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Aminita muscaria, Amanita pantherina and others

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
    AMINITA MUSCARIA & AMANITA PANTHERINA
    AND OTHERS

    International Programme on Chemical Safety
    Poisons Information Monograph (Group monograph) G026
    Fungi

    Please note that further information on Sections 1, 3.1, 3.2 and 8 is
    pending.

    1.  NAME

        1.1  Scientific name

             Species of the genus Amanita.  The species known to
             cause the majority of toxic exposures are: Amanita muscaria
             and Amanita pantherina.

             The toxins are all isoxazole derivatives.

             Other Amanita mushrooms contain the same toxins and
             induce similar toxicity:

             Amanita muscaria var. Kamtschatica Langsdorff ex. Fr.
             Amanita regalis (Fr.) R. Mre. (A. muscaria var. umbrina Fr.)
             Amanita muscaria var. formosa
             Amanita muscaria var. alba
             Amanita gemmata (Fr.) Bertillon
             Amanita velatipes Atk.
             Amanita cothurnata Atk.
             Amanita flavovolvata Sing.
             Amanita strobiliformis (Vitt.) Quel.
             Amanita pantherina (DC ex Fr.) Secr.
             Amanita pantherina multisquamosa
             Amanita pantherina velatipes
             Amanita pantherina pantherinoides
             Tricholoma muscaria

        1.2  Family

             Agaricaceae ( Agaricales)

             The genus is Amanita  (Amanitaceae)

        1.3  Common name(s) and synonym(s)

             Amanita muscaria

             English   Fly Agaric
             German    Fliegenpilz, Roter fliegenpilz
             Spanish   Falsa oronja, Amanita matamoscas
             French    Amanite tue-mouche,
                       Agaric aux mouches,
                       fausse oronge
             Italian   Ovulo malefico, Uovolaccio
             Polish    Muchomor czerwony

             Amanita pantherina

             English   Panther cap.
             German    Pantherpilz, Braunner Knollenblätterpilz
             Spanish   Amanita pantera, galipiermo falso
             French    Amanite panthère, Fausse golmelle
             Italian   Tignosa bigia, Tignosa regata, Agarico panterino
             Polish    Muchomor plamisty

    2.  SUMMARY

        2.1  Main risks and target organs

             The most frequent cause of intoxication is the
             consumption of Amanita muscaria by people who mistake it
             and ignore its toxicity. Amanita muscaria might also be
             ingested in order to obtain mind-altering effects.  The
             central nervous system is the major target organ.

        2.2  Summary of clinical effects

             Symptoms appear 30 to 90 minutes after ingestion and
             last usually for 6 hours but may persist for 12 to 24 hours. 
             The primary effects are central nervous system depression and
             stimulation, which may alternate.  Symptoms usually begin
             with drowsiness followed by a state of confusion, with
             ataxia, dizziness, euphoria resembling alcohol intoxication
             and may proceed to increased activity, illusions, or even
             manic excitement.
             These periods of excitement may alternate with periods of
             somnolence, deep sleep or stupor.  The illusions are
             primarily a misinterpretation of sensory stimuli.  The
             prognosis is usually good with symptomatic treatment.  Death
             from these mushrooms is extremely rare.

        2.3  Diagnosis

             Based upon history of ingestion and clinical features.

        2.4  First aid measures and management principles

             Treatment includes prevention of absorption of the
             toxins and treatment of the signs and symptoms of
             intoxication as they occur.  Atropine is not recommended.
             Induction of emesis is NOT recommended because of the
             potential central nervous system depression and seizures.
             There is no specific antidote for Amantia muscaria and
             Amanita pantherina poisoning.

        2.5  Poisonous parts

             All parts of the fruiting body of Amanita muscaria and
             Amanita pantherina are toxic.

        2.6  Main toxins

             The main toxins are: ibotenic acid, muscimol and
             muscazone. These three toxins are found in certain species of
             mushrooms throughout the world. They are related and are all
             isoxazole derivatives.

    3.  CHARACTERISTICS

        3.1  Description of the fungus

             3.1.1  Special identification features

                    Identification: Complete and precise
                    identification of the mushroom (if available) should
                    be accomplished by a mycologist.  If no mycologist is
                    available, colour photographs may be helpful for a
                    first identification. Identification is difficult when
                    the mushrooms have been altered by cooking, eating or
                    storage.
    
                    Description of Amanita muscaria
    
                    Cap:     8 to 12 cm diameter, occasionally over 20 cm;
                             conical when young, flattening in age;
                             viscid, adorned with white to pale yellow
                             warts or small patches.  This mushroom has a
                             variety of color variants, ranging from
                             yellow through orange, orange-red to
                             blood-red or scarlet.

                             The yellow, orange or orange-red caps 
                             (A. muscaria var. formosa) occurs in eastern
                             North America.  The scarlet cap 
                             (A. muscaria var. muscaria) occurs in western
                             North America, throughout Europe and
                             Asia.
                             Flesh firm, white throughout.
    
                    Gills     (lamellae): crowded, free or just touching
                             stalk, broad, white, minutely hairy
                             edges.
    
                    Stalk:   8 to 15 cm long, 20 to 30 mm thick enlarging
                             towards base and becoming bulbous; white,
                             covered with silky hairs.
                    Ring:     (annulus): large, membranous, white to
                             yellowish, median to superior, resistant
                             though margin usually frayed.
    
                    Cup       (volva): the remains of the volva are often
                             only 2 or 3 concentric rings above the bulb;
                             white to straw.
    
                    Spores:  white spore print (in mass); 8 - 11 by 6 - 8
                             microns, ellipsoid, thin walled, no amyloid
                             reaction.
    
                    Description of Amanita pantherina

             3.1.2  Habitat

                    Scattered or abundant, sometimes in fairy rings
                    under hardwoods and conifers from spring to
                    autumn.

             3.1.3  Distribution

                    These species are widely distributed throughout
                    the planet.  Amanita muscaria grows in summer and
                    autumn under coniferous and deciduous trees, from the
                    lowland up to the subalpine zone.  It occurs
                    practically all over the temperate and subtropical
                    zones in Europe, North Africa, South Africa, Asia,
                    Japan, Australia, North America (in the Western States
                    of the USA more often than in the Eastern States) and
                    in South America.  (Seeger & Stijve, 1978).

        3.2  Poisonous parts of the fungus

             All parts of the fruit body of A. muscaria are toxic. 
             The isoxazoles are NOT distributed uniformly in the mushroom.
             Most are detected in the cap of the fruit, then in the base,
             with the smallest amount in the stalk (Lampe, 1978; Tsunoda
             et al., 1993).  Drying A. muscaria in the sun or with
             heater caused an increase of muscimol in the mushroom, though
             a lot of precursors of ibotenic acid was lost.  Ibotenic acid
             and muscimol in the mushroom were stable on storage under dry
             or salt conditions (Benedict et al., 1966; Tsunoda  et al.,
             1993).
             Whilst ibotenic acid and muscimol are rapidly released from
             the mushrooms by cooking and boiling, these processes do not
             eliminate all toxic substances.

        3.3  The toxin(s)

             3.3.1  Name(s)

                    The main toxins are: ibotenic acid, muscimol
                    and muscazone.
    
                    These three toxins are found in certain species of
                    mushrooms throughout the world.  They are related and
                    are all isoxazole derivatives (Eugster, 1979). 
                    Ibotenic acid and muscinol are mainly responsible for
                    the toxic effects (Takemoto et al., 1964; Bowden and
                    Mogey, 1965; Eugster et al., 1965; Muller and Eugster,
                    1965).

             3.3.2  Description, chemical structure, stability

                    Ibotenic acid and muscimol have similar
                    structure to glutamic acid and GABA (Krogsgaard-Larsen
                    P. et al., 2000).

