetylcysteine for instance. IV (if possible) silybinin, a hepatoprotective agent and direct stimulant of certain RNA polymerase enzymes has had very good things said of it, and is often used.

Mechanical means such as dialysis and plasmapheresis have been done obviously, but the results aren't fantastic, better than nothing but not fantastic.

Failing that, it is either a liver transplant, in addition to those measures, or meeting the new horseman on the job.


Species containing amatoxins, not exclusive list, but wide ranging nevertheless

Amanitas of the subgroup Phalloidea, inc.:

A.phalloides, the death cap (including its white form, A.phalloides var.alba
A.virosa, destroying angel, death angel, white death cap (erroneous name really, this properly refers to A.phalloides var.alba)
A.verna (sensu roger phillips) the spring amanita
A.ocreata, the western north american destroying angel (along with A.bisporigera, this one is a particularly grim sonofabitch, packing a massive quantity of amatoxins, even compared to the other Phalloidea, and vastly more than Galerinas by orders of magnitude)
A.bisporigera, the north american destroying angel
A.exitialis-south chinese species, rich in amatoxin, contains some beta-carboline also.
A.magnivelaris
A.arochae-greyish, known as hongo gris in mexico, this is the main one found in south america of the Phalloidea

Lepiota species inc.:

L.brunneo-incarnata this bugger looks worryingly like a parasol (L.procera, although taxonomically seperated by some authorities into the genus Macrolepiota) and like the parasol and shaggy parasol, the ring is mobile on the stem. This species has caused deaths.

Probably L.cristata, unaware of any deaths, but I am not an authority on fungi, so I couldn't tell you for sure. I sure woudn't fuckin' eat the buggers though thats for sure.
L.helveola
L.clypeolaria has caused deaths I believe, maybe not, but it does contain amatoxins.
L.josserandii definately has.
L.subincarnata-this one is in fact, commonly named the fatal dapperling, again, full of amatoxins, and has caused fatalities.

(I reccomend only Lepiota procera syn.Macrolepiota procera, the parasol, be eaten, L.rhacodes is sort of edible, doesn't contain amatoxins, but causes GI upset undercooked or raw, and some people are made violently ill by it even then. Its phylogenetic relationship to the genus Chlorophyllum precludes it from my personal dinnerplate anyhow)




                                         

Toxins of the genus Amanita, act II-nephrotoxins

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Next we come to some rather less vicious, but still certainly not something you want to contend with, the allenic norleucine toxins from some Amanitas in the subgroup Lepidella, these are 2-amino-4,5-hexadienoic acid and IIRC, chlorinated derivatives, 2-?amino-?4-?pentynoic acid (propargyl-glycine) is present in some of the nephrotoxic Lepidellas also, this is an interesting compound, as it inhibits an enzyme that is responsible for metabolic endogenous production of H2S, both a vasodilator and imflammatory marker (or possibly proimflammatory, I am not sure, not too well up on the endogenous gasotransmitter system). It fucks about with blood sugar levels also IIRC.
 
Typical symptoms are kidney failure starting after a delayed onset of around 8-10 hours (lower back pain, insatiable thirst, GI symptoms initially, inability to piss, or passing very little, highly concentrated urine) maybe some liver damage, but primarily kidney failure and initial GI upset.

Prognosis from these is not so grim as after ingestion of the orellanine found in Cortinarius spp.

Typical mushroom species containing these:

Amanita smithiana-decidedly nasty, has gotten quite a few people now.
A.thiersii has been shown to be able to cause kidney failure, although 'temporary' in nature, which implies to me it is perhaps one of the lesser toxic species of this toxic Amanita group
A.proxima
A.pseudoporphyria
Amanita abrupta is a really nasty one, of this group, quite seriously hepatotoxic in addition to being a kidney-rapist, this is the one that contains the chloro-derivative, namely (2S,4Z)-2-amino-5-chloro-6-hydroxy-4-hexenoic acid, not as deadly as the amatoxins though, but still capable of causing extensive hepatic cytotoxicity and necrosis, thought to have killed in the past.

Treatments-supportive, nothing specific, although similar measures taken with amatoxic poisoning wouldn't hurt. Dialysis should be undertaken.


                           

     Act III-Toxins present in the genus Amanita subsection Amanita

Amanita subsection Amanita includes some notable species, and those we use entheogenically or recreationally, I.E the A.muscaria complex, A.pantherina (iffy, more there in a moment, people, bear with me) and A.gemmata (avoid, white spored, white amanita...eat this and you are essentially asking for a dinner-date with that skinny new horseman on the job)

The main toxins in that lot, and a couple of others, are isoxazoles, an isoxazolecarboxylic acid, ibotenic acid, which is a NMDA receptor selective excitotoxin, which decarboxylates to muscimol after slow heat-curing to dryness, its a GABAa agonist binding at the GABA recognition site itself, the psychotropic agent in these fungi, and traces of the cholinergic agonist neurotoxin muscarine, a quat, which is as such, due to the charge it bears, restricted to the PNS. Causes much of any nausea with these mushrooms, as well as all the sweating, lachrymation and salivation, as well increased urination. Only traces, mere traces of muscarine in a.muscaria and A.pantherina etc, don't treat with atropine in case of severe intoxication, the effects are due to the other two compounds. However buscopan, the IBS medicine can be used to premedicate to avoid the cholinergic nastiness if your local strain causes any, its a scopolamine quat.amine and won't cause any central antimuscarinic troubles as atropine or scopolamine itself can.

