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At least 19 recordsLinked to original sources
PubMed1997

[Poisonous mushrooms, mushroom poisons and mushroom poisoning. A review].

Of 1,500 different types of Norwegian mushrooms, 60-100 are considered poisonous. Fatal intoxications occur very infrequently. Lack of knowledge of picking and preparing mushrooms and accidental or deliberate consumption are recognised causes of mushroom poisoning. Delayed onset of symptoms (> 5-6 hrs) indicates serious poisoning, and these patients must be admitted to hospital. Cytotoxic toxins (e.g. amatoxin, orellanin) cause serious damage to the visceral organs (liver, kidney) and require intensive treatment, including hemoperfusion. Neurotoxic toxins may cause dramatic, but less harmful peripheral or central symptoms affecting the peripheral and central nervous systems, including hallucinations. Some mushrooms cause gastroenteritis of low clinical significance within a few hours after consumption. Interaction between mushrooms and alcohol may lead to a disulfiram-like effect. Induced vomiting and activated charcoal are important initial therapeutic measures. The precise history of the patient and the collecting of mushroom remnants, including vomitus, may help to identify the particular mushroom. In Norway, the National Poison Information Centre may be contacted for further advice.

Humans↗
PubMed1998

[Differential diagnosis of mushroom poisoning].

Mushroom poisoning is a very urgent problem of internal medicine. Mushroom picking is one of the most popular hobbies in the Czech and Slovak Republic. This is one of the main reasons of the rising incidence of mushroom poisoning, incl. fatal cases. Mushroom poisoning is characterized by a very varied clinical picture which is reflected also in recent classification systems. The main objective of the present work is to draw attention to cardinal symptoms and signs of different types of mushroom poisoning which respect new findings in the diagnosis and differential diagnosis of mushroom poisoning.

Diagnosis, Differential↗
PubMed1976

Amanita preissii "mushroom" poisoning.

"Mushroom" poisoning has rarely been reported in Australia. We present six cases of Amanita preissii poisoning successfully treated with atropine sulphate. The symptoms and signs were typical of muscarinic poisoning, which suggests that this alkaloid is the principal toxic component. A short time interval between the ingestion of poisonous fungi and the onset of symptoms, in our cases within one hour, indicates a good prognosis. The dangers of mistaking poisonous for edible varieties of fungi are emphasized, particularly in relation to immigrants not conversant with Australian fungi. Public education and control of marketing are advised.

Adult↗
PubMed1985

Intravenous mushroom poisoning.

Mushrooms of the genus Psilocybe frequently are ingested by recreational drug users for their hallucinogenic effects. We present the case of a 30-year-old man who allegedly received an intravenous injection of an extract of Psilocybe mushrooms. His clinical course was characterized in part by vomiting, severe myalgias, hyperpyrexia, hypoxemia, and mild methemoglobinemia, and it was similar to two previously reported cases. The patient improved rapidly with supportive care.

Adult↗
PubMed1976

[Mushroom poisoning. New possibilities for treatment].

Poisonous species of fungi in Germany are very few. Dangerous is the ingestion of raw, spoiled or poisonous mushrooms. There exist no reliable tests to determine whether a mushroom is safe except by expert examination and identification of the mushroom. In clinical practice the classification of mushroom poisoning is possible in muscarine-syndrome, gastroenteritic syndrome and in two-phase-syndrome. 90-95% of lethal mushroom poisonings are due to ingestion of Amanita phalloides. In severe cases extensive hepatic necrosis occurs, characterized by profound abnormalities in liver function caused by hepatic coma. In deep coma mortality rates amount to 70% or more. A new therapeutic measure (coated charcoal hemoperfusion)-first applied in liver failure by Chang (1972) and Williams (1973)-has been performed in 3 patients with severe poisoning after ingestion of Amanita phalloides (each patient had eaten at least 7-10 fungi Amanita phalloides). Two of the patients survived.

Adult↗
PubMed1993

Clinical symptomatology and management of mushroom poisoning.

Among poisonous mushrooms, a small number may cause serious intoxication and even fatalities in man. Humans may become symptomatic after a mushroom meal for rather different reasons: (1) ingestion of mushrooms containing toxins, (2) large amounts of mushrooms may be hard to digest, (3) immunological reactions to mushroom-derived antigens, (4) ingestion of mushrooms causing ethanol intolerance, and (5) vegetative symptoms may occur whenever a patient realizes that there might be a possibility of ingestion of a toxic mushroom after a mushroom meal. Based on the classes of toxins and their clinical symptoms, seven different types of mushroom poisoning can be distinguished: (1) phalloides, (2) orellanus, (3) gyromitra, (4) muscarine, (5) pantherina, (6) psilocybin, and (7) gastrointestinal mushroom syndrome. Two other entities of adverse reactions to mushrooms are (8) coprinus and (9) paxillus syndrome. Phalloides, orellanus, gyromitra and paxillus syndrome may lead to serious poisoning, which generally requires treatment of the patient in an intensive care unit. Diagnosis of mushroom poisoning is primarily based on anamnestic data, identification of mushrooms from leftovers of the mushroom meal, spore analysis, and/or chemical analysis. Therapeutic strategies include primary detoxification by induced emesis, gastric lavage and activated charcoal, secondary detoxification, symptomatic treatment and rarely specific antidotes. Owing to progressing fulminant hepatic failure, lethality associated with phalloides syndrome is still high (5-20%). Basic treatment includes administration of silibinin and penicillin G, although controlled studies on its therapeutic efficacy are still lacking. In serious phalloides syndrome, orthotopic liver transplantation has to be considered. Fortunately, the prognosis in most other mushroom poisonings is excellent.

Animals↗
PubMedDate not supplied

Birth weight and congenital anomalies following poisonous mushroom intoxication during pregnancy.