                    Muscimol

                    CHEMICAL NAME: 3-Isoxazolol, 5-(aminomethyl)-
                    CAS REGISTRY NUMBER: 2763-96-4
                    SYNONYMS:
                             3(2H)-ISOXAZOLONE, 5-(AMINOMETHYL)-3-
                             HYDROXY-5-AMINOMETHYLISOXAZOLE
                             3-Hydroxy-5-aminomethylisoxazole-agarin
                             3-HYDROXY-5-AMINOMETHYLISOXAZOLE-AGARIN
                             AGARIN
                             5-(Aminomethyl)-3(2H)-isoxazolone
                             5-(Aminomethyl)-3-isoxazolol
                             5-Aminomethyl-3-hydroxyisoxazole
                             5-Aminomethyl-3-isoxyzole

                             Agarin
                             AGARINE
                             Muscimol
                             Pantherin
                             PANTHERINE
                             RCRA waste number P007
                    OTHER NUMBERS: 6036
                             NIOSH/NY3325000
                             NY3325000
                             (Ref: IPCS INTOX CD-ROM, 2000, 1)
    
                    Ibotenic acid
    
                    CHEMICAL NAME: 5-Isoxazoleacetic acid,
                    alpha-amino-3-hydroxy-, monohydrate
                    CAS REGISTRY NUMBER: 60573-88-8
                    SYNONYMS
                             alpha-Amino-2,3-dihydro-3-oxo-5-
                             isoxazoleacetic acid
                             alpha-Amino-3-hydroxy-5-isoxazoleacetic acid
                             hydrate
                             alpha-Amino-3-hydroxy-5-isoxazolessigsaure
                             hydrat
                             Amino-(3-hydroxy-5-isoxazolyl)acetic acid
                             Ibotenic acid
                             Ibotensaeure
                             Isotenic acid
                             Pramuscimol
                    OTHER NUMBERS
                             NY2100000
                             (Ref: IPCS INTOX CD-ROM, 2000, 1)

                    The toxins are thermostable and are NOT destroyed by
                    cooking.

             3.3.3  Other physico-chemical characteristics

                    Molecular weight:
                    Ibotenic acid:          176.15
                    Muscimol                114.12

        3.4  Other chemical contents of the fungus

             Bufotenine (Waser, 1979)
             Amavadin: a vanadium compound (Kneifel et al, 1986).
             Stizolobic and Stizolobinic acid: L-DOPA oxidation products
             (Chilton et al. 1974; Bresinsky & Besl, 1985).
             Muscaflavin, Muscaurin: colorant principles (Depovere & Moens
             1984)
             Muscarine (Eugster, 1979)

    4.  USES/CIRCUMSTANCES OF POISONING

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Amanita muscaria and Amanita pantherina are
                    not and have not been used in medical practice.
    
                    In the past it has been used in different populations
                    and cultures as a fly-killer and an inebriant
                    (Siberia), an ecstasy agent (India), and a
                    hallucinogenic (Indian peoples of Meso-America).  In
                    Japan, a derivative of muscinol is presently being
                    used as a pesticide.  An extract of ibotenic acid has
                    been found to be some 20 times more powerful than
                    monosodium glutamate as a flavour enhancer (Wasson,
                    1964, 1968, 1972, 1979).

        4.2  High risk circumstances

             The most frequent course of intoxication is the
             consumption of Amanita muscaria and Amanita pantherina by
             people who mistake it and ignore its toxicity.  Amanita
             muscaria and Amanita pantherina might also be ingested in
             order to obtain psychotic effects and especially to expand or
             alter spatio-temporal awareness.
             Death from this kind of mushroom is rare, or rarely reported. 
             If so, it is due to complications.  However, it would be
             unwise to consider eating them because the toxins are
             complex, variable in quantity, and not completely
             understood.

        4.3  High risk geographical areas

             These species are widely distributed throughout the
             planet.

