This document discusses various types of mushroom poisoning, including those caused by Amanita mushrooms, Gyromitra mushrooms, Cortinarius mushrooms, Inocybe mushrooms, and Coprinus mushrooms. It describes the clinical effects of each type of poisoning as well as recommended treatment approaches. The poisoning types are distinguished based on factors like onset of symptoms and target organ systems.

1. M&P poisoningM&P poisoning
Prof. Dr. Saad S Al Ani
Senior Pediatric Consultant
Head of Pediatric department
Khorfakkan Hospital
Sharjah ,UAE
saadsalani@yahoo.com

2. 2
MushroomMushroom PoisoningPoisoning
06/19/13M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

3. MushroomMushroom PoisoningPoisoning
• Mushrooms are a great source of nutrition
• They are:
- Low in calories
- Fat free
- High in protein
Making them an ideal food except for the
fact that some are highly toxic if ingested
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13 3

4. Cont.Cont.
• The clinical syndromes produced by
mushroom poisoning are divided
according
to the:
- Rapidity of onset of symptoms
- Predominant system involved.
•The symptoms are due to the principal toxin
present in the ingested mushrooms
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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5. Cont.Cont.
• The eight major toxins produced by mushrooms
are categorized as:
1. Cyclopeptides
2. Monomethylhydrazine
3. Muscarine
4. Hallucinogenic indoles
5. Isoxazole
6. Coprine (disulfiram-like reaction)
7. Orellanine
8. Gastrointestinal tract–specific irritants
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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6. Cont.Cont.
• The wild mushroom:
-Tricholoma equestre has been associated
with delayed rhabdomyolysis
-Clitocybe amoenolens and Clitocybe
acromelalgia have been reported to
cause
erythromelalgia.
• The toxins responsible for these effects
are unknown.M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
606/19/13

7. Gastrointestinal: Delayed Onset
Amanita Poisoning
•Poisonings by species of Amanita and
Galerina account for 95% of the fatalities
due to mushroom intoxication
•The mortality rate for this group is 5-10%.
•Cells with high turnover rates, such as those
in the gastrointestinal mucosa, kidneys, and
liver, are the most severely affected.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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8. • Most species produce two classes of
cyclopeptide toxins:
(1)Phallotoxins, which are heptapeptides
believed to be responsible for the early
symptoms of Amanita poisoning
(2) Amanitotoxin, an octapeptide that
inhibits RNA polymerase and subsequent
production of messenger RNA.
Cyclopeptide toxins
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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9. Pathogenesis
Amanita poisoning causes:
• Cellular necrosis which may occur
throughout the gastrointestinal tract,
the most heavily exposed site.
• Acute yellow atrophy of the liver
• Necrosis of the proximal renal tubules
are found in lethal cases.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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10. The clinical course of poisoning
• The clinical course of poisoning with
Amanita or Galerina species is biphasic.
• Nausea, vomiting, and severe abdominal
pain ensue 6-24 hr after ingestion.
• Profuse watery diarrhea follows shortly
thereafter and may last for 12-24 hr.
• During this time, as much as 9 L of fluid
may be lost.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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11. Cont.
• From 24-48 hr after poisoning, jaundice
,hypertransaminasemia (peaking at 72 to
96 h), renal failure, and coma occur.
• Death occurs 4-7 days after the ingestion.
• A prothrombin time less than 10% of
control is a poor prognostic factor.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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12. Treatment
•Treatment for Amanita poisoning is both
supportive and specific.
•Fluid loss from severe diarrhea during the
early course of the illness is profound,
requiring aggressive therapy for correction
of this loss.
• In the late phase of the disease, management
of renal and hepatic failure is also necessary.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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13. Cont.
• Specific therapy for Amanita poisoning
is designed to remove the toxin rapidly
and to block binding at its target site.
• Oral activated charcoal and lactulose
combined with fluid and electrolyte
replacement are recommended as part
of the initial treatment for children with
Amanita poisoning.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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14. Cont.
• Forced diuresis should be avoided,
since this increases renal exposure.
• Intravenous penicillin G (400,000 U/kg/
24 hr) administered as a continuous
infusion
• Silybin dihemisuccinate, the water-soluble
isomer of the flavolignone silymarin (in an
intravenous dosage of 20-50 mg/kg/24 hr
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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15. Cont.
• Silybin dihemisuccinate, act synergistically
to:
1.Inhibit binding of both toxins
2.Interrupt enterohepatic recirculation of
amanitotoxin,
3.Protect from further hepatic injury from
the toxins. .
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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16. Monomethylhydrazine Intoxication
• Species of Gyromitra contain mono-
methylhydrazine (CH3NHNH2), which
inhibits central nervous system (CNS)
enzymatic production of γ-aminobutyric
acid (GABA).
• Monomethylhydrazine also oxidizes
iron
in hemoglobin, resulting in methemo-
globinemia.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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17. Cont.
•Children with Gyromitra poisoning
experience:
vomiting, diarrhea, hematochezia
and abdominal pain within 6-24 hr
of ingestion of the toxin.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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18. Cont.
• Symptoms of CNS depression and
seizures develop later in the clinical
course.
•Hemolysis and methemoglobinemia
are potential life-threatening
complications of monomethylhydrazine
poisoning.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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19. Treatment
•Hypovolemia due to gastrointestinal fluid
losses and seizures requires supportive
intervention.
•Pyridoxal phosphate, the coenzyme that
catalyzes the production of GABA, can
reverse the effects of monomethylhydrazine
when administered in high doses.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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20. Cont.
• Pyridoxine hydrochloride (25 mg/kg) is
administered intravenously at a
frequency
dependent on clinical improvement.
• Parenteral administration of methylene
blue is indicated if the methemoglobin
concentration exceeds 30%;
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
2006/19/13

21. Cont.
• Severe methemoglobinemia may require
dialysis.
•Blood transfusions may be required for
significant hemolysis
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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22. Renal: Delayed Onset
Orellanine Poisoning
•Species of Cortinarius contain the heat-
stable toxin bipyridyl orellanine, which
causes severe non-glomerular renal injury
characterized by interstitial fibrosis and
acute tubular necrosis.
22
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital
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23. •The exact mechanism of injury is unknown.
• Cortinarius poisoning is characterized by:
nausea, vomiting, and diarrhea
That manifest 36-48 hr after ingestion.
Orellanine Poisoning (Cont.)
23
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

24. Orellanine Poisoning (Cont.)
• Although the initial symptoms may be
trivial, more serious renal toxicity
occurs in several days.
• Acute renal failure occurs in 30-50%
of those affected, beginning with
polyuria and progressing to renal
failure
24
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

25. Treatment
• Treatment for orellanine poisoning is
supportive.
• Early presentation, within 4-6 hr after
ingestion, can be treated with activated
charcoal and gastric lavage
25
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

26. Treatment (Cont.)
• Hemodialysis may be needed in
patients
suffering from renal failure.
• Most patients recover within 1 mo but
chronic renal insufficiency develops in
one third to one half of patients
26
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

27. Autonomic Nervous System: Rapid Onset
Muscarine Poisoning
•Mushrooms of the genera Inocybe and, to a
lesser degree, Clitocybe contain muscarine
or muscarine-related compounds.
•These quaternary ammonium derivatives
bind to postsynaptic receptors, producing
an exaggerated cholinergic response.
27
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

28. Cont.
• The onset of symptoms is rapid (30
min to 2 hr after consumption) and
the
disease spectrum is characterized by
the following:
-Hypercholinergic response
diaphoresis
- Excessive lacrimation
- Salivation and vomiting
- Miosis
- Urinary and fecal incontinence 28
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

29. Cont.
• Respiratory distress caused by broncho-
spasm and increased bronchopulmonary
secretions is the most serious complication
•The symptoms subside spontaneously within
6-24 hr.
29
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

30. Treatment
•Atropine sulfate, the specific antidote, is
administered intravenously (0.01 mg/
kg; max 2 mg).
•This is repeated until the pulmonary
symptoms resolve or the patient becomes
overtly tachycardic
30
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

31. Coprine Ingestion
• Coprinus atramentarius and Clitocybe
clavipes contain coprine.
•Like disulfiram ,coprine inhibits the
metabolism of acetaldehyde after ethanol
ingestion.
• The clinical manifestations result from
accumulation of acetaldehyde.
31
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

32. Cont.
• Coprine intoxication becomes apparent
after ethanol ingestion and may occur
up to 5 days after consumption of the
mushroom.
•Hyperemia of the face and trunk, tingling
of the hands, metallic taste, tachycardia,
and vomiting occur acutely.
•Hypotension may result from intense
peripheral vasodilation.
32
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

33. Cont.
• The syndrome typically is self-limited
and lasts only several hours.
• No specific antidote is available.
• If hypotension is severe, vascular
reexpansion with isotonic parenteral
solutions may be required.
• Small oral doses of propranolol have
also been suggested.
33
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

34. Central Nervous System: Rapid Onset
Isoxazole Intoxication
•Although Amanita muscaria and Amanita
pantherina may contain muscarine, the
toxins responsible for the CNS symptoms
after
ingestion of these mushrooms are muscimol
and ibotenic acid, the heat-stable derivatives
of the isoxazoles.
•Muscimol, a hallucinogen, and ibotenic
acid, an insecticide, have anticholinergic
effects. 34
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

35. Cont.
• From 30 min to 3 hr after ingestion, CNS
symptoms appear: obtundation, alternating
lethargy and agitation, and, occasionally,
seizures.
•Nausea and vomiting are uncommon.
• If large amounts of muscarine are contained
in the mushroom, symptoms of cholinergic
crisis also may occur.
35
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

36. Cont.
• Specific therapy must be carefully
selected
• If an exaggerated cholinergic response is
observed, atropine should be administered.
• Because ingestions of A. muscaria often
are associated with anticholinergic findings
the acetylcholinesterase inhibitor
physostigmine is often used to reverse the
delirium and coma.
36
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

37. Cont.
• Benzodiazepines also are used for the
agitation and delirium.
• Seizures can be controlled with diazepam
•In most cases, however, early treatment
with ipecac (if the patient is conscious)
and close observation are all that is
required.
37
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

38. Indole Intoxication
• Mushrooms belonging to the genus
Psilocybe (“magic mushrooms”) contain
psilocybin and psilocin, two psychotropic
compounds.
• Within 30 min after ingestion, patients
experience euphoria and hallucinations, often
accompanied by tachycardia and mydriasis.
38
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

39. Cont.
• Fever and seizures have also been observed
in children with psilocybin poisoning.
• These symptoms are short-lived, usually
lasting for 6 hr after consumption of the
mushroom.
•Severely agitated patients may show response
to diazepam.
39
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

40. Gastrointestinal: Rapid Onset
• Many mushrooms from various genera
produce local gastrointestinal
manifestations.
•The causative toxins are diverse and
largely unknown.
• Within 1 h of ingestion, patients
experience acute abdominal pain,
nausea, vomiting, and diarrhea.
•Symptoms may last from hours to days
depending on the species of mushroom
40
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

41. Treatment
• Treatment is mainly supportive.
• Children with large fluid losses may
require parenteral fluid therapy.
• It is imperative to differentiate ingestion of
mushrooms of this class from ingestion
of Amanita and Galerina species containing
cyclopeptide toxins.
41
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13

42. 42
PotatoPotato PoisoningPoisoning
06/19/13M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

43. Potato Poisoning
• Solanine is a mixture of several related
toxins found in greened and sprouted
potatoes.
•Potatoes exposed to light and allowed to
sprout produce a number of alkaloid
glycosides containing the cholesterol
derivative solanidine.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13 43

44. Solanine Poisoning
• Two of these glycosides, α- solanine and
α- chaconine, are found in highest concentration
in the peels of greened potatoes and in the
sprouts.
•Some solanine can be removed by boiling but
not by baking.
M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 06/19/13 44

45. Solanine Poisoning
•The major effect of α-solanine and
α- chaconine is inhibition of cholinesterase
•Cardiotoxic and teratogenic effects have
also been reported.
4506/19/13M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

46. Clinical manifestations of solanine and chaconine poisoning
•Intoxication occur within 7-19 hr after
ingestion.
•The most common symptoms are:
vomiting, abdominal pain, and diarrhea
• In more severe instances of poisoning
neurologic symptoms, including:
drowsiness, apathy, confusion, weakness,
and vision disturbances, are rarely
followed
by coma or death.
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47. Treatment of solanine poisoning
• Is largely supportive.
• In the most severe cases, symptoms resolve
within 11 days.
•Atropine treatment has not been evaluated.
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48. References
• Bedry R, Baudrimont I, Deffieux G, et al:
Brief report: wild mushroom intoxication as a cause of rhabdomyolysis.
N Engl J Med 2001; 345:798-804.
•Diaz JH:
Syndromic diagnosis and management of confirmed mushroom poisonings.
Crit Care Med 2005; 33:427-436.
•Berger KJ, Guss DA: Mycotoxins revisited: part II. J Emerg
Med 2005; 28:175-183
•Korpan YI, Nazarenko EA, Skryshevskaya IV, et al: Potato
glycoalkaloids: true safety or false sense of security?. Trends
Biotechnol 2004; 22:147-151.
•Ruprich J, Rehurkova I, Boon PE, et al: Probabilistic modelling of
exposure doses and implications for health risk characterization:
glycoalkaloids from potatoes. Food Chem Toxicol 2009; 47:2899-
2905.
•http://www.crazyaboutmushrooms.com/mushroom_poisoning.html
06/19/13 48M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

49. Thank You