A series of 22 women who suffered from mushroom poisoning while pregnant have been identified among adults receiving treatment between 1960 and 1993 in a specialist clinic in Budapest, Hungary. In most cases, the poisonings were attributed to Amanita phalloides, verna, and related species. Of these, 20 went to term, and data were collected on gestational age, birth weight, and both major and minor congenital anomalies. Mean birth weight (but not gestational age) was lower than in the control series, suggesting that maternal poisoning may have led to intrauterine growth retardation. Two children were identified with major abnormalities (one of whom had fetal alcohol syndrome related to alcohol abuse by the mother). The prevalences of both major and minor anomalies were similar to the prevalence in the matched control group and to the rate in a more recent control series examined according to the same protocols. However, the statistical power to detect teratogenic effects is limited, especially as only five of the mothers suffered the poisoning episode during the first trimester.

Adult↗
PubMed1986

Mushroom poisoning due to Cortinarius speciosissimus: electron microscope study in rats.

The effects of a poisonous mushroom, Cortinarius speciosissimus, on rat kidney were studied by transmission electron microscopy. Suspension of dried mushroom (500 mg/kg body weight) was administered as a single dose directly into the esophagus. The kidneys were fixed by perfusion, and both cortex and medulla were sampled. C. speciosissimus toxin acted primarily on the epithelial cells of the proximal tubules. No changes were seen in the glomeruli. First ultrastructural changes were observed at 2 days in the renal cortex. The most prominent damage occurred at 5 days, when most of the proximal tubular cells appeared necrotic. Dark bodies (diameter 0.15-0.5 micron) spaced by 25-45 nm were frequently found in the damaged tubular cell nuclei. Regeneration of the tubular cells was seen at 10 days. After 2 months, increased amount of collagen fibres were seen between tubules. The nuclear changes in the damaged tubular cells and the slowly manifesting toxicity suggest that C. speciosissimus toxin acts on nuclei or nucleoli and/or metabolic pathways associated with them.

Animals↗
PubMed2004

Acute and late effects on induction of allodynia by acromelic acid, a mushroom poison related structurally to kainic acid.

1. Ingestion of a poisonous mushroom Clitocybe acromelalga is known to cause severe tactile pain (allodynia) in the extremities for a month and acromelic acid (ACRO), a kainate analogue isolated from the mushroom, produces selective damage of interneurons of the rat lower spinal cord when injected either systemically or intrathecally. Since ACRO has two isomers, ACRO-A and ACRO-B, here we examined their acute and late effects on induction of allodynia. 2. Intrathecal administration of ACRO-A and ACRO-B provoked marked allodynia by the first stimulus 5 min after injection, which lasted over the 50-min experimental period. Dose-dependency of the acute effect of ACRO-A on induction of allodynia showed a bell-shaped pattern from 50 ag x kg(-1) to 0.5 pg x kg(-1) and the maximum effect was observed at 50 fg x kg(-1). On the other hand, ACRO-B induced allodynia in a dose-dependent manner from 50 pg x kg(-1) to 50 ng x kg(-1). 3. N-methyl-d-aspartate (NMDA) receptor antagonists and Joro spider toxin, a Ca(2+)-permeable AMPA receptor antagonist, inhibited the allodynia induced by ACRO-A, but not by ACRO-B. However, other AMPA/kainate antagonists did not affect the allodynia induced by ACRO. 4. Whereas no neuronal damage was observed in the spinal cord in ACRO-A-treated mice, induction of allodynia by ACRO-A (50 fg x kg(-1)) and ACRO-B (50 ng x kg(-1)) was selectively lost 1 week after i.t. injection of a sublethal dose of ACRO-A (50 ng x kg(-1)) or ACRO-B (250 ng x kg(-1)). Higher doses of ACRO-A, however, could evoke allodynia dose-dependently from 50 pg x kg(-1) to 500 ng x kg(-1) in the ACRO-A-treated mice. The allodynia induced by ACRO-A (500 ng x kg(-1)) was not inhibited by Joro spider toxin or NMDA receptor antagonists. These properties of the late allodynia induced by ACRO-A were quite similar to those of the acute allodynia induced by ACRO-B. 5. ACRO-A could increase [Ca(2+)](i) in the deeper laminae, rather than in the superficial laminae, of the spinal cord. This increase was not blocked by the AMPA-preferring antagonist GYKI52466 and Joro spider toxin. 6. Taken together, these results demonstrate the stereospecificity of ACRO for the induction of allodynia and suggest the presence of a receptor specific to ACRO.

Animals↗
PubMed1998

[Mushroom poisoning in Turkey].

Mushroom poisoning constitutes the main part of plant intoxications in Turkey. Not only in rural areas, but also in Istanbul, gathering mushrooms is a habit among villagers who have moved to the city and settled in the vicinity of a forest. Phalloides syndrome, Pantherina syndrome and gastro-intestinal syndrome are the most frequently encountered types of mushroom poisonings. Amanita phalloides which is growing widely in Istanbul forests is responsible for many serious cases every year. Haemoperfusion and penicillin are used for the treatment, because Legalon-SIL is not imported in Turkey.

Agaricales↗
PubMed1999

[Prevention and treatment of mushroom poisoning].

In the submitted review the author gives an account on basic aspects of primary, secondary and tertiary prevention of mushroom poisoning. Mushroom poisoning is not caused only by toxic mushrooms (true intoxications) but under certain conditions also by edible mushrooms (false intoxications and pseudointoxications). The basis of primary prevention is not to pick and eat mushrooms which could damage health, and knowledge of basic facts, and types of mushroom poisoning. The main objectives of secondary prevention of mushroom poisoning are to prevent absorption of toxins from the digestive tract into the human organism and their effective elimination from the organism.

Humans↗