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Ingestion of mushrooms is the most common cause of
             intoxication.

        5.2  Inhalation

             No data available

        5.3  Dermal

             No data available

        5.4  Eye

             No data available

        5.5  Parenteral

             No data available

        5.6  Others

             No data available

    6.  KINETICS

        6.1  Absorption by route of exposure

             Based on the time of onset of clinical symptoms, the
             rate of absorption of the toxins of Amanita muscaria and
             pantherina from the gastro-intestinal tract seems to be
             rapid. However, the exact rate and the proportion of
             absorption is still unknown.

        6.2  Distribution by route of exposure

             Muscimol and ibotenic acid, presumably cross the
             blood-brain barrier via some active transport system. 
             Neither muscimol nor ibotenic acid is removed from the
             receptor by the GABA or glutamate active uptake system. 
             Inefficient removal of these false neurotransmitters once
             they have passed the blood-brain barrier may be an important
             contributing factor to their central nervous system effect
             (Balcar & Johnston, 1972; Kronsgaard-Larsen & Johnston, 1975,
             2000).

        6.3  Biological halflife by route of exposure

             Both ibotenic acid and muscimol may be detected in human
             urine within one hour after the ingestion of the mushrooms. 
             The peak of excretion of ibotenic acid appears at the second
             hour after the ingestion.

        6.4  Metabolism

             Metabolites include pantherin, tricholomic acid and
             solitaric acid.
             In humans, a substantial amount of ingested ibotenic acid is
             excreted in urine unmetabolized.  Some is converted to
             muscimol which is more pharmacologically active.

        6.5  Elimination and excretion

             In human beings, a substantial fraction of ingested
             ibotenic acid is excreted in the urine unmetabolized. 
             Virtually no muscimol is excreted when pure ibotenic acid is
             eaten, but muscimol is detectable in the urine after eating
             A. muscaria, which contains both, ibotenic acid and
             muscimol.  The ibotenic acid that does pass through the body
             is excreted rapidly, between 20 and 90 minutes after
             ingestion (Chilton, 1975).  It should be noted that major
             symptoms appear after the first 60 minutes to 2 hours and
             reach their greatest intensity after the excretion of
             ibotenic acid. Major signs and symptoms of major or severe
             intoxication lasts more than 5 hours after the peak in
             excretion of ibotenic acid.
             According to animal experiments, most of the muscimol
             delivered by intra peritoneal injection in the mouse is
             excreted in the urine as muscimol or metabolites of muscimol
             within 6 hours.  About 1/3 is excreted as muscimol, 1/3 as a
             cationic conjugate, and 1/3 as an oxidation product (Ott J.
             et al, 1975).
    
             In fact, the urine retains the pharmacological activity of
             the Fly Agaric, and in the sacred rituals in eastern Siberia,
             the urine of the Shamans and their acolytes was ingested by
             some followers  and considered a better inebriant or
             hallucinogen (Efron et al 1979).

    7.  TOXINOLOGY

        7.1  Mode of action

             Ibotenic acid is structurally similar to glutaminic acid
             and mimics its effects in animals. Ibotenic acid is rapidly
             converted to muscimol, which structurally resembles GABA.
             Muscimol has a high affinity for GABA receptor sites and
             imitates the action of GABAB in animals and humans,
             inhibiting and controlling the recruitment and multiplication
             of nerve impulses mediated by many positive neurotrasmitters
             (Page, 1984).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             The threshold for observation of
                             central nervous system disturbances in human
                             is about 6 mg of muscimol or 30 to 600 mg of
                             ibotenic acid (Waser, 1979).  This dose is
                             potentially available in a single
                             A. muscaria or A. pantherina
                             mushroom.
    
                             In human volunteers, effects were measurable
                             about 1 hour after ingestion of 7.5 to 10 mg
                             of muscimol, or 50 to 90 mg of ibotenic acid. 
                             These effects continued for 3 to 4 hours,
                             with some residual effects lasting as much as
                             10 to 24 hours in some subjects.  Hangover
                             was noted the next day (Chilton, 1975;
                             Eugster, 1979).
    