Ibotenic acid-this decarboxylates on either boiling, or heat-curing, over a low flame, such as overnight at the minimum setting of your oven. IUPAC nomenclature for ibotenic acid is the following: (S)-2-amino-2-(3-hydroxyisoxazol-5-yl) acetic acid (for the S isomer, the one found in nature of course)


The result is muscimol, the intoxicant, this binds with high affinity to GABAa and the GABAc receptor (more properly GABAa-rho, mainly expressed in the retina, with some distribution also to the CNS, composed entirely of GABAa-rho type subunits) acting as an agonist.
Effects are both excitatory and inhibitory in nature. Whilst ibotenic acid just just a pure and simple neurotoxin, muscimol displaces GABA, and at the same mimics its action (it binds, unlike the benzos, barbs, neurosteroids, loreclezole, the valproate-like compounds in valerian, etc. not at an allosteric regulatory site, but at the GABA binding site itself, located between an alpha and a beta-type subunit combination, this displacement of GABA, the main inhibitory neurotransmitter of the CNS* causes excitation due to the removal of GABA from its binding sites, and also sedation and inhibitory effects due to the agonist nature of muscimol itself. Quite a complex interaction, so I believe.

Here we are, muscimol, 5-(aminomethyl)- isoxazol-3-ol:

 (*the main other being glycine, which is primilarily functional, I believe, at the spinal level, concerned with reflexive action amongst other things, antagonists of which include the toxin tutin, from Coraria bushes, and the well known convulsant poison strychnine, but anyway, back to business)

Interestingly, there are a few other, more minor constituents of the A.muscaria group, amavadine, a chelated vanadium complex is present, at quite staggering levels, compared to background levels of vanadium in plants and fungi, it appears to bioconcentrate the element in large quantities.

Muscarine is present in trace, harmless quantities, able to do little more than cause a bit of sweating and salivation, as is muscazone, a keto-derivative of ibotenic acid which will almost certainly decarboxylate likewise, this is formed by photocatalytic rearrangement of ibotenic acid.

Muscarine: (2S,4R,5S)-(4-hydroxy-5-methyl-tetrahydrofuran-2-ylmethyl)-trimethyl-ammonium cation)

Muscazone:



The synthetic muscimol derivative thiomuscimol (the isothiazole derivative) is much more potent than muscimol is.


A.pantherina contains more of the above than does A.muscaria, however, I would avoid its use, I personally will not use it.
The panthercap contains two aminoacid neurotoxins, stizolobic acid and stizolobinic acid, which bear some similarity to the generally nonlethal but most tormenting, torturous acromelic acids from certain Tricholoma species. There are only traces present, but they are incredibly fuckoff potent (femtomolar concentrations are sufficient to cause toxicity )



Action varies in invertebrates, amphibians and mammals, in all it appears glutamatergic excitotoxin in nature, I believe in mammals they are kainate receptor agonists, I theorise that they are subtype selective, given the mode of action does not produce, as far as I know, the protracted allodynia and hyperalgesia caused by the acromelic acids. Stizolobic acid is more potent than stizolobinic acid.

hxxp://www6.ufrgs.br/favet/imunovet/molecular_immunology/chemicalcausesfungi.html THIS site claims it in mammals to be an AMPA antagonist (they refer to the AMPAr as quisqualate receptor here) but I don't think so, it doesn't fit at all with other reports, and they make some other rather....odd....claims about other fungi and their bioactive constituents.

Any effects produced by it, are likely, given the response in humano to acromelic acids, or other excitotoxins to be prolonged in nature.

There appears to be a poisonous lookalike for A.muscaria, this I only recently learned of, the mushroom is Amanita aprica

A.aprica description:

This appears to be an northamerican species, and it appears, as far as I know, to possess the same psychotropic properties as the Muscaria/Pantherina/Gemmata group within the subsection Amanita of the genus Amanita, however there seem to be quite a few reports of it causing severe muscle cramping in addition to this. It associates with coniferous trees, including hemlock (the spruce-like tree, not the deadly umbelliferous herb Conium maculatum, or the even deadlier water hemlocks/cowbanes of the genera Circuta and Aethusa) and pines of varying kinds.

Looks like the fly agaric, ranging from orange to yellowish golden color, gills, white, sometimes tinged with yellow-gold, stem, likewise. Spores-white, elongated, thin-walled, smoothe, inamyloid reaction to Melzer's reagent.

Cap becomes covered with volva remnants, similar to the fly agaric, but in A.aprica these become embedded into the cap and won't easily scrape off, as they will do off A.muscaria. Frosty-velvety appearance of these embedded partial veil remnants rather than the warty, lumpy morphology of the warts on the surface of a muscaria cap.

Known chemical reactions: Phenol-reddish discoloration of the cap flesh and stem tissue (please, somebody test A.muscaria with phenol? I will have to try and remember to do so next time I see them growing), I would guess of the gills also, this takes between ten and 15 minutes.  15-20% KOH or NaOH, orange discoloration of partial veil within 5-10 minutes, negative rxn to both FeSO4 and diluted H2SO4.


Amanita toxica* (DEADLY POISONOUS, WARNING!)

Note, the name 'Amanita toxica' sensu Lazo has been declared nomen invalidum. There is somewhat of a taxonomic clusterfuck with the whole 'Gemmata-like' subgrouping within Amanita subsection Amanita, they are really hard to ID, and there exists considerable variation between them, including possible hybridisation between both Gemmata-like taxa, and A.muscaria or A.pantherina....Lazo originally took A.toxica 'Lazo's deadly amanita' for a Gemmata, but it is obviously not. A.gemmata causes pantherine-type intoxication, isoxazoles are present, but this one is nasty, very nasty from what little info I have about it. Drop you suddenly dead nasty. Most unlikely to be suspected as a fungal culprit too.

I have seen very few pictures of this species, even then it has been as a dried voucher specimen. Looks brown, similar size to the larger members of Amanita subs.Amanita, retaining some warty veil remnants on the cap.

 
South american species, relatively newly described in chile, no other known member of Amanita subsection Amanita is lethal, at least, not barring complications such as preexisting heart conditions, the convulsant effects that occur instead of GABAergic inhibitory ones in little children who eat those fungi, etc.

This one is different, it appears to contain a cardiotoxin, which is incredibly unusual amongst macrofungi, I only know of one other species which does, unless we count the cardiac effects of those fungi which contain large quantities of muscarine, but other than the mushroom responsible for yunnan sudden death syndrome, in china, then I know of no other fungal cardiotoxins in the macrofungi, period. Grows in association with conifers/pines,

It is noted that this cardiotoxic principle is possibly similar in nature to oubain (strophanthin-G), this is a cardioactive steroid glycoside found in Strophanthus hispidus, a plant in the Apocynacea, the dogbane family, a family, including both the famous Iboga plant, and a great many extremely poisonous plants, many of which are used for arrow or dart poisons, also found in Akocanthera, the bushman's poison bush. Similar cardioactive steroids occur in foxglove (digitalis), the source of the very old, but still very valuable heart drug digoxin, oleander sap, twigs, flowers, nectar and foliage, the venom of certain toads in the genus Bufo (lick me, squeeze me, or try smoking me and you will pay the price, fuckers )
and the deadly Upas tree of java, Antiaris toxicaria, a mere scratch from whos twigs can kill a man within a half hour, if any of the toxic latex is introduced into the system, this is used for arrows and blowgun darts, tipped with a mixture of an extract of Antiaris, arsenic salts, lime juice and 3-4 other highly toxic plants, little more than a couple of cm length of one of these darts, which the natives pare down near the tip, so as to cause its breaking off in the wound on impact will fell a top predator such as a tiger within a couple of hours at most, take down the biggest game, and rapidly kill a person so hit, cardiac glycosides are very effective poisons so I do not doubt the lethality of Amanita toxica.

Assuming this is indeed a cardioactive steroidal glycoside type poison, in this mushroom species, it may be treatable, and it will cause some characteristic clinical presentations (other than dropping dead of a heart attack that is)

The heart rate will be slowed, but made more forceful in the case of minor, sub-toxic doses of the poison, little is known about this species, so I don't have a huge amount of data to give you, but it is known to have killed quite a lot of people in chile, where it occurs and is reported to be one of the most highly poisonous fungi in chile, indeed, quite possibly ranking amongst some of the deadliest in south america, so one can safely assume that a sub toxic dose isn't going to be very much at all.

Possible symptoms include nausea, double vision/blurring of vision, bradycardia, vomiting, diuresis possibly, confused state of mind, delirium or psychotic behaviour, seizure, in the case of digitalis at least, it can cause an unusual effect on the vision, although not common, where green/yellow halos are percieved round seen objects or lights, color perception is altered also possibly, but I don't know weather this is specific to digitalis.

Likely is at first, ventricular tachycardia will present,  followed by bradycardia, with severe hypotension, degenerating into, as the poisoning progresses a ventricular tachyarrythmia, the EKG is likely to show a shortened QRS complex, inversion of the T-wave component of the action potential, and severe A-V block. A specific and very suggestive marker on the EKG will be A-V blockade with paroxysmal atrial tachycardia, this is highly indicative of cardiac steroidal glycoside poisoning, especially when coupled with a presentation like the above. Likely in severe cases to progress to complete heart block, and sudden death.

Some of those steroids are extremely potent, for example a typical dose of digoxin for heart issues is 0.125mg/d-0.250mg/d via SLOW IV push, or 1mg per os, the collection of cardiac glycosides in Antiaris toxicaria is almost certainly much more potent, and possessed of a singularly great rapidity and violence of action.

If somebody ingesting these mushrooms even makes it to hospital, although it is entirely plausible that a fatal outcome might occur shortly after feeling merely quite ill, or kill the patient before they can get to hospital, if they do get help, then the treatment course I advise is to get them hooked up to a 12 lead EKG, and commence bloodwork straight away, but without waiting for the results. Treatment with atropine may be necessary, IV lidocaine may well be useful for helping combat the arrythmias, it isn't impossible that adenosine may have to be used, in an emergency to short-circuit an atrial tachycardia or arrythmia, or SVT, although quite probably in this case a very bad idea in most instances, and certainly not to be done in the case of pre-existing heart block. It is quite possible for a dangerous interaction with adrenergic pressors such as adrenaline, NA or DA.

These are supportive measures however, ideally, and as rapidly as possible digibind (an antibody preparation) should be given by IV
This is an antibody fragment directed at digitalis toxins, which has been produced from antibodies raised in sheep immunized with a digoxin derivative. This is polyvalent against digitalis, and quite a few other cardiac glycosides, so there is a chance that it will bind and neutralise the fungal toxin. This however cannot be guaranteed, but it would rapidly reverse the poisoning if it is indeed crossreactive with digi-FAB.

I have frequently seen A.gemmata itself noted as one of the species responsible for the typical isoxazole-mediated 'pantherine syndrome', there appears to be some contentious reports though, Phillips lists it as deadly poisonous, many other sites list A.gemmata as merely poisonous, and grouping it with A.muscaria, A.pantherina and others containing ibotenic acid/muscimol. There appears, perhaps, to be something squirrely going on with this Chilean species, if species it is....very little information appears available on either the putative toxin, or indeed Amanita toxica sensu Lazo itself, but the following reference appears to support the putatitive presence of a cardioactive toxic fraction within some varieties of A.gemmata

"A ouabain like compound present in Amanita gemmata (Fr) Gillet"
IRCS Medical Science: Library Compendium 1981, 9(4), p.297

This again casts aspersions on at least Chilean populations of A.gemmata, this time listing severe hepatic failure and kidney damage, reminiscent of amatoxin poisoning. Amanita gemmata is, however, a pretty tricky little bugger, and not particularly easy to identify to species level, they can look quite similar to pale A.phalloides so it isn't impossible that the mushrooms responsible for this were not in fact A.gemmata. I don't have these references in full, any chance somebody might grab them for me?

Rev Med Chil. 1994 Jul;122(7):795-802.
[Mushroom poisoning in the IX region. Role of Amanita gemmata]
PMID: 7732230

At any rate, I certainly do not reccomend that anybody experiment with A.gemmata, well, actually, I take that back, I do encourage people to experiment as much as they can on this species, but NOT by eating the things, Meixner test 'em, after definite ID (remember, whilst it will detect amatoxins, it is not a specific test, and will crossreact with other indolic compounds, since this is quite probably at least in some instances/races/strains/subspecies an isoxazole containing fungus, and quite certainly not one containing psilocybin, a positive Meixner test would be interesting. Its very rare here where I am, and certainly its not likely, in the UK to be the same species/chemorace/strain(s) as is/are knocking people off in Chile, so if anybody is interested enough and in that area, do go check them out, report back with microscopy, chemical tests, same goes for US specimens, and those from the UK, or the continent, if you see this species, hit 'em with the Meixner test, phenol, ferrous sulfate, KOH/NaOH solution, Meltzer's, etc. be creative.)

One thing should be concluded though at least...Amanita gemmata is off the menu

Thats it, for now, although I will work on this more, finish off the Amanita subsection Amanita toxicology section later, and then start work on the hydrazines, coprine, the bypyridyl nephrotoxins of the genus Cortinarius, the immunotoxin involutin, the myotoxic species, sudden yunnan death syndrome-the mushroom-barium connection, muscarine, misc. neurotoxins and GI toxicants, and the most unusual macrofungal source of tricothecenes, and perhaps the very deadliest of all macrofungi, Podostroma cornu-damae.

[The Lone Stranger]

Wow !!!! Well done . Thats a shit load of information and you put it together in 2 days !!!!! It should either be made a sticky or put in a special information section only for sensible factual information = posts like this one should be cut out , or two threads made.......this one for the facts and another to talk about them and the facts thread so that this one doesnt get full of arguments.......... it looks like a potential part for the proposed site wiki to me .

[Tsathoggua]

Well thanks, not finished yet. I need to edit the section on Amanita subsection Amanita toxins, to include A.aprica (a nasty fly agaric lookalike of the A.gemmata complex, which whilst apparently hallucinogenic, appears to have something else, rather more noxious in there) and to add a few other things here, there, and elsewhere.

2 days? 2-maybe 3 hours is more like it. Just drawing on memory so far, but I guess I should do at least a little research and see what (or who) else I can dig up. Not bad, I hope, considering I was rather pissed at the time

For now I have to give the lovecraftian toad god directions to the local hardware store, and possibly piss through somebody's letterbox, and then go to sleep, after telling toadie a few things about why not to mix GAA, TETA-acetate and certain combinations of nitroparaffins and carbonyl compounds............oh, and get another large glass of the rather tasty coconut rum I pinched off toadface while he was busy inspecting his fridge and the funny goings on of some chlorobutanol in there....he won't notice, he is lazy, too full of crazed cultist human sacrifices, and at several epochs old, his memory isn't all that likely to let him know how much went missing

[Tsathoggua]

                                   

Section II: Gyromitrin: of False morels and rocket fuel

Where shall we look next, in my small and humble class on elementary mycotoxicology for the pot hunter and drug enthusiast, hmm?

The hydrazines, I think.

