Management of Poisoning by Unknown Fungi
MANAGEMENT OF POISONING BY UNKNOWN FUNGI
This guideline is intended to be only the basic set of instructions to
manage cases of unknown mushroom ingestion, and is by no means
exclusive. There may be exceptions to the guidelines contained, and
the user should refer to the individual PIMs, other treatment guides,
or more detailed literature for specific management of poisoning cases
due to mushrooms which have been identified.
Specific antidotal therapy is available for very few intoxications by
fungi, therefore mainstays of treating poisoning are: decontamination,
symptomatic and/or supportive therapy, clinical observation and good
nursing care.
GENERAL APPROACH TO THE POISONED PATIENT
1. Stabilization and complete patient evaluation
Apply general clinical measures to prevent further deterioration of
the patient. Fortunately, poisoning by fungi is NOT a frequent
life-threatening situation, but if airway, breathing or circulation
are compromised, perform appropriate resuscitative measures. The
primary survey of the patient should be carried out simultaneously
with resuscitation in case of life-threatening poisoning. After
stabilization of the vital signs, an accurate history helps guide
further management.
Routine questions should include:
* what fungus/fungi did you intend to collect
* what type of tree was it growing near
* was it growing in the woods or in the field or the garden
* on what substrate was the fungus growing
* did the fungus have an odor, what was the size and
colour, were there gills or "sponge"
* how many species of fungi were consumed
* how many persons ate the fungus
* was the fungus eaten at more than one meal (what
were the exact times of ingestion)
* how long after exposure did the symptoms begin to appear
* how was the fungus prepared (raw vs. cooked)
* how were the fungi stored between collection and the
time of preparation
* how were the already prepared fungi stored before
ingestion
* was any alcohol consumed with the meal
* are all people ill who consumed the fungus
* are there other ill persons in the group who did NOT
consume the fungi
* did the patient ever eat this fungus before
* were the mushrooms bought, and if so, where.
If the mushrooms are available and the diagnosis is still unclear, try
to have them analysed by a mycologist, but start treatment without
delay if serious poisoning is suspected.
In some places the "newspaper" test (the newspaper must contain
lignin) is being used: press the mushroom on the newspaper, let it dry
and add one drop of hydrochloric acid. The paper may then turn to a
blue or bluish-green colour indicating the presence of amatoxins. The
test is not 100% conclusive.
2. Fungus identification
Accurate identification of the fungus involved (genus and species)
helps guide appropriate treatment. In managing the patient poisoned
by a fungus, it is mainly more important what the fungus is NOT,
rather than what it is. There are only a few fungal species in which
the toxin (e.g. cyclopeptides, orellanine, gyromitrin) is of such a
magnitude that the treatment of the patient must be more than only
symptomatic in nature. If available, a trained mycologist should be
consulted to help eliminate from consideration the more toxic fungal
species.
3. Reduction of absorption
The mainstay in the reduction of absorption is the administration of
activated charcoal. Since it only takes a few minutes to adsorb
toxins, it should be administered even before gastric lavage or emesis
is induced (dosage: 50 to 100 g in adults, 10 to 25 g in children).
In general emesis or lavage only removes about one-third of ingested
material, so sufficient activated charcoal administration should prove
more effective. If microscopic analysis of gastric contents is to be
performed, do the sampling, if possible, before administration of a
charcoal.
4. Enhancement of elimination
Dialysis and haemoperfusion may be indicated only in very few fungal
intoxications (e.g. by cyclopeptides, orellanine), but to be effective
it must be undertaken on an early stage of poisoning.
SPECIFIC APPROACH TO THE POISONED PATIENT
5. Specific fungal antidotes
Few antidotes are available for fungal intoxications. Many proposed
antidotes have NOT been proven to be useful in controlled clinical
studies, but still have their international proponents.
6. Main fungal syndromes and their treatment
Symptomatic treatment of the patient should begin before
identification of the fungus in question. Knowledge of certain
syndromes characteristic of fungal poisoning is important. Always
keep in mind that there can be many causes of symptoms which are NOT
directly related to an exogenous fungal toxin: panic reactions (fear
of having ingested a highly poisonous fungus), difficulties to digest
the fungi, bacterial contamination (Salmonella, Staphylococcus, in the
worst botulism), raw fungi (many edible species give arise to
gastrointestinal symptoms if not prepared properly), individualized
allergic reactions or, rarely, pesticide residues.
It must be remembered that when dealing with fungal toxins, that the
longer the time interval (usually > 6 to 12 hours) between ingestion
and the onset of symptoms, the more severe the type of fungal toxin
(e.g. amatoxin, orellanine, gyromitrin). Long onset indicates the
possibility of a severe poisoning.
