TOX 12 - Mushroom poisoning

Question 1

Rapid onset type: onset and from what

Answer 1

• effect within 15-30 min
• mushrooms containing MUSCARINE

Question 2

Rapid onset type: signs

Answer 2

Muscarinic excess (sweating, salivating, bradycardia, nausea, vomiting)

Some mushrooms contain atropine like poison as well, which causes CNS stimulation and hallucinations

Question 3

Delayed onset type: contents, onset

Answer 3

Contains a-amanitin (harmful to parenchymal tissues) and phalloidin (hepatotoxic)

Onset 6-12 hours after ingesting

Question 4

Delayed onset type: signs

Answer 4

Initial - nausea, vomiting, diarrhea, shock

days later - hepatotoxicity, nephrotoxicity

Question 5

Delayed onset type: therapy

Answer 5

Decontamination and symptomatic treatment

Question 6

. Hepatotoxins (protoplasmic toxins) MOA, agent, effects(early, progressive)

Answer 6

Toxin induces direct cellular damage to susceptible cells (highaffinity to hepatocytes), followed by end-organ failure.

Amanita phalloides (‘death cap’):mechanism: blocks RNA polymerase → inhibits mRNA transcription and protein synthesis → apoptosis

• Early phase (6-24 h’ of ingestion) - Abdominal pain, Nausea, vomiting, Diarrhea
• Progressive phase (48-96 h’ of ingestion) - Fulminant hepatic failure (hypoglycemia, coagulopathies, hepatic encephalopathy), Acute kidney injury, Acute pancreatitis

ingestion of full cap is lethal

Question 7

Muscarine (neurotoxin) MOA, agent, effect, treatment

Answer 7

Toxin stimulates peripheral muscarinic receptors; acts like Ach, but is not degraded by cholinesterase, and therefore, has a longer duration of action.

Agents - Inocybe (‘fiber cap’)

• Cholinergic syndrome, develops within 5 min’ - 5 h’.
• ‘DUMBBELS’: diarrhea, urination, miosis, bradycardia, bronchoconstriction, excitation (CNS), lacrimation, secretion (sweating, salivation)
• Toxicity is generally self-limited; resolves within 12 h’ of ingestion

Question 8

Inebriating toxins (neurotoxin)

Answer 8

These mushrooms contain Ibutenic acid (glutamate NMDA agonist) and Muscimol (GABAA agonist).

Ibutenic acid is unstable and easily decarboxylated to muscimol.

Agents - Amanita muscaria, Mechanism: - ibotenic acid agonist at central glutamic acid receptors → CNS stimulation.

• Muscimol(active agent of ibotenic acid ): agonist GABA receptors → sedation.

,Amanita pantherine

• Clinical syndrome consists of alternating periods of CNS excitation (hysteria, hyperkinetic behavior, seizures, myoclonic twitching) and CNS depression (alterations of time and space perception, ataxia, respiratory depression)

Clinical/ symptoms: vomiting and diarrhea, anticholinergic symptoms ( mydriasis, dry mouth, tachycardia). euphoria with hallucinations.

Management: supportive ( rehydration). phyostigmine with severe anticholinergic symptoms.

• Symptoms occur 30-180 min’ after ingestion, peak at 2-3 h’, and disappear within 6-9 h’

Question 9

treatment hepatotoxin, muscarine, inebriating toxins

Answer 9

1. Hepatotoxins (protoplasmic toxins) -

• Decontamination by active charcoal and
• limit the enterohepatic circulation by nasoduodenal tube,
• intensive care ,
• Potential antidote - Silymarin (silibinin)
• • N-Acetylcysteine
• • Penicillin

2. Muscarine (neurotoxin) -

• supportive care ,
• Atropine IV in case of Bradycardia

3. Inebriating toxins (neurotoxin) -

• supportive care,
• Benzodiazepine and
• barbiturates may control agitation and seizures,
• Mechanical ventilation may be necessary