Anybody ever tasted morels? fresh, or dried, to be rehydrated and made into gravy (they go particularly well when the smoky, rich flavour of the true morel is coaxed out of its shell with a little offering of heat-dried Amanita muscaria), soup, stews and what have you, very tasty indeed, as long as one cuts them open, for they are hollow inside, and make, I find, a rather comfortable abode for slugs, snails and other assorted critters of the many-legged, mushroom-eating pursuasion, remember that, next time you find some, for saving you an unwelcome guest or three in your meal aside altogether, its an important salient point when it comes to the morphology of something altogether less desirable, the false morels.

Some people do eat false morels, sometimes known as lorchels, of the genus Gyromitra, and some similar looking fungi, morphologically speaking, in the genus Helvella, all funky shaped ascomycete fungi, but personally I think the edibility is dubious at the absolute most fantastically optimistic best, and you are about to read why.

This is a true morel, Morchella conica I think from the look, I have some of these in my kitchen actually, dried, awaiting the day I make soup or next have steak (bah, I didn't have the energy to cook for several days recently and lost a perfectly good two steaks, a whole load of fresh oyster mushrooms and shiitake and one lot of morel, cep, fly agaric and chanterelle gravy, after sleeping for two days and nights, I went to make it and found my gravy had maggots in it and my steak was off, that was going to be a cracker of a dinner )



A true morel in cross section, this is not Morchella conica, but another species, most likely Morchella esculenta.


Note the irregular, fairly deep pits in what passes for a cap in the morels, at least those of the genus Morchella, the half-free morels of the genus Mitrophora are much smaller, and a bit more traditionally 'mushroom' shaped, and as I said, they are HOLLOW INSIDE. False morels, on the other hand are not, they have multiple small cavities when sliced down the middle, and look distinctly brain-like, both within and without, actually, in cross section, I think they somewhat resemble and MRI image of the brain. Below is a Gyromitra esculenta, whole, and in cross section.

The true morels DO contain small quantities of the hydrazine based nasties, and are not to be eaten raw, but they are safe to eat, there are some people who have a bad reaction, but this is never as severe as eating a poisonous species like the false morels, and they are widely consumed, and sought after worldwide, I'm adventurous when it comes to wild mushrooms, but I'm not stupid, or incautious, I do eat the true morels and enjoy them, but I have never, and will never eat Gyromitra spp. or the helvellas.





There is something out there though that is just begging to trip people up, Ptychoverpa bohemica, the early false morel. It looks really like the true yellow/white morels (M.esculenta) and contains enough gyromitrin to strike it off my list (to remove Ptychoverpa from my list, that is, if ever I run into the true morels, you bet they are getting taken home) There are a couple of distinguishing features though, one being the peculiar folded, convoluted interior of the stem, and the other main one being the fact that the cap is actually that, rather than a continuation of the stipe, as a one-piece outfit, as the true morels are.

Ptychoverpa bohemica


The stipe of Ptychoverpa bohemica

Gyromitrin itself, why, its a fairly simple molecule, the acetaldehyde hydrazone of n-formyl-n-methylhydrazine, present in quite large quantities (grams, even,per kilogram of mushroom tissue), and is well known to be highly toxic, or rather, its metabolic product, monomethylhydrazine is. MMH has another use also, where its toxicity was likewise found to be high, NASA, funny enough, for MMH is used as a hypergolic propellant for spacecraft in combination with dinitrogen tetroxide.

This is gyromitrin:



Its action is by inhibiting the activated phosphate derivative of pyridoxal, vitamin B6, quite reminiscent of a clinically used drug, actually, another hydrazine-based nasty, the anti-tuberculosis drug isoniazide, N-nitroso derivatives are formed by hepatic cytochrome-P450 pathways which damage the liver in cases of false morel poisoning (or presumably, an accident at NASA involving MMH rocket fuel, assuming it doesn't blow you halfway to hell first of course), there are changes in blood chemistry, methaemoglobinaemia, sometimes acidosis, along with headaches, severe vertigo, nausea/vomiting and seizure. GABAergics can be used to control seizure, although vitamin B6 should also be given in large doses, given the specific mode of action, it results in less synthesis of GABA via inhibition of pyrodoxal phosphate, which is a requisite cofactor for the actions of aminoacid decarboxylases which usually operate to produce the monoamine neurotransmitters.

Neuropathy can also result.

I would think, that barbiturate type GABAa agonists would serve better than benzos in this case, given the way that glutamate decarboxylase is inhibited, for two reasons, one being that benzos increase the effectiveness of GABA by increasing the open frequency of the chloride channel, into response to GABA binding, whereas barbs open it longer also, the more direct gating of the GABAa ion channel would, I think, make barbs a more effective choice where seizure control is needed. In addition, unlike benzos, barbiturates are AMPA type glutamate receptor antagonists. Less GABA being produced from glutamate via the decarboxylase enzyme thanks to lacking the B6 phosphate cofactor means more glutamate hanging about, which means more tendency to seizure, as well, potentially, as excitotoxic memory damage, although I do not specifically, personally know of any case reports emphasizing this, it doesn't mean there aren't any, all it means, is I haven't read them.

This won't prevent hepatorenal toxicity however. IV silymarin wouldn't be a bad idea. Oh, and its carcinogenic too.

Whats this? I hear you ask, people EAT these things?