                             Purified ibotenic acid and muscimol produced
                             hallucinations, delirium, muscular spasm, and
                             sleep in volunteers (Theobald et al., 1968,
                             Waser, 1979).

                    7.2.1.2  Children

                             No data available.

             7.2.2  Relevant Animal data

                    Muscimol lacks cholinergic effect at the
                    neuromuscular junction.  It inhibits tremor induced by
                    tremorin but does not stop the associated salivation
                    and lacrimation.  A low dose of muscimol affects the
                    EEG of cats and rabbits (Scotti et al., 1969; Theobald
                    et al., 1968).  These observations further support a
                    localization of action of muscimol in the brain rather
                    than in the peripheral nervous system.
    
                    Muscimol and ibotenic acid administered to rats and
                    mice intraperitoneally affects brain in the levels of
                    serotonin (5-hydroxytryptamine), noradrenaline and
                    dopamine as do LSD, psilocybin and mescaline
                    (Koenig-Bersin et al., 1970; Waser, 1979). 
    

                    Ibotenic acid and glutamic acid produce convulsions in
                    immature rats, in which the blood-brain barrier is not
                    completely developed (Johnston, 1973).  Muscinol has
                    been shown to produce electroencephalographic
                    alterations distinct from hallucinogens such as LSD or
                    mescaline (which is in accord with the clinical
                    observations).  Neither ibotenic acid nor muscimol
                    appears to act on receptors acetylcholine, dopamine,
                    or 5-hydroxytryptamine receptors in the central
                    nervous system. It has been suggested that both
                    muscimol and ibotenic acid act similarly by activation
                    of the gamma-aminobutyric acid (GABA) receptor (Brehm
                    et al., 1972; Walker et al., 1971).
    
                    The acute LD50 of muscimol in rats ranges from 4.5
                    mg/kg intravenously to 45 mg/kg, p.o.  Experiments in
                    dogs suggest that the effects of 20 mg/kg/day, p.o.
                    are not cumulative (Waser, 1979).

             7.2.3  Relevant in vitro data

                    No data available.

        7.3  Carcinogenicity

             No data available.

        7.4  Teratogenicity

             No data available.

        7.5  Mutagenicity

             No data available.

        7.6  Interactions

             Muscimol-treated animals, administered small doses of
             diazepam or phenobarbital, displayed flaccid paralysis and an
             electroencephalographic pattern similar to deep anesthesia
             Theobald et al. (1968) and Scotti de Carolis et al. (1969). 
             These data cannot be extrapolated to humans.

    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)

                             A convenient analytical method for
                             ibotenic acid (IBO) and muscimol (MUS) in a
                             toxic mushroom, Amanita muscaria 
                             (A. muscaria), was developed.  IBO and MUS in
                             the mushroom were extracted with 70%
                             methanol.  After filtration, IBO and MUS in
                             the extract were determined by high
                             performance liquid chromatography (HPLC) with
                             a UV detector set at 210 nm.  The HPLC system
                             adopted was ion-pair chromatography in the
                             reverse-phase mode on an IRICA RP-18 (C18)
                             column  (4.0 mm with sodium dodecyl sulfate
                             as a counter ion.  Recoveries of IBO and MUS
                             added to the sample were more than 98% and
                             the minimum detectable concentration of IBO
                             or MUS was about 1 ppm.  The concentrations
                             of IBO and MUS in A. muscaria ranged from
                             258 and 471 ppm and from 18 to 27 ppm,
                             respectively.  Neither of the compounds was
                             detected in commercial edible mushrooms
                             (Abstract: Tsunoda K, Inoue N, Aoyagi Y,
                             Sugahara T, J Food Hyg Soc Jpn; 34(1). 1993.
                             12-17).

