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Gyromita species

1. NAME
   1.1 Scientific name
   1.2 Family
   1.3 Common name(s) and synonym(s)
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First aid measures and management principles
   2.5 Poisonous parts
   2.6 Main toxins
3. CHARACTERISTICS
   3.1 Description of the fungus
      3.1.1 Special identification features
      3.1.2 Habitat
      3.1.3 Distribution
   3.2 Poisonous parts of the fungus
   3.3 The toxin(s)
      3.3.1 Name(s)
      3.3.2 Description, chemical structure, stability
      3.3.3 Other physico-chemical characteristics
   3.4 Other chemical contents of the fungus
4. USES/CIRCUMSTANCES OF POISONING
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstances
   4.3 High risk geographical areas
5. ROUTES OF EXPOSURE
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological halflife by route of exposure
   6.4 Metabolism
   6.5 Elimination and excretion
7. TOXINOLOGY
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Relevant Animal data
      7.2.3 Relevant in vitro data
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological Analyses and their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple Qualitative Test(s)
         8.2.1.2 Advanced Qualitative Confirmation Test(s)
         8.2.1.3 Simple Quantitative Method(s)
         8.2.1.4 Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple Qualitative Test(s)
         8.2.2.2 Advanced Qualitative Confirmation Test(s)
         8.2.2.3 Simple Quantitative Method(s)
         8.2.2.4 Advanced Quantitative Method(s)
         8.2.2.5 Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
   8.6 References
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 Central nervous system (CNS)
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid and electrolyte disturbances.
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic/specific treatment
   10.3 Decontamination
   10.4 Enhanced elimination
   10.5 Antidote/antitoxin treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
12. Additional information
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S) DATA (INCLUDING EACH UPDATING), COMPLETE ADDRESSES



    GYROMITA SPECIES

    International Programme on Chemical Safety
    Poisons Information Monograph (Group monograph) G029
    Fungi

    Please note that further information on Sections 1,  3 and 8 is
    pending.

    1.  NAME

        1.1  Scientific name 

             Species known to cause poisoning include:

             Gyromita esculenta
             Gyromita ambigua
             Gyromita infula

             Species suspected of causing poisoning include:

             Gyromita gigas
             Gyromita fastigiata
             Gyromita californica
             Gyromita sphaerospora

             The main toxin is Gyromitrin.

        1.2  Family

             Helvellaceae.

        1.3  Common name(s) and synonym(s) 

             Brain Mushrooms;
             Elephant's Ears;
             Beefsteaks;
             False Morels;
             Lorchels;
             Frulingslorchel" ("Spring Gyromitra")  [German];
             Spugnola bastarda" ("Inferior or False Sponge") [Spanish];
             Uchac obecny" [Czechoslovakian];
             "Piestrzenica kasztanowata" [Polish];

             For the fungus  Gyromitra esculenta, some of the
             international common names include:

             Smrz obecny [Czech];
             Korvasieni [Finnish];
             Fausse morille [French];
             Gyromitre comestible[French];

             Morillon moricaude [French];
             Lorchel [German];
             Fruhjahrslorchel [German];
             Laurich [German];
             Verdachtige [German];
             Marugola [Italian];
             Tobiiro-noboririo [Japanese];
             Shaguma-amigasatake [Japanese];
             Piestrzenica kasztanowata [Polish];
             Usiak obycajny [Slovakian];

    2.  SUMMARY

        2.1  Main risks and target organs 

             Liver, nervous system, and gastrointestinal tract.

        2.2  Summary of clinical effects 

             Nausea, abdominal cramps, gassy feeling, vomiting, and
             watery diarrhoea.  In severe cases one might see the
             development of jaundice, seizures, liver failure, and coma. 
             Deaths have been documented from this fungal toxin!

        2.3  Diagnosis 

             The onset of symptoms usually follows a delay of 5 to 12
             hours post exposure.

        2.4  First aid measures and management principles

             Induction of vomiting, if early in the exposure. 
             Multiple dose Activated Charcoal to retard absorption.  Dose:
             adult = 50 to 100 grams, paediatric = 1 gram per
             kilogram.

        2.5  Poisonous parts 

             All parts of the fungus are potentially toxic.