Yes, people do, although its a bloody crazy thing to do, some people really have a taste for them, particularly the Finns, apparently you can buy canned false morels in Finnland, which must, by law come with a prominent warning as to their toxicity and detail the mandatory preparation.

Eat any false morel or the other species containing them raw, and its likely to be the last thing you ever do, but...

Gyromitrin, and some structurally similar compounds (albeit in lesser quantities than gyromitrin itself, nevertheless, they convert likewise to MMH) are volatile, likewise the hydrazine derivative. So, false morels can be eaten...sort of...personally I would feel safer eating fugu. They MUST be cooked, if you must eat them, after cleaning, first remove the stems, then boil them, throw away the water, boil them again, throw the water, boil, throw, boil throw, then cook them for use in the meal. Eat only a little, peoples vulnerability to the poison varies immensely, as does the levels of it within the mushroom on a per species basis, and per population basis, likewise to the season and place found growing. The stems contain the highest quantities of gyromitrin within the mushroom fruitbody (this goes for Gyromitra esculenta, and probably the other Gyromitras, no idea about Helvellas, Verpa spp. and of course, the various members of the genus Pezziza do not have a stem to begin with, they are cup fungi, so this is of course a moot point there) Apparently mushrooms from a higher altitude (Gyromitra spp.) contain less toxin than do those from lower down.

When I say susceptibility varies....a meal that could be shared by a hypothetical family of 6 adults (on no account should a child, or an epileptic person ever, ever  EVER eat these!!!!!!), maybe everyone eats, is fine, but maybe not, with the same batch of mushrooms, maybe one person is very vulnerable to MMH/gyromitrin, and either gets very sick, or dies, maybe the reverse and everybody but one person does...you just have no idea until you eat the things, even having eaten them before. 

And just a wondering, nothing specific to back it up but theory...being a hydrazone of acetaldehyde, it wouldn't surprise me much if including the false morel in a meal also containing a mushroom that packs coprine, such as Coprinus atramentarius, the common ink cap, which inhibits aldehyde dehydrogenase, and will make you damn sick, although won't kill you, fungal disulfiram basically by mode of action, might well make you sick in and of itself, having eaten ink caps with, or a day or two beforehand of consuming alcohol. (excluding the shaggy ink cap/lawyer's wig, C.comatus which doesn't contain coprine, or if it does, not significant quantities)

If you absolutely have to eat them....don't travel in a closed car with them, and don't carry them home in a vehicle also carrying a pet animal, ideally, strap them to a roof-rack in a container, if you haven't got one, put them in the boot, in a bag, and open all the windows as wide as they can go. Likewise, don't cook them in an enclosed kitchen, as the toxin is cooked off by repeated parboiling, it can, and has killed people before. There have been cases where the chef cooked them, but ate none, but got gassed in his/her kitchen making them ill, or killing them.

If they are to be dried for future use (this was at one time thought to reduce the gyromitrin levels to safe quantities, this is incorrect, and dried false morels must be treated just the same, rehydrated in water, which must be gotten rid of somewhere safe, then repeatedly boiled and the water changed several times just as fresh ones would have to be treated, and after this, then cooked in the meal.

I include the cooking instructions here for the sake of safety only, my stance is that they should never be eaten, and the instructions, are there for if somebody is determined to eat false morels, or any of the other species I will list as containing gyromitrin, then they should at least know how to prepare them. Take note of the fact I didn't say 'how to prepare them safely'.

In cases of poisoning by the fumes while cooking, it acts much faster than it otherwise would do, there can in some cases of oral ingestion leading to poisoning, be a delay, like there is with the death cap and other amatoxic species of 6-8 hours before onset of severe symptoms, not always, but sometimes. Via inhalation it is likely to be MUCH faster, maybe even while they are still being prepared.

Notable species which contain MMH/gyromitrin are:

Gyromitra esculenta (the false morel)
G.infula (the lobed false morel)
Probably G.gigas, and the other Gyromitra spp.

Helvella species (interesting tidbit-if you hold a Helvella to your ear, you can hear them hissing and crackling when they are at the stage where they are releasing spores, due to the way they are fired from the asci)

Verpa species also, notably V.bohemica and probably V.conica.

Sarcosphaera coronaria (this apparently also bioaccumulates arsenic...yum yum)

I think certain Pezizza species also contain the stuff (Sarcospharea is a monotypic genus now, with the other species being reclassified in this genus)

[Tsathoggua]

Section III: Muscarine, and its many hideouts in the fungal world

Many of you guys may well already be familiar with muscarine. This quaternary ammonium-based neurotoxin was the ligand for which the muscarinic type of  the acetylcholine receptor family was named. Along of course, with the nicotinic acetylcholine receptor, no prizes for guessing where that got its name from...

There are a great many macrofungal basidiomycete species which contain muscarine, its not very pleasant stuff, but it has at least, some redeeming features. Number one amongst them, is the fact that unlike most fungal toxins, such as amatoxins, orellanine (coming up in the next installment) and the other various GI irritants, neurotoxins and what have you, there exists a specific antidote to muscarine poisoning. The muscarinic acetylcholine receptor antagonist, or anticholinergic, in the common parlance, atropine.