             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

                    Symptoms appear within 30 to 90 minutes and are
                    most marked at 2 or 3 hours.  They may include:
                    drowsiness, confusion, dizziness, ataxia, euphoria,
                    delirium, visual and auditory disturbances with
                    hallucinations, muscle cramps and spasms.
                    Gastrointestinal disturbances and convulsions may also
                    be seen.

             9.1.2  Inhalation

                    No data available.

             9.1.3  Skin exposure

                    No data available.

             9.1.4  Eye contact

                    No data available.

             9.1.5  Parenteral exposure

                    No data available.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    No data about chronic toxicity available.

             9.2.2  Inhalation

                    No data available.

             9.2.3  Skin exposure

                    No data available.

             9.2.4  Eye contact

                    No data available.

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Toxic effects appear 30 to 90 minutes after ingestion
             and last usually for 6 hours but may persist for 12 to 24
             hours.  Hangover is often observed the following day.  The
             prognosis is usually good with symptomatic treatment.  Death
             from these mushrooms is extremely rare (Chilton, 1978).
             Although they sometimes produce dramatic intoxications with
             extensive psychological and neurological effects these
             mushrooms have a totally unwarranted reputation for being
             "deadly poisonous".

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Pulse and blood pressure are usually normal.
                    In one case, the patient developed cardiac
                    fibrillation (Lincoff & Mitchel, 1977), also
                    bradycardia was observed (Benjamin, 1992).

             9.4.2  Respiratory

                    Respiration is not usually affected (Bosman et
                    al., 1965); but respiratory depression is possible as
                    a result of over treatment (Benjamin, 1992).

             9.4.3  Neurological

                    9.4.3.1  Central nervous system (CNS)

                             The primary effects are CNS
                             depression and stimulation, which may
                             alternate.  Symptoms usually begin with
                             drowsiness followed by a state of confusion,
                             with ataxia, dizziness, euphoria resembling
                             alcohol intoxication and may proceed to
                             increase activity, illusions, or even manic
                             excitement.
                             These periods of excitement may alternate
                             with periods of somnolence, deep sleep or
                             stupor (Ammirati et al., 1985;  Benjamin,
                             1992).
                             The illusions are primarily a
                             misinterpretation of sensory stimuli such as
                             changes in color vision, echo images (seeing
                             through walls), identification of hospital
                             personnel as divine figures, and the like,
                             rather than true hallucinations caused by
                             Psilocybe, or Paneolus.
                             However, vivid hallucinations associated with
                             accidental poisoning by this Amanitas have
                             been reported occasionally (McDonald, 1980;
                             Carter et al., 1983).
                             Seizures are observed primarily in children
                             (Benjamin, 1992).

                    9.4.3.2  Peripheral nervous system

                             Muscimol lacks cholinergic effects
                             at the neuromuscular junction

                    9.4.3.3  Autonomic nervous system

                             Neither muscarinic nor atropinic
                             effects have been observed in poisoning due
                             to A. muscaria or A. pantherina.
                             Occasionally, sweating and salivation have
                             been reported (Lampe, 1978; Waser, 1979;
                             Benjamin, 1992).

                    9.4.3.4  Skeletal and smooth muscle

                             Muscle jerks, fasciculation and
                             spasms in the extremities are observed
                             (Chilton, 1978; Benjamin, 1992).

             9.4.4  Gastrointestinal

                    Dyspepsia and vomiting may occur (Chilton,
                    1978, own data).

             9.4.5  Hepatic

                    Amanita muscaria has no hepatotoxic effects.

             9.4.6  Urinary

                    9.4.6.1  Renal

                             No data available.

                    9.4.6.2  Other

                             No data available.

             9.4.7  Endocrine and reproductive systems

                    No data available.

             9.4.8  Dermatological

                    Skin may be warm and flushed (Benjamin, 1992).

             9.4.9  Eye, ear, nose, throat: local effects

                    Miosis as well as mydriasis or intermittent
                    mydriasis were observed in children (Benjamin,
                    1992)

             9.4.10 Haematological

                    No data available.

