Topic 17 - Mycetism: mushroom poisonings in humans Flashcards
Mycetism
Health hazard caused by ingestion of toxic substances present in macro fungal sporocarps
Mycetisms of animals
Little is known
Livestock usually not treated, if poisoned →slaughter
Pets meet rarely with macrofungal sporocarps
Susceptibility of wild animals to fungal poisoning poorly studied
Mycetism in humans
Macrofungal poisonings with a long latency period
Phalloides syndrome
Orellanus syndrome
Gyromitra toxicity
Mycetism in humans
Macrofungal poisonings with a short latency period (hallucinogenic fungi)
Muscarinic syndrome
Pantherina syndrome
Psilocybin syndrome
Other macrofungal poisonings
Disulfiram syndrome
Paxillus syndrome
Gastrointestinal syndrome
Consumption of raw mushrooms
Phalloides syndrome: symptoms and poisonous compounds
Latency period: 6-24 hours
Starts with stomach complaints → vomiting and diarrhoea (fever) → high risk of dehydration (gastrointestinal phase)
Acute symptoms end within 1-2 days, but continue with liver damages, liver enlargement, jaundice, haemorrhages in the stomach and intestines, and disturbance of consciousness
Toxic compounds of phalloides syndrome
Amatoxins, phallatoxins, virotoxins
Death cap poisoning: mechanism of action
Toxins can inactivate the RNA polymerase II enzyme and terminate the protein synthesis at the level of transcription → hepatocytes die
Phallotoxins and virotoxins
Less toxic (worse absorption rate in the tissues)
Phallotoxins inhibit cell division and destroy cell membranes
Virotoxins supposed to have effects similar to that of phallotoxins
Lethal dose of death cap poisoning
LD50 for humans: 0.1 mg/bwkg
A single sporocarop of 20-25 g of A. phalloides contains 5-8 mg of amatoxins
Treatment of death cap poisoning
Removal of toxins from the intestinal tract and the blood must be immediately started after the appearance of the first symtoms → inhibition of liver toxicity → Recovery of electrolyte metabolism of body
Detoxification of blood
Chemotherapy
Transplantation of liver
Detoxification of blood
By hemodialysis and plasmaphoresis
Chemotherapy
Various liver defences: application of lipoic acid, cytochrome C, silymarin, high dose antibiotics, and vitamin C
Taxa causing Orellanus syndrome
Cortinarius orellanus (fool’s webcap) C. orellanoides C. rubellus (deadly webcap) C. splendens (cortinarin) C. gentilis C. fluorescens ...
Orellanus syndrome symptoms
Long latency (2-17 days), symptoms not always associated with the idea of mushroom poisoning
Repeated mushroom ingestion → toxins accumulated in the tissues
Initial symptoms: anorexia, fatigue, headache, thirst, chills, high fever, GI symptoms
Later symptoms: pain in joints, lumbar region, muscles, kidney damage, and less frequent: liver damage and manifestation of nervous system
Final outcome: kidney faliure, death
Cause of orellanus syndrome
Orellanin
- colorless
- Fluoresces in blue
- has bipyridyl structure
- has been detected from the renal tubules, highly probable to affect them
Treatment of orellanus syndrome
Symptomatic treatment of kidneys
Dialysis
Transplatnation of kidneys
Prevention of orellanus syndrome
little is knownabout the toxins of Cortinarius species hence, the consumption of all the related taxa should be avoided
Taxa causing Gyromitra toxicity
Gyromitra esculenta(false morel) G. fastigiata(brown false morel) G. gigas(snow morel) G. infula (hooded false morel) Cudonia circinans Helvellaspp. (elfin saddles) Discinaspp.