Yup, the same drug that comes from deadly nightshade, otherwise known as belladonna, a real beauty of a plant, although highly poisonous. Atropine in small doses can be used to directly reverse the effects of muscarine. However, there exists another remedy, if one should get the wrong mushrooms, and be poisoned by muscarine containing fungi, some medications for irritable bowel syndrome, buscopan being the one I know of, although atropine methylnitrate is available I believe. Buscopan is OTC in the UK at least, and available online. Its scopolamine/hyoscine, another potent anticholinergic, but in the form of the butylbromide quaternary ammonium derivative, just like muscarine itself, being a quat, its charge, and cannot pass the blood-brain barrier, so will not exert central symptoms, both it and muscarine are restricted to the peripheral nervous system.

Atropine isn't nice stuff, it will give you the drymouth from hell, increase your heart rate (muscarine will usually slow it down), make it nigh on impossible to take a piss, blur your vision, and too much will make you go stark raving batshit crazy, and probably result in your being arrested, after being found sitting in the road, thinking you are playing poker with glow in the dark space pigeons, whilst in actuality, you are legging it arse naked down the road, chewing on a little old lady's arm as if it were a sausage sandwich.

The butylbromide of scopolamine/hyoscine cannot do that, it can't penetrate the CNS, so at worst, the peripheral symptoms, if too much is given,would present, but the anticholinergic deliriant psychosis will not.

The signs of muscarine poisoning, and there are a great many mushrooms it is found in a wide range of mycoflora, from Inocybe, to Boletus species, lead to what clinicians know by the acronym SLUDGE.

Salivation, Lachrymation, Urination, Defacation, G.I upset, and Emesis.

So you drool like a catholic priest in a nursery, you can't see shit for your eyes are watering like crazy, you piss yourself, shit yourself, whilst feeling awfully sick and with severe stomach pains, and to top it all off, you are continuously throwing up, until there is nothing left to throw but your innards.

The good news, is you are very, very unlikely to die. Its treatable, easily so, and it will teach you a thorough lesson in why you should be paying attention to whats going in that mushroom soup.

Also presenting will be pronounced miosis (contraction of the pupils of the eye to pinpoints, just as opioids do, but more so), sweating, running of the nose, bradycardia, muscle spasms/jerking and difficulty breathing.

Present in a great many fungi, including, most famously, Amanita muscaria, hence the species epithet. Muscarine was long thought to be the primary toxin in this species, and the related ones such as the panther cap, and other similar fungi in the genus Amanita, subsection Amanita. Not so, however, as there are only tiny fractions of a percent in the fly agaric, enough to cause some sweating, and tearing of the eyes, and pupil constriction if ones strain is one that is relatively high in muscarine, but without exception, ibotenic acid and muscimol (ibotenic acid being a glutamatergic neurotoxin, which on heat curing, decarboxylates to muscimol) is the primary toxin, or depending on who is writing, and who is harvesting the mushrooms, the desirable compound/active drug. Atropine should NOT be given if somebody is actually genuinely poisoned by psychoactive Amanitas. The result will not be pleasant. Buscopan in small doses can be used however, to counteract any muscarinic side effects and allow for an un-tainted, more pleasant experience with the fly agaric.

Many, possibly most of the genus Inocybe on the other hand, contain, as opposed to the merest traces in fly agarics, maybe up to 3-4 percent of total weight in muscarine, and are real nasty little buggers. Most of them are little brown nondescript mushrooms, commonly known as the fibercaps, I know of not one single member of this genus that is fit for the table, although a small handful are psychedelic, and contain psilocin/psilocybin, and one, Inocybe aeruginescens, contains a rather unusual structure for a tryptamine, the sole known source of the alkaloid aeruginescin, the n,n,n-trimethyltryptammonium derivative of psilocybin. Won't pass the BBB, and as far as I know, it is a highly potent 5HT3 agonist, which is the polar opposite of the mode of action of some very efficient antiemetic/antinauseant drugs, which makes me think, that this particular shroom might well cause very, very severe nausea and vomiting if used recreationally.

That little off-topic niblet of info aside, back on track.

Other fungi containing muscarine in significant amounts, are certain Clitocybe species, notably C.dealbat and C.rivulosa, both of these are highly toxic, and potentially lethal. Some boletus species also contain it, in general, unless you know exactly what you are doing whilst identifying your finds, avoid eating any bolete with red pores (the peppery bolete, Chalciporus piperatus is an exception, its quite easy to identify visually, by habitat, growing in association with the silver birch, just as fly agarics do, indeed, often growing alongside them, and the fact that nibbling a tiny piece of peppery bolete between your teeth on the tip of your tongue, will reveal an intense burning, peppery chilli-fire heat, and the pores of this species are a dull brownish red, whereas the majority of poisonous Boletus species are of a bright, intense vivid red color)

A specifically notable bolete that has a load of muscarine within, is Boletus pucherrimus. This little bastard, whilst looks beautiful, is HIGHLY poisonous, and on one occasion, has caused death, the cause of death in the husband, of a man and wife who ate it, was an infarct of the mid-gut, which is highly atypical of muscarine poisoning however. It is in there....but, some boletes, as I will come to in a later section, contain some potent cytotoxic proteins, which would be much more likely to be responsible.