(i) Cyclopeptides
These are a group of major fungal toxins, accounting for approximately
90% of the fungal fatalities internationally. The fatality rate in
untreated cases is between 20 and 30%. Patients show a relatively
long time interval, that goes from 6 to 24 hours, between exposure and
onset of symptoms. Multiple dose activated charcoal is warranted in
an attempt to interrupt the entero-hepatic recycling that can occur
with these toxins. Enhanced diuresis and the possibility of using
specific antidotes could be considered. Patients generally pass
through four phases: (1) latent asymptomatic period, (2)
gastro-intestinal phase with massive diarrhoea, vomiting, and
dehydration with metabolic consequences like metabolic acidosis and
hypoglycemia, (3) lessening of symptoms with a period of apparent
well-being, and (4) hepatic phase (normally starting 36 to 48 hours
after ingestion) with a rise in liver enzymes and acute hepatic
failure. Patients who might have been exposed to these fungal toxins,
will need close monitoring for liver damage and possible kidney
damage, and could possibly require a liver transplant in the most
severe cases. The principle is that unless these cyclopeptide
containing fungi can NOT be ruled out from consideration in the case,
it must be assumed that this is what the medical treatment team is
facing.
Example fungi: Amanita bisporigera, Amanita ocreata, Amanita
phalloides, Amanita virosa, Amanita verna, Gallerinaspp.,
Lepiota josserandii, Lepiota subincarnata and others; see PIM
on amatoxin containing mushrooms.
(ii) Orellanine-Orelline
Cases of orellanine poisoning have been confirmed only in Europe. The
toxin is mainly nephrotoxic with a very long delay (3 to 11 days)
between exposure and onset of renal symptoms. Occasionally there may
be mild gastrointestinal symptoms during the latency period. The
toxin is probably a bipyridyl oxide (orellanine).
The mortality rate is thought to be approximately 15%. Patients
usually present with: myalgia, particularly lumbar pain, headache,
chills, rigors, a severe burning thirst and oliguria. On admission
to hospital (often after several days post ingestion) the patients
show signs of renal damage that may progress into complete renal
failure.
Treatment is mainly symptomatic, but if the patient is admitted to
hospital within 24 hours after the meal (very unusual),
gastrointestinal decontamination and hemodialysis should be performed
in an attempt to eliminate the toxin.
Example fungi: Cortinarius gentilis, Cortinarius orellanus,
Cortinarius semisanguineus, Cortinarius specciossimus and
others .
(iii) Gyromitrin-Monomethylhydrazine (MMH)
The fungal toxin gyrometrin, yields upon hydrolysis the toxic compound
monomethylhydrazine (MMH). The toxin has a boiling point of 87.5o C,
and as it may be distilled off during the cooking process, it may
produce a toxic atmosphere for the cook. Once again, the relatively
long onset of symptoms (6 to 12 hours) indicates that it may be a
severe poisoning. The intoxication is characterized by some initial
effects: fatigue, dizziness, vertigo, severe headache, a feeling of
bloatness, abdominal pain, and possibly emesis. In more serious cases
convulsions, coma, hemolysis and acute hepatitis may occur.
Pyridoxine (Vitamin B6) is the antidote for life-threatening symptoms
such as convulsions and coma. Otherwise treatment is symptomatic and
supportive. Not all individuals who consume this fungus may develop
symptoms, as each person has their own individualized tolerance, below
which there are no visible symptoms.
Example fungi: Gyromitra esculenta, Gyromitra gigas, Gyromitra
infula and others; see PIM gyromitrin containing mushrooms.
(iv) Coprine
The fungal toxin coprine, blocks the enzyme acetaldehyde
dehydrogenase, which stops the metabolism of ethanol at the
acetaldehyde stage. It acts very similar to the drug disulfiram used
in the treatment of alcoholism. If ethanol is NOT consumed with the
meal, these fungi may be edible. Onset of symptoms is generally short
(30 minutes to 1 hour). The symptoms which generally only appear if
ethanol has been consumed with the meal or within 24 hours after the
meal, consist of: skin flushing, anxiety, a feeling of swelling or
paresthesia in hands and feet, nausea, vomiting, a metallic taste,
tachycardia, and chest pain. Treatment is symptomatic and supportive,
and remission takes place in a few hours.
Example fungi: Coprinus atramentarius, Coprinus insignis,
Coprinus quadrificus and others .
(v) Muscarine
The fungal toxin muscarine, is physiologically very similar to the
neurotransmitter acetylcholine, and therefore causes a cholinergic
syndrome. The onset of symptoms is usually short (30 minutes to 2
hours), and consists of perspiration, salivation, and lacrimation,
along with blurring of vision, abdominal cramps, loose-watery stools,
flushing of the skin, miosis, hypotension, and bradycardia.
Bronchorrea and bronchoconstriction may also be observed. Atropine is
the drug of choice for the treatment of cholinergic symptoms.
Example fungi: Clitocybe spp., Inocybe spp., Mycena
pura and others; see PIM on muscarine containing mushrooms.
(vi) Ibotenic Acid-Muscimol
The fungal toxin ibotenic acid and its reduction product muscimol, are
compounds that act on the nervous system as agonists of
gamma-aminobutyric acid ( GABA). Central nervous symptoms may
alternate between depression and stimulation. Symptoms appear after
30 to 90 minutes after ingestion and include drowsiness, confusion,
dizzines, euphoria, but may proceed to CNS excitation with agitation,
illusions and manic excitement. Seizures are observed primarily in
children. Muscle jerks, fasciculations and muscle spasm in the
extremities are observed. Treatment is symptomatic and supportive.
For anxiety, agitation and convulsions benzodiazepines may be useful.
Although one would think that the species named muscaria implies
that muscarine is the main toxic agent found in the mushrooms, it is
only present in small amounts.
Example fungi: Amanita cothurnata, Amanita muscaria, Amanita
pantherina and others; see PIM Isoxazole containing mushrooms.
(vii) Hallucinogenic compounds (including psilocybin,
psilocin, baeocystin)
These fungal compounds affect the central nervous system, causing
LSD-like symptoms. Usually after 30 to 60 minutes post exposure, the
patient will exhibit: laughter, confusion, disorientation,
depersonalization, derealization, visual and auditory hallucinations,
hyperkinetic compulsive movements. Treatment is symptomatic and
supportive, in a quiet environment, talk-down therapy, and sedation
when necessary. NOTE: Fungi sold on the street as substances of
abuse, may be either hallucinogenic fungi, or may have been
adulterated with other mind-altering compounds, or merely have no
mind-altering potential at all.
Example fungi: Gymnopilus spp., Panaeolus spp ., Psilocybe spp.
and others ; see PIM on Psilocybin containing mushrooms.
(viii) Gastrointestinal irritants
These fungal toxins are a collection of as yet mostly unidentified
compounds which seem to cause most of their symptomatology in the
gastro-intestinal tract: nausea, vomiting, diarrhea. Onset of symptoms
is generally short (30 minutes to 2 hours). Treatment is symptomatic
and supportive.
Example fungi: Agaricus hondensis, Boletus eastwoodiae, Boletus
frostii, Boletus satanus, Enteloma luridus, Hebeloma
crustiliniforme, Lactarius torminosus, Omphalotus olearius,
Paxillus involutus, Pholiota squarrosa, Ramaria formosa,
Russula emetica, Scleroderma aurantium, Verpa bohemica and
others .
(ix) Other fungal toxins
More research is required on other fungal toxins which seem to be
associated with some unique toxic syndromes. Some of the fungi which
have been implicated with toxic syndromes include: Amanita
smithiana and A. proxima (renal failure), Auricularia
auricula (easy bruising and excessive bleeding), Hypholoma
fasiculare (hepatic injury), Paxillus involutus (immune
hemolytic anemia), Clitocybe acromelalga , Lepiota inversa,
Clitocybes amaenoens (erythromelalgia, paresthesia and dysesthesia
remaining for over one year - personal communication from J.
Trestrail).
FOLLOW-UP AND CONTINUING CARE OF THE POISONED PATIENT
7. Continuing care.
After diagnosis and initial treatment, an adequate observation period
should be established, especially if the poisoning is severe.
Psychiatric evaluation and counseling is indicated in the case of
intentional poisoning (e.g. suicide, substance abuse).
Education is recommended in cases of accidental poisoning by fungi, in
order to prevent further poisoning incidents.
Prevention and educational material is available in a number of
poisons centres.
Author:
John H. Trestrail, III, RPh. FAACT, DABAT
Toxicologist
Grand Rapids, Michigan, USA
Date: August 30, 2000
Reviewed by:
Luc De Haro, Heinz Faulstich, Barbara Groszek, John Haines, Jonas
Hojer, Christine Karlson-Stiber, Hans Persson, Jenny Pronczuk, John H.
Trestrail III, Thomas Zilker.
Stockholm, Sweden, 21st October, 2000
Erfurt, Germany, 9th November, 2000