Gyromitra toxicity symptoms
Two-phase course
Long latency period
Starts with GI symptoms (nausea, abdominal pain, vomiting, diarrhoea, headache)
May lead to liver damages and nervous system symptoms (nervousness, excitement, delirium)
2-3 days → circulation system of the patient may collapse; death is often due to respiratory failure
Gyromitrin: mechanism of action
Thermo-instable compound
Serious poisoning may happen only when large amounts of raw mushrooms are ingested
Liver → transformed into monomethyl hydrazine
Inhibit enzymes; are teratogenic, mutagenic and carcinogenic effects have also been shown
Treatment of gyromitra toxicity
Similar to death cap poisoning
vitamin B used to support liver
Muscarinic syndrome - muscarine mechanism of action
Muscarine → structural analog of acetylcholine: able to bind to all types of muscarinic acetylcholine receptors and activate them
Parasympathetic nervous system uses chiefly acetylcholine as its neurotransmitter → muscarine causes parasympathetic predominance
Symptoms of muscarinic syndrome
Short latency period
Characteristic parasympathetic neurological symptoms (perspiration, salivation, lacrimation) can be observed with a low heart rate and blood pressure, and narrowpupils
Other symptoms: shortness of breath, visual disturbances
Treatment of muscarinic syndrome
The antidote of muscarine is atropine (it causes sympathetic predominance) (injection)
Pantherina syndrome symptoms
Short latency period
Symptoms similar to alcohol intoxication
Personality disorders, time and space perception disorders, increased emotional state, fiery speech, strong motor restlessness
Stuporous, fall deep asleep → wake up without any adverse effects
Pantherina toxins
Symptoms mainly caused by isotonic acid, present in large amounts in A. pantherina, can be transformed into muscimol or muscason
Muscimol
Structural analog of neurotransmitter gamma-aminobutyric acid (GABA), which is a general inhibitory neurotransmitter in the CNS
Have insecticidal effects
Symptomatic treatments applied
Psilocybin syndrome symptoms
Latency period: from 30 minutes to 2 hours
Physical symptoms: headache, dizziness, disturbance of consciousness, numbness, slow pulse, low blood pressure
Psychic symptoms: happiness, fear, feeling of liberation, time and space perception disorders, depression, tantrum, delirium
Effects may take 6 to 10 hours
Psilocybin syndrome: toxins
Neurotoxins, antagonists of serotonin: psilocybin, psilocin, beocystin,bufotenin
Psilocybinforms acolor-less crystal, structurallysimilar to lysergic acid
Blue compounds are pro-duced when psilocybin is oxidized → fungi with bluesporocarps are often hallucinogenic
Active ingredients of psychotherapeutic drugs
Disulfiram syndrome symptoms
The related fungal species are not poisonous
Symptoms occur only after drinking alcohol: feeling hot, face flushed, sweating, trembling, elevated heart rate, blood pressure drop, characteristic metallic taste in the mouth, fainting, symptoms disappear after a few hours
Disulfiram syndrome toxins
The active constituent iscoprine, aninhibitorof acetaldehyde dehydrogenase enzyme
In the body,coprineis transformed into aminocyclopropanol; it inhibits the conversion of alcohol to acetaldehyde then to acetate ion; symptoms occur due to the temporary increase of acetaldehyde
Disulfiram syndrome treatment
does not require special therapy
After eating these fungi → no alcohol for 3 days
Pauxillus syndrome symptoms
1-2 hours after the ingestion of raw sporocarps, gastro-intestinal symptoms (vomiting, diarrhea) occur for everybody; no symptoms when cooked
Consumed repeatedly
the cooked sporocarps can also cause serious sepsis in the susceptible persons;
Symptoms: bloody urine, urinary retention, pain in the kidneys, death (in severe cases)
Pauxillus syndrome - course
The number of antibodies produced against the fungal proteins increases antigen-antibody → complexes are developed that cause agglutination of red blood cells → hemolysis (immunohemolytic anemia)
Blood hemoglobin content decreases dramatically; sometimes the sensitivity is developedafteryears of repeated ingestionsof P. involutus
Pauxillus syndrome - treatment
Symptomatic treatments: gastric lavage, laxation, support of blood circulation
Transfusion of blood
In case of renal failure: dialysisis applied
Gastrointestinal syndrome - symptoms
Mild symptoms occur in 15 minutes to 2 hours
Vomiting, diarrhea, nausea, abdominal cramps, but muscle crampsand circulation disorders can also occure
Gastrointestinal syndrome toxins
chemically different compounds with an unpleasant odour, or a pungent taste (e.g.: terpenes, sesquiterpenes, anthraquinones) irritating the stomach and the intestines
Gastrointestinal syndrome treatment
recovery of electrolyte metabolism