Most of these toxic boletes bruise bright blue or blue-purple, a characteristic also shared by the Psilocybin mushrooms in many cases. These are NOT psychoactive, some contain muscarine, and some contain cytotoxic lectins, some have both, and none should be eaten. There are a handful of species fitting this description which can be eaten, some must, must be cooked, although I do not reccomend it at all, due to the risk of misidentification, and the dubious edibility of them in the first place.

More hosts for this toxin include certain Mycena species, Omphalotus (most of these, the jack'o'lanterns, glow in the dark, and contain in addition to muscarine, some rather unpleasant terpenoids) and a few other minor species of lesser interest.

I think, that concludes this chapter, there isn't much more I can say about it, if I think of anything to add though, I will do. For now, I shall bugger off, and plan what to add next. Orellanine, the insidious, slow-acting bipyridyl nephrotoxin of the deadly webcaps, I think.

[Hawkwind]

Very impressive post!

Gary Lincoff, author of the Audubon guide, tells a story about how he ate A. muscaria in the United States for years and never got off.  While in a berry and Amanita patch in Russia surrounded by bears, he got down on the ground like a bear and started eating them, and hasn't come down since.

[Tsathoggua]

Awful, awful, rotten idea to try eating them raw, Possibly quite a lot worse doing so surrounded by bears. They don't just shit in the woods, get 'em pissy and they rip people's faces off in the woods too:D

And thanks. Its still a work in progress. I have to cover orellanine, T2 toxin, satratoxin-H (these are almost exclusively a product of unicellular moulds, but there is one macrofungus that contains both, and has been responsible for whacking a few japs that messed with it, And then the cytotoxic lectins in Boletus species, a couple of terpenoid nasties, and a couple of hitherto thought great edibles, that in fact, contain a rather vicious, demyelinating neurotoxin of a most unusual structure to find in nature, After that, just sudden yunnan death syndrome, the mushroom/barium connection, polyporic acid, fasiculol derivatives and the Tricholoma/Russula myotoxins. That I can think of, probably I will think of more. I'm shattered right now, been busy slaving my arse off welding stuff all day and oh boy, the heat, the sodding heat...One ice cold can of rocket fuel-grade lager and I dare not take any chlormethiazole, which I was otherwise intending to do (damn do I ever have a neat doctor, all I had to do was ask to be changed from a benzo script to a barb-sensitive GABAa binding site ligand, and the only question was 'which one do you want', previously, without any benzo tolerance, and maybe fortnightly use, or two doses in two weeks now and then, but even up to 60-70mg nitrazepam scarcely touches me, one capsule of chlormethiazole on the other hand, and as long as I take an antihistamine with it, to prevent the rather odd side effect of a sharp, very localised pain behind the bridge of my nose, its as effective as a hammer to the back of the neck, but a whole lot more pleasant:D....best give it a few hours, if I can even stay awake for ten minutes longer, seeing as how one drink affected me after *working my furry autie arse off all day in the blazing heat, welding torch lit non stop in a small, very well insulated shed....)

Fuck...won't be working on this tonight, thats for sure.



(*figuratively speaking, its not THAT furry

[Hawkwind]

Awful, awful, rotten idea to try eating them raw, Possibly quite a lot worse doing so surrounded by bears. They don't just shit in the woods, get 'em pissy and they rip people's faces off in the woods too:D

I didn't get a chance to talk to Gary, but I think he would agree with you on both the advisability of cooking mushrooms (even Agaricus) and avoiding bears.  The great psychedelic rangers sometimes get a little carried away (some on this board may resemble that remark) and sometimes can be idiot savants.

Here's another reason I like Gary (besides co-discovering P. tampanensis with Pollock).  After the drum circle and dance at the mycology conference, the party started thinning out in the common area about 2 a.m.  At 4 a.m. I looked around, turned to the guy sitting next to me and said, "you know, now we're down to my kind of people."  And in walked Gary with big eyes (I of course assumed he's just an insomniac or night owl).

And thanks again to C**** for that garbage bag full of P. weilii he brought to the conference for early bioassays.  Of course I didn't try any, I'm just an insomniac and night owl. . . .

[Sedit]

Tsathoggua or anyone else for that matter do you have information on an orange/yellow mushroom that grows relatively low to the ground with an inverted cap, its a zonate shape if I understand this correctly? Its bruising blue/violet with a touch of green due to the skin color, its a meaty mushroom. It was found in a cedar tree forest.

I thought possibly a gymnopilus species hence my interest in it in the first place but I now don't think that it is.

It looks similar to Lactarius porninsis photos I have seen yet the stalk is very thick and I know of no Lactarius which bruises blue. It has a faint smell but others have noted it to have a much stronger smell claiming it to smell like rotten milk . Im also looking into canthearellus species but once again I know of no bluing reaction in these.

I wish I could provide more details and a photo but its not in the best of shape and in even worse shape since I have been cutting it and examining it so I will have to wait till I find another sample to photograph.

Can you think of any mushrooms off the top of your head that semi fits this description and is poisons?

[Sedit]

The more I look the more I think what I found might be a chanterelle mushroom. They like the type of forest it was in, its the right time of year the color is pretty much dead on, I have found similar ones around that are white instead of yellow however so that confuses me. At the same time I have seen Gym species that look relatively similar.

It still does not explain the mild bluing that occures as this does not happen in chanterelle mushrooms. Its a faint bust distinct blue that fades over time to rusty brown I guess you would call it.