        2.6  Main toxins 

             N-methyl-N-formylhydrazone acetaldehyde (also known as
             Gyromitrin), and its hydrolysis product Monomethylhydrazine
             (MMH), with a chemical formula of CH3-NH-NH2.

    3.  CHARACTERISTICS

        3.1  Description of the fungus

             3.1.1  Special identification features 

                    The surface of the fungus is generally colored
                    orange-brown to brown.  The flesh is usually brittle,
                    and a cross-section of the stalk (stipe) shows
                    chambered areas.
    
                    Species of Gyromitra are grouped with the
                    Ascomycetes, with their spores developing in a
                    sac-like structure ("ascus").  They are medium to
                    large fungi.  The surface is convoluted like a brain. 
                    The cap may also be saddle shaped in some
                    species.

             3.1.2  Habitat

                    Usually found growing on the ground or on
                    rotting wood.  These fungi are usually found in the
                    early Spring time (March-June).

             3.1.3  Distribution 

                    World wide distribution. Most fatalities have
                    occurred in Europe, with it being a major problem in
                    Eastern Europe.

        3.2  Poisonous parts of the fungus

             All parts are potentially toxic.  Cooking, freezing, or
             drying the fungal material may still leave significant
             concentrations of the toxin in the tissue.

        3.3  The toxin(s)

             3.3.1  Name(s)

                    N-methyl-N-formylhydrazone acetaldehyde (also
                    known as Gyromitrin), and its hydrolysis product
                    Monomethylhydrazine (MMH), with a chemical formula of
                    CH3-NH-NH2.
    

                    MMH is well known in the space industry as it is a
                    rocket fuel used to control the attitude of
                    spacecraft.  It was from the toxicological
                    investigations of potential worker related exposures
                    to MMH, that much became known of the toxicology of
                    Gyromitrin.

             3.3.2  Description, chemical structure, stability

                    The hydrolysis product MMH boils at 87.5
                    degrees Centigrade, and thus can produce toxic fumes
                    in the air, above the cooking utensils, which may
                    effect the individual preparing the fungi for
                    consumption.   It is believed by many consumers of
                    this fungus, that by cooking them in two changes of
                    water, it renders them toxin free.  However, multiple
                    cases of toxic patients who have cooked them in this
                    manner, and still become toxic, renders this a
                    probably fallacy!

             3.3.3  Other physico-chemical characteristics

                    No other data available.

        3.4  Other chemical contents of the fungus 

             None of importance.

    4.  USES/CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    This fungus is collected for food, with almost
                    all collectors knowing exactly what they have
                    collected.  The problem arises from the fact that they
                    refuse to believe that these fungi contain a toxin
                    which may be harmful to them or others.

        4.2  High risk circumstances

             Individuals collecting wild fungi for consumption, or
             for commercial purposes.

        4.3  High risk geographical areas 

             Europe, North America.

    5.  ROUTES OF EXPOSURE

        5.1  Oral 

             This is the most common route of exposure.

        5.2  Inhalation 

             Inhalation of the volatile fumes during the cooking
             process may prove dangerous,

        5.3  Dermal

             Not applicable

        5.4  Eye 

             Not applicable

        5.5  Parenteral 

             Not applicable

        5.6  Others

             Not applicable

    6.  KINETICS

        6.1  Absorption by route of exposure 

             When ingested, there is generally a long latent period
             of 6 to 24 hours before symptoms appear.  If inhaled,
             symptoms may appear in 2 to 8 hours.

        6.2  Distribution by route of exposure 

             Information presently unknown.

        6.3  Biological halflife by route of exposure 

             Information presently not known.

        6.4  Metabolism 

             The toxin Gyromitrin is initially converted to
             N-methyl-N-formylhydrazine (MFH), which is ultimately
             converted to Monomethylhydrazine (MMH).

        6.5  Elimination and excretion 

             Exact routes are presently unknown.

