Mushroom poisoning

Mushroom poisoning

Introduction

Mushroom poisoning can cause a range of symptoms from mild, mostly gastrointestinal, disturbances to organ failure or even death.

  • Represent 5.8% of total poisonings in the US

Aetiology

Amatoxin containing mushroom species:

  • Amanita group:
    • Amanita phalloides (Death Cap)
    • Amanita virosa  (Destroying Angel)
    • Amanita verna (Fool’s Mushroom)
    • Others: A. ocreata, A. bisporigera, A. suballiacea
  • Lepiota group: 
    • L. helveola, L. chlorophyllum, L. brunneolilacea, L. josserandi, L. fulvella, L. subincarnata, L. brunneoincarnata
  • Miscellaneous:
    • Galerina autumnalis (Autumn skullcap), Galerina venenata, Galerina sulcipes, Conocybe filaris

Pathophysiology

Amanitin toxin:

Heat stable toxin (remains toxic whether eaten raw or cooked) that inhibits RNA polymerase, causing disruption of transcription of mRNA. As a result, hepatocytes cannot synthesize key protein coding genes, leading to the disintegration of nucleoli and pathologically centrilobular hepatic necrosis. This leads to the insidious onset of liver failure over 48 hours.
Amanitin disintergrates hepatic cell nucleus. | Litten W. The most poisonous mushrooms. Sci. Am. 1975;232:90–101.

Phallotoxin

Late onset (> 6 hours after ingestion) of vomiting and watery diarrhea occur due to the second component in some of these mushrooms which are phallotoxin. Lepiota species lack phallotoxins so may not have the onset of vomiting and diarrhea until after 12 hours post-ingestion, or may just present with symptoms of liver failure at 24 hours post ingestion.
Phalloidin attacks the cell membranes causing leakage of calcium atoms, followed by loss of potassium ions. | Litten W. The most poisonous mushrooms. Sci. Am. 1975;232:90–101.

Clinical features

Clinically silent phase:

Often foragers comment on how good the food made from Amanita species tastes, and there are no signs of a problem for at least 6 hours.

First stage: 6-12 hours after ingestion

  • GI phase: Onset of nausea, abdominal cramps, profuse watery diarrhea, and signs of dehydration.
  • Physical examination: Dry mucosal membranes and tachycardia, and given sufficient dehydration, hypotension.

Second stage: 2-3 days after ingestion

Patient appears to recover transiently, and GI symptoms resolve, but ongoing liver damage continues
  • Rising liver function transaminase, bilirubin
  • Development of coagulopathy
  • Progression to hepatic encephalopathy

Third stage:

Both liver and renal function become compromised. Occur rapidly after laboratory signs of liver injury, and death can occur in three to seven days.
  • Hepato-renal syndrome
  • Hepatic encephalopathy
  • Death

Management

  • IV N-acetyl-cysteine (treat potential liver injury, and provide glutathione)
  • High-dose IV penicillin (compete with liver uptake of amatoxin)
  • IV silymarin (OAT-P transporter inhibitor that slows the entry of amatoxin into the liver)
  • Activated charcoal (reduce absorption of amatoxins if given early after ingestion and may also prevent toxin readsorption hours later as amatoxins undergo enterohepatic recirculation)

Summary:

Tavassoli, M., Afshari, A., Arsene, A. L., Mégarbane, B., Dumanov, J., Paoliello, M., Tsatsakis, A., Carvalho, F., Hashemzaei, M., Karimi, G., & Rezaee, R. (2019). Toxicological profile of Amanita virosa – A narrative review. Toxicology reports, 6, 143–150. https://doi.org/10.1016/j.toxrep.2019.01.002
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