             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

                             Light or mild dehydration may be
                             observed, as a consequence of
                             vomiting.

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    No data available.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks

                    No data available.

        9.5  Other

             No data available.

        9.6  Summary

             Symptoms onset is usually within 30 to 90 minutes,
             peaking at 2 to 3 hours. Initial drowsiness is followed by
             ataxia, confusion, agitation, illusions or even manic
             excitement.  These periods of excitement may alternate with
             periods of somnolence, deep sleep or stupor.  Muscle jerks,
             fasiculations and spasms in the extremities were
             observed.


    10. MANAGEMENT

        10.1 General principles

             Treatment includes prevention of absorption of the
             toxins and treatment of the signs and symptoms of
             intoxication as they occur, especially sedation.
             Induction of emesis is NOT recommended because of the
             potential CNS depression and seizures.

        10.2 Life supportive procedures and symptomatic/specific
             treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status of the patient.
             Control convulsions with appropriate drug regimen, sedation
             with benzodiazepines is required (see IPCS Treatment
             Guidelines).

        10.3 Decontamination

             Emesis is not recommended.
             Administer activated charcoal, most effective when
             administered within one hour of ingestion.
             Gastrointestinal emptying and/or charcoal is however, rarely
             indicated and only in very recent ingestion, while the
             patient is asymptomatic.

        10.4 Enhanced elimination

             Forced diuresis
             Not necessary, although possibly effective on
             theoretical grounds. 
    
             Hemodialysis
             Although the toxins may be removed by hemodialysis (Mitchell
             and Lumack, 1978) this procedure is considered unnecessary in
             view of the good prognosis of clinical cases.

        10.5 Antidote/antitoxin treatment

             10.5.1 Adults

                    There is no specific antidote for Amanita
                    muscaria and Amanita pantherina poisoning.

             10.5.2 Children

                    There is no specific antidote for Amanita
                    muscaria and Amanita pantherina 
                    poisoning.

        10.6 Management discussion

             Treatment includes prevention of absorption, with
             activated charcoal, of the toxins and treatment of the signs
             and symptoms of intoxication as they occur.
             Induction of emesis is not recommended because of the
             potential central nervous system depression and seizures.
             There is no specific antidote for Amantia muscaria and
             pantherina  poisoning.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             Accidental poisoning
    
             There are numerous reports in the medical literature of this
             type of intoxication. Intoxication with A. muscaria and
             pantherina have more recently become more common as the
             result of deliberate attempts by individuals to induce
             hallucinations.  Special recipes are even now appearing for
             ways to prepare a broth from these mushrooms so that one can
             retain their psychoactive effects without the
             gastrointestinal irritating effects.
    
             Voluntary ingestion
    
             Agnus McDonald experimented the self-administration of whole
             A. muscaria (1978). He prepared capsules with dried and
             powdered mushrooms, collected in Northern California. With 12
             g of dried A. muscaria a noticeable effect was felt.
    
             "In summary, 12 g of dry red A. muscaria produced mainly
             these following symptoms: a marked nausea that tapered off
             over the first three hours; 2) a conspicuous absence of
             reflective thought combined with a sense of tiredness, and 3)
             a slight transient euphoria around the fourth hour that
             alternate with and finally was overwhelmed by a general sense
             of fatigue.  It was not an inspiring experience, and the
             initial nausea was so great that I had no desire to repeat
             it.  I decided on a compromise.  I made an infusion by
             soaking 30 g of dried mushrooms in a cup of water. Within one
             hour I was obviously feeling a greater effect than I had from
             eating 12 g. I felt again as if I were in a state of
             suspended animation, this time with a much stronger desire to
             sleep. Although my environment seemed somehow "bright", there
             were no hallucinations of obvious visual distortions.  My
             stream of consciousness seemed notably empty, and when I
             contemplated writing down something about how I felt, I could
             think of nothing to say.  I noticed a marked increase in my

             usual level of saliva production.  By 5 1/2 hours after
             ingestion, the effects were waning.  By 7 hours later, they
             were nearly gone, and I succumbed to my desire to sleep. 
             There were no sequelae the following morning".
    