    7.  TOXINOLOGY

        7.1  Mode of action 

             The nervous system is acted upon by MMH, through the
             interference of the normal utilization of Pyridoxine (Vitamin
             B6).  The main problem is that MMH exhibits the "all or none"
             phenomenon with respect to the development of symptoms.  Each
             individual has a unique threshold below which no symptoms
             appear.  Once their threshold has been exceeded, the patient
             is into full-blown toxicity.  The analogy of a light switch
             can be used to illustrate this phenomenon.  In toxicology,
             one would believe that if you increase the dose, you
             therefore increase the toxicity, the result of which is an
             increase in the exhibited symptoms.  In the case of MMH, the
             switch is not like a dimmer switch which can gradually
             increase or decrease the light (symptoms), but is more like a
             typical on-off switch, in which there is either light
             (symptoms) or none.  It is this phenomenon which probably
             allows the majority of individuals to consume this fungus and
             not exhibit any visible symptoms.  And then for some as yet
             unexplained reason, they exceed their individual threshold,
             and exhibit toxic symptoms.  It could be that the
             individualized threshold changes with the age of the
             individual, or maybe with the status of their physical
             health.  It could also be that the amount of toxin in the
             fungi differs from prior years due to some as yet unexplained
             effect (climate, substrate, and so on), which causes them to
             exceed their individualized threshold in this particular
             instance.
    
             Symptoms of MMH intoxication closely resemble those seen from
             intoxication by the drug Isoniazid (INH), which is also a
             hydrazine compound.

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             The lethal dose of Gyromitrin in
                             adults is estimated to be from 20 to 50
                             micrograms per kilogram.  MMH can be proven
                             to present by the use of gas liquid
                             chromatography (GLC).  A GLC method was
                             established by Pyysalo, Niskanen, and Stijve. 
                             The material is heated with water in a sealed
                             tube for several hours at 123 degrees
                             Centigrade, so that the chemically bound
                             poisons are also liberated.  Chloroform
                             extraction under Nitrogen is then carried
                             out, and the GLC analysis that follows
                             enables 10 micrograms of Gyromitrin to be
                             detected. 

                    7.2.1.2  Children 

                             The lethal dose of Gyromitrin in
                             children is estimated to be from 10 to 30
                             micrograms per kilogram.

             7.2.2  Relevant Animal data

                    See 7.3

             7.2.3  Relevant in vitro data

                    No other data available.

        7.3  Carcinogenicity 

             In experimental animals, MMH has been found to be
             carcinogenic, with an increase in the formation of malignant
             tumors.

        7.4  Teratogenicity 

             Found in experimental animals.

        7.5  Mutagenicity 

             MMH had been found to be carcinogenic and mutagenic in
             experimental animals.

        7.6  Interactions 

             Unknown

    8.  TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses 

                             In the majority of cases the fungus
                             will be readily identified by the patient. 
                             These cases are for the most part, NOT a case
                             of misidentification of the fungus. 
                             Therefore, an analysis of the suspected
                             fungus, in order to most appropriately treat
                             the patient, is NOT required.  Studies of
                             European specimens of this fungus, have found
                             that each kilogram of dried Gyromitra
                             tissue, may contain from 14.7 to over 6400
                             milligrams of the toxin Gyromitrin.  Other
                             studies have found that in fresh fungal
                             tissue, one may find from 1200 to 1600
                             milligrams of Gyromitrin per kilogram.
    
                             MMH can be proven to present by the use of
                             gas liquid chromatography (GLC).  A GLC
                             method was established by Pyysalo, Niskanen,
                             and Stijve.  The material is heated with
                             water in a sealed tube for several hours at
                             123 degrees Centigrade, so that the
                             chemically bound poisons are also liberated. 
                             Chloroform extraction under Nitrogen is then
                             carried out, and the GLC analysis that
                             follows enables 10 micrograms of Gyromitrin
                             to be detected (Bresinsky, 1990, page
                             10).

                    8.1.1.2  Biomedical analyses 

                             No data available.

                    8.1.1.3  Arterial blood gas analysis

                             No data available.

                    8.1.1.4  Haematological analyses

                             No data available.

                    8.1.1.5  Other (unspecified) analyses 

                             A microscopic examination of the
                             spores in a water mount, which may be
                             detected in recovered gastric contents, will
                             show one or two conspicuous oil droplets. 
                             The fruiting bodies may take several weeks
                             before they produced mature spores.

