Poisonous Mushrooms
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Foodborne Illnesses

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  Background
Amanitin poisoning
MHH poisoning
Orellanine poisoning
Coprine (antabuse-like) poisoning
Muscarine posioning
Ibotenic Acid-Muscimol Poisoning
Psilocybin-Psilocin poisoning
Gastro-Intestinal Irritants
 
 
 
 
. Background:    
  Many epicureans delight in the exquisite taste of mushrooms owed largely to their unique texture and succulence.    There is ,however, a more odious role for fungi which cast quite a darker shadow.    Mycotoxicosis is a disease with many origins all of which share a common denominator which is illness (and even death) as a direct result of toxic ingestion of mushroom and mold toxins (both of which are members of the Fungi Family) that act upon the central nervous system, liver, gastrointestinal tract, bone marrow, or kidneys.   
 
 
  Amanitin poisoning  
 

     The number one cause of mycotoxicosis is the consumption of wild mushrooms by so- called mushroom hunters many who have tempted fate by mistaking a harmful and relatively innocuous mushroom for a lethal one.   The deadliest of these is Amanita virosa (infamously referred to as the 'Destroying Angel') found in eastern N. America or Amanita phalloides ('The Death Cap'), found in the west and whose cap is lethal even in small quantities.   The toxins from these mushrooms come in two forms, known as the amatoxins (amanitans) and the phallotoxins (phalloidins).   In fact, it is estimated that the phallotoxins are ten times more lethal than cyanide when injected.  Fortunately, stomach acids break down or neutralize the majority of these toxins.   On a more grim note, amatoxins are not inactivated by digestive juices and remain quite deadly.  These amatoxins rapidly damage intestine, kidney, and liver.   Furthermore, amatoxins are known to bind cellular machinery which ultimately blocks protein synthesis bringing the machinery of the cell to a grinding halt.   This is a major problem for cells of the liver, kidney and gastrointestinal tract which have a high turnover rate.  Lastly, there is no antidote and symptoms occur late after much of the damage is already done.  

Treatment for Amanita poisoning is comprised of attempts at: (1) removing the toxin from the body by haemodialysis, haemoperfusion, and apheresis (2) increasing the rate of excretion, and (3) supportive measures.

 
 
 
  MHH poisoning  
       The  morel (Morchella esculenta) is a prized delicacy which complements steak and a good red wine.   Their uncanny resemblance to the false morel (Gyromitra esculenta) has caused many inadvertent poisonings for untutored mushroom hunters unfortunate enough to chance upon them.   In fact, it is thought that as many as 4% of fatal mushroom poisonings are a result of eating these.  The precursor toxin secreted by this mushroom is called gyromitrin and is hydrolyzed into MMH which incidentally is used as rocket fuel and is extremely toxic.  Symptoms of poisoning appear 2-12 hours (usually about 6 hrs) after a meal.   An initial bloated feeling is surpassed by nausea, vomiting, diarrhea, fever and abdominal cramps.  Some victims lose control of their muscles and in the most severe cases, jaundice, convulsions, coma and death may ensue 7 days post- ingestion.  Affected internal organs include the central nervous system, the liver, and the gastro-intestinal tract.

Treatment:   include evacuation if caught right away, otherwise piridoxine hydrochloride should be administered as a specific physiological antagonist.   Supportive measures may be needed.

 
 
 
  Orellanine poisoning  
       Death by kidney failure has been linked to the fatal consumption of yet one more toxic mushroom Cortinarius orellanus.  Poisoning by this european mushroom  is different than many other toxigenic mushrooms in that it has a slow onset and even severe cases rarely present symptoms for 3-4 days after being consumed.   In milder cases, the latency can extend to 10-17 days.   Most deaths associated with these poisonings occur as a result of kidney failure and in most cases occur after 2 or 3 weeks (in rare cases this can extend to months).  While no confirmed cases exist in North America numerous cases have been described in Poland, France, Germany, Switzerland, and Czechoslovakia.

Symptoms: initial intense thirst, accompanied by burning and dryness of the mouth, headache, chills, abdominal or loin pain, nausea, vomiting.   One of the clinical features is an increased BUN (blood urea nitrogen) which is common for kidney failure.