             McDonald conducted also an assay with six human volunteers
             who ate the 12 g does of dried-powdered Fly Agaric.  All
             experimented nausea, although only two of them vomited.  All
             six experienced tiredness, and three of the six reported
             increased salivation.  Only two of the subjects related
             visual distortions that might pass for low-grade
             hallucinations.
    
             The experiences of Waser (1979), who experimented himself the
             effects of pure substances (ibotenic acid and muscimol),
             merit to be mentioned here:
    
             "A 20 mg ibotenic acid dose ingested in water tastes like
             mushrooms, but produces little immediate action.  Within half
             an hour a warm and slightly flushed face was noticed, without
             changes in blood pressure or heart rate, with no physic
             stimulation, but lassitude followed by sleep.  A day later a
             migraine with classical one-sided visual disturbance
             developed for the first time in my life.  The occipitally
             localized headache continued in a milder form for two
             weeks.
    
             Next I turned to muscimol.  A dose of 5 mg in water orally
             ingested had little effect except a feeling of laziness.  Ten
             mg produced a slight intoxication after 90 minutes with
             dizziness, ataxia and elevated mood, psychic stimulation (in
             psychological tests), no hallucinations but slight changes in
             taste and color vision.  Some myoclonic muscle twitching
             followed, then sleep with dreams.  After two to three hours I
             felt normal, rested and able to undertake anything, even
             work.  During the next night I slept well, deep and long.  No
             other signs followed.
    
             With 15 mg of muscimol administered orally the intoxication
             started after 40 minutes and was more pronounced.  Dizziness
             made walking with closed eyes impossible, but reflexes were
             not changed.  Speech was sometimes inarticulate and
             dysarthric. Appetite and taste were diminished.  After a
             phase of stimulation, concentration became more difficult. 
             Vision was altered by endlessly repetitioned echopictures of
             situations a few minutes before.  Hearing became noisy and
             sometimes was followed by echo.  Most disturbing were
             repeated myoclonic cramps of different muscle groups.  I felt
             sometimes as if I had lost my legs, but never had
             hallucinations as vivid and colorful as with LSD. The pupils
             remained always the same size.  After 2 hours I fell asleep,

             but I cannot remember any dreams.  Two hours later I awoke
             again and was glad that the muscle twitching was less
             frequent.  I did not feel relaxed and fresh as after 10 mg
             muscimol but rather dull and uncertain.  Blood pressure was
             only a little elevated during the psychoactive phase".
    
             Muscimol induces a state of psychosis with confusions,
             dysarthria, disturbance of visual perception, illusions of
             colour vision, myoclonia, disorientation in place and time,
             weariness, fatigue and sleep.  Concentration tests showed
             improved performance with small doses (5 mg) but diminished
             performance and learning with an increased number of errors
             with higher doses (10 to 15 mg).

    12. Additional information

        12.1 Specific preventive measures

        12.2 Other

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

        Author:     J. Piqueras
                    Department of Haematology & Haemotherapy
                    General Hospital Vall d'Hebron
                    Autonomous University of Barcelona
                    08035 Barcelona
                    Spain
    
        Date:       10 January 1990
    
        Reviewer    Dr Barbara Groszek
                    Department of Clinical Toxicology
                    College of Medicine of the Jagiellonian University
                    31-826 KRAKOW
                    POLAND
    
                    Tel: +48 12 647 55 85 or +48 12 647 11 05
                    Fax: +48 12 647 55 85 or +48 12 647 11 05
                    E-mail: mfgrosze@cyf-kr.edu.pl
    
        Date:       16 October 2000
    
        Reviewed by:
    
        *    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)
    





















    See Also:
       Toxicological Abbreviations