             8.1.2  Storage of laboratory samples and specimens

                    8.1.2.1  Toxicological analyses

                             No data available.

                    8.1.2.2  Biomedical analyses

                             No data available.

                    8.1.2.3  Arterial blood gas analysis

                             No data available.

                    8.1.2.4  Haematological analyses

                             No data available.

                    8.1.2.5  Other (unspecified) analyses

                             No data available.

             8.1.3  Transport of laboratory samples and specimens

                    8.1.3.1  Toxicological analyses

                             No data available.

                    8.1.3.2  Biomedical analyses

                             No data available.

                    8.1.3.3  Arterial blood gas analysis

                             No data available.

                    8.1.3.4  Haematological analyses

                             No data available.

                    8.1.3.5  Other (unspecified) analyses

                             No data available.

        8.2  Toxicological Analyses and their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

                    8.2.1.1  Simple Qualitative Test(s)

                             No data available.

                    8.2.1.2  Advanced Qualitative Confirmation Test(s)

                             No data available.

                    8.2.1.3  Simple Quantitative Method(s)

                             No data available.

                    8.2.1.4  Advanced Quantitative Method(s)

                             No data available.

             8.2.2  Tests for biological specimens

                    8.2.2.1  Simple Qualitative Test(s)

                             No data available.

                    8.2.2.2  Advanced Qualitative Confirmation Test(s)

                             No data available.

                    8.2.2.3  Simple Quantitative Method(s)

                             No data available.

                    8.2.2.4  Advanced Quantitative Method(s)

                             No data available.

                    8.2.2.5  Other Dedicated Method(s)

                             No data available.

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

                    8.3.1.1  Blood, plasma or serum

                    8.3.1.2  Urine

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

                    No data available.

             8.3.3  Haematological analyses 

                    A methaemoglobin (MeHb) level that is elevated,
                    is significant as a prognostic factor of a poor case
                    outcome.

             8.3.4  Interpretation of biomedical investigations

                    No data available.

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

             No data available.

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             No data available.

        8.6  References

             Not applicable.


    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    The gastrointestinal phase may include:
                    headache, vertigo, nausea, abdominal cramping,
                    bloated/gassy feeling, vomiting, and watery diarrhoea. 
                    Haemolysis may be observed.  In the more severe
                    hepatorenal phase,  one might see the development of
                    delirium, jaundice, seizures, liver failure, and coma. 
                    Deaths have been documented from this fungal
                    toxin!

             9.1.2  Inhalation 

                    Effects similar to ingestion.

             9.1.3  Skin exposure 

                    Not applicable

             9.1.4  Eye contact 

                    Not applicable

             9.1.5  Parenteral exposure 

                    Not applicable

             9.1.6  Other

                    Not applicable

        9.2  Chronic poisoning

             9.2.1  Ingestion 

                    Same as for acute exposures.
    
                    This type of exposure is NOT commonly a chronic
                    problem.  Although continually eating this fungus at
                    multiple meals, during its fruiting season, may force
                    the patient to exceed their personal threshold for
                    tolerance to the toxic chemical.

             9.2.2  Inhalation 

                    Effects similar to ingestion.

             9.2.3  Skin exposure 

                    Not applicable

             9.2.4  Eye contact 

                    Not applicable

             9.2.5  Parenteral exposure 

                    Not applicable

             9.2.6  Other

                    Not applicable

        9.3  Course, prognosis, cause of death

             The gastrointestinal phase may include: headache,
             vertigo, nausea, abdominal cramping, bloated/gassy feeling,
             vomiting, and watery diarrhoea.  In the more severe
             hepatorenal phase,  one might see the development of
             delirium, jaundice, seizures, liver failure, and coma. 
             Deaths have been documented from this fungal toxin!

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    No data available.

             9.4.2  Respiratory 

                    No data available.

             9.4.3  Neurological 

                    9.4.3.1  Central nervous system (CNS)

                             Seizures have been reported.

                    9.4.3.2  Peripheral nervous system

                             No data available.

                    9.4.3.3  Autonomic nervous system

                             No data available.

                    9.4.3.4  Skeletal and smooth muscle

                             No data available.

