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.