 
 
 
  Coprine (antabuse-like) poisoning  
  There are anecdotal reports that workers at a rubber plant  routinely exposed to the anti-oxidant disulfuram could no longer hold their liquor quickly becoming ill.   Further analysis of this compound revealed physiological evidence of a much altered response to alcohol and subsequently provided the basis for its use in treating chronic alcoholism.  Coprinus atramentarius produces a similar effect and has an onset of seven days.   Coprine, the causal agent blocks alcohol metabolism causing an accumulation of acetaldehyde.   Thus, the symptoms present are actually a result of acetaldehde poisoning.  Curiously, the mushroom itself is not toxic by itself and only elicit an effects after it is mixed with alcohol.    Symptoms experienced by one unfortunate to mix these two substances involve hot flashes, a metallic taste, tingling limbs, numbness in the hands, palpitations, throbbing headache, nausea, and vomiting.   The good news is that much like a hangover, the symptoms will abate and this condition is not fatal.  
 
 
 

Muscarine poisoning

 
  Some members of two common genera, Clitocybe and Inocybe, contain significant amounts muscarine.   Muscarine poisoning rarely fatal although it can be fatal if large enough quantities are consumed.  After 30 minutes to 2 hours the exocrine glands (producers of perspiration, salivation, and lacrymation) are potently stimulated, accompanied by constriction of pupils, blurred vision, muscle spasms, diarrhea, slow heart beat, and a drop in blood pressure.    A successful treatment regime normally involves careful administration of atropine, a drug which antagonizes the activity of muscarine.  
 
 
  Ibotenic Acid-Muscimol poisoning  
       

The beloved Amanita muscaria may be best recognized by its fairy-tale like features.  Perhaps it is the red cap containing bubbly white circles which has captured the imaginations of many.  Amanita was in fact discovered long ago, and my numerous cultures.  Its popularity as a religious or recreational intoxicant was celebrated in both the ancient soma hymns of the sacred Indian book, the Rig Veda, as well as in certain Siberian tribes.   

The Siberians learned early on that the principal intoxicant could be recycled.   This they learned through the observation that reindeers, who normally have a fondness for urine, can be intoxicated simply by lapping up the urine of affected reindeer.   As unappealing as it may sound to most, this behavior actually came in handy for poor tribesman who could not afford the mushrooms when they were scarce and would actually wait to drink the urine of their more affluent yet inebriated brethren.

While fresh mushrooms are psycoactive, the dried mushroom is far more potent.  This can be explained by the fact that as ibotenic acid degrades, the product muscimol is 5-10 times as active.   Death from overdose is uncommon, but can occur from ingestion of about 10 caps.  Recover from the average 'trip' is complete and treatment is usually unnecessary unless many have been eaten.  Under these circumstances it is advised that the stomach be evacuated, convulsions treated pharmacologically, and the atropine not be administered.

 
       
 
        Psilocyin-Psilocin poisoning  
       

Classic tales of mycology tell of two Americans who managed to penetrate the wall of silence between the ancient Aztec "Oaxaca" people.   These people were ostracized by Christian Spanish Conquistadors for their use of hallucinogenic mushrooms used during their rites of divining and curing.   As these rites were practiced for the first time in hundreds of years in front of non-oaxacans the secret of 'Teonacatl' - the flesh of the gods- was released.   Participating in the shamanic ritual, the scientists ate these magic mushrooms and what followed was history.   As the hallucinations slowly began kaleidoscopic images transformed through space, time and reality followed by emotions of euphoria and peace.   The effects lasted a total of four and a half hours followed imperceptibly by deep somnolescence.

Four agaric genera including Psilocybe (most commonly used in Mexico), Panaeolus, Conocybe (coastal US and British Columbia), and Gymnopilus.  Psilocybe cubensis are often cultivated and in fact these spores are often purchased by mail order.  Other species of Psilocybe, most notably P. semilanceata and P. pellicula (these two are known as 'Liberty Caps').

The principle psycoactive compounds are psilocybin and psilocin, which are derivatives of a common neurotransmitter, serotonin.    2 grams of mushroom is considered the average dose and even though the hallucinogenic effects are overwhelming though they rarely cause serious poisoning (unless large numbers are consumed).   Though treatment is usually unnecessary it may prove useful to provide reassurance or tranquilizers for adults on so-called "bad trips".  Children don't tolerate these mushrooms as well as adults do and may develop a high grade fever or suffer convulsions.  Treatment of  seizures imay involve the use of chlorpromazine, and the fevers should not be treated with aspirin but instead these children should be kept cool with mildly cool water or wet towels. 

 
       
 
        Gastro-Intestinal Irritants  
           
       

 
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