             9.4.4  Gastrointestinal

                    Nausea, vomiting, diarrhoea and abdominal
                    cramping.

             9.4.5  Hepatic

                    Damage has been documented, in the later stages
                    of the intoxication.  Hepatic coma has lead to
                    fatalities.

             9.4.6  Urinary

                    9.4.6.1  Renal

                             Damage has been documented.

                    9.4.6.2  Other

                             None known.

             9.4.7  Endocrine and reproductive systems 

                    Unknown.

             9.4.8  Dermatological 

                    Unknown.

             9.4.9  Eye, ear, nose, throat: local effects 

                    No data available.

             9.4.10 Haematological 

                    Methemoglobinemia and haemolysis may develop.

             9.4.11 Immunological

                    No data available.

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             No data available.

                    9.4.12.2 Fluid and electrolyte disturbances.

                             There may be electrolyte imbalances
                             produced by the excessive loss of body fluids
                             due to severe vomiting and
                             diarrhoea.

                    9.4.12.3 Others

             9.4.13 Allergic reactions 

                    Patients may exhibit allergic reactions to
                    these type of fungi, as well as other fungi.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks

                    Deaths have been documented!  This mushroom
                    toxin has a fatality rate second only to the more
                    highly toxic fungal Amatoxins.

        9.5  Other

             No data available.

        9.6  Summary 

             Nausea, abdominal cramps, gassy feeling, vomiting, and watery
             diarrhoea.  In severe cases one might see the development of
             jaundice, seizures, liver failure, and coma.  Deaths have
             been documented from this fungal toxin!

    10. MANAGEMENT

        10.1 General principles 

             If early in the exposure, it is advised that Activated
             Charcoal (DOSE: 50 to 100 grams in adults, 25 to 50 grams in
             children from 1 to 12 years of age, and 1 gram per kilogram
             in children under 1 year of age) be given to attempt to
             adsorb any toxin remaining in the gastro-intestinal tract. 

             The Charcoal should be administered without a cathartic, as
             the patient more than likely has, or will, develop a
             significant diarrhoea anyway.  All individuals with severe
             symptoms should be admitted to hospital for treatment and
             observation.

        10.2 Life supportive procedures and symptomatic/specific treatment

             Intravenous glucose for hypoglycemia, intravenous
             fluids to correct electrolyte imbalances, enhanced diuresis
             to avoid renal damage, and sedation where necessary.

        10.3 Decontamination 

             Activated Charcoal

        10.4 Enhanced elimination 

             Not applicable.

        10.5 Antidote/antitoxin treatment

             10.5.1 Adults

                    Pyridoxine (Vitamin B6) can be given, but ONLY
                    for life threatening symptoms (e.g. convulsions, and
                    coma).  The usual dose for adults and children is 25
                    milligrams per kilogram.  The dose is diluted at least
                    1:5 and given as an intravenous drip over 15 to 30
                    minutes.  The dose can be repeated, but should NOT
                    exceed 20 grams (for adults, less in children) per 24
                    hours.  A case has been documented,  in which an
                    excessive amount of Pryidoxine (132 and 183 grams,
                    over a 3 day period) was used to treat this type of
                    fungal intoxication, and which resulted in the
                    development of peripheral neuropathies in a husband
                    and wife (Albin et al., 1987).
    
                    Seizures should be controlled with an anticonvulsant
                    such as Diazepam, in the usual dosage as recommended
                    for such a condition.

             10.5.2 Children 

                    Same as for adults, with the proper
                    adjustments for paediatric dosages.

        10.6 Management discussion 

             Dialysis may be necessary if there is evidence of
             developing renal damage.  Throughout the treatment procedure
             the condition of the liver must be continually monitored and
             liver support given where required.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature 

             Case #12911912-91, from the regional poison centre in
             Grand Rapids, Michigan, USA, is illustrative of how a patient
             who has repeatedly eaten these fungi, can suddenly develop
             problems.  A 25 year old female, 4 months postpartum, with a
             history of eating "Beefsteak" fungi for years with no
             problems, became ill approximately 11 hours post ingestion. 
             Her initial symptoms consisted of some diarrhoea and episodes
             of vomiting, which continued for almost 22 hours.  The
             patient appeared jaundiced and was hospitalised for treatment
             of her immediate problems.  The patient was given
             Prochlorperazine for her vomiting, and complained of being
             dizzy and tired.  Laboratory values indicated a total
             bilirubin of 8.2 mg/dl (normal 1.1 mg/dl), conjugated
             bilirubin of 0.8, unconjugated bilirubin of 6.3 mg/dl, direct
             bilirubin of 1.9, SGOT 289 U/l, SGPT 228 U/l, blood sugar 152
             mg/dL, and a BUN of 20.  After observing the patient and
             providing symptomatic treatment, she was discharged from
             hospital after 3 days, with no apparent sequelae.
    
             Case #12914612-91, from the regional poison centre in Grand
             Rapids, Michigan, USA, involved a 70 year old man, who had a
             history of congestive heart failure (CHF).  He admitted that
             he had consumed "Beefsteak" fungi for 65 years with no ill
             effects.  One week after consuming some of these fungi, he
             was admitted to hospital with elevated liver enzymes: LDH
             15000, SGOT 4500, and an SGPT 2600.  The patient never
             experienced any vomiting, and only a slight jaundice was
             noted.  After 10 days hospitalisation, with observation and
             symptomatic care, he was discharged with no apparent
             sequelae.

    12. Additional information

        12.1 Specific preventive measures

             These fungi should NEVER be consumed.  It is truly a
             form of "fungal roulette"!

        12.2 Other

             Because of the possible unpredictable toxic outcome,
             these fungi should never be sold commercially for human or
             animal consumption!  It should also be noted that some
             species of mycological related fungi may also be toxic.  Some
             of these potentially toxic genera include: Helvella,
             Sarcosphaera,  Peziza, Disciotis, and Verpa.

    13. REFERENCES

        Albin RL, Albers MD, Greenberg HS et al. (1987) Acute sensory
        neuropathy from pyridoxine overdose, Neurology, 37, 1729-1732.
    
        Ammirati JF, Traquair JA, Horgen PA (1985) Poisonous Mushrooms of
        the Northern United States and Canada. University of Minnesota
        Press, Minneapolis, Minnesota, USA.
    
        Benjamin Dr (1995) Mushrooms: Poisons and Panaceas. W. H. Freeman
        and Company, New York, New York, USA.
    
        Bresinsky A, Besl H (1990) A Colour Atlas of Poisonous Fungi.
        Wolfe Publishing Ltd., London, England.
    
        Lincoff G, Mitchell DH (1977) Toxic and Hallucinogenic Mushroom
        Poisoning: A Handbook for Physicians and Mushroom Hunters, Van
        Nostrand Reinhold Co., New York, New York, USA.
    
        Rumack BH, Salzman E (1978)  Mushroom Poisoning: Diagnosis and
        Treatment, CRC Press, Boca Raton, Florida, USA.
    
        Smith-Weber N (1988) A Morel Hunter's Companion. Two Peninsula
        Press, Lansing, Michigan, USA.
    
        Spoerke DG &  Rumack BH (1994) Handbook of Mushroom Poisoning:
        Diagnosis and Treatment, CRC Press, Boca Raton, Florida,
        USA.

    14. AUTHOR(S), REVIEWER(S) DATA (INCLUDING EACH UPDATING), COMPLETE
        ADDRESSES

        John H. Trestrail, III, RPh, FAACT, DABAT
        Toxicologist
        Regional Poison Center
        1840 Wealthy, S.E.
        Grand Rapids, Michigan 49506, USA
    

        Tel: +1 616 774 5329
        Fax: +1 616 774 7204   
        E-mail: john.trestrail@spectrum-health.org
    
        REVISION DATED: August 23, 2000
    
        REVIEWER(S):
    
        *    Dr Barbara Groszek, Dr John Haines, Dr Johan Holmdahl, Dr
             Jenny Pronczuk and Dr John Trestrail (Meeting on Mushroom
             Poisoning, 19-21 October 2000, Stockholm, Sweden). 
    
        *    Dr B. Groszek and Dr H. Persson (INTOX-12, 6-11 November
             2000, Erfurt, Germany.