Micetismos: Parte 4: Síndromes tempranos con síntomas complejos / Mushroom poisonings. Part 4: early-onset syndromes with complex symptoms / Intoxicações por cogumelos. Parte 4: Síndromes precoces com sintomas complexos

En esta Parte 4 de la serie de cuatro artículos sobre micetismos se analizan los síndromes que se caracterizan por presentar un período de latencia muy corto, con la aparición de síntomas complejos en menos de 6 horas después de la ingestión de los macromicetos. Se discuten los siguientes micetismos: 1) Toxíndrome muscarínico o colinérgico periférico por especies de Inocybe y Clitocybe. 2) Toxíndrome inmunohemolítico o hemolítico por Paxillus. 3) Toxíndrome neumónico alérgico por Lycoperdon perlatum y por Pholiota nameko. 4) Toxíndrome panterínico o neurotóxico glutaminérgico por compuestos isoxazólicos o síndrome pantherina/muscaria. 5) Toxíndrome coprínico o cardiovascular. 6) Toxíndrome neurotóxico alucinogénico por psilocibina y derivados indólicos. 7) Toxíndrome psicotrópico por estirilpironas y gimnopilinas de Gymnopilus spectabilis o G. junonius. 8) Toxíndrome agudo de rabdomiólisis por Russula subnigricans. 9) Toxíndrome cianogénico por Marasmius oreades. 10) Toxíndrome inmunosupresor por tricotecenos macrocíclicos de Podostroma cornu-damae. 11) Toxíndrome hemolítico debido a ostreolisina de Pleurotus ostreatus y especies relacionadas. Se analizan los síntomas, las toxinas involucradas, los mecanismos de acción, cuando se conocen, y las especies causantes de los micetismos.

This Part 4 of the series of four articles on mushroom poisonings refers to early-onset syndromes, which are characterized by a very short latency period, and the appearance of complex symptoms in less than 6 hours after mushroom ingestion. The following mycetisms are discussed, (1) Peripheral cholinergic, or muscarinic syndrome due to Inocybe and Clitocybe species. (2) Immunohaemolytic or haemolytic syndrome by Paxillus. (3) Allergic pneumonic syndrome due to Lycoperdon perlatum, and Pholiota nameko. (4) Glutaminergic neurotoxic, or pantherinic syndrome by isoxazole compounds or pantherina/muscaria syndrome. (5) Coprinic or cardiovascular syndrome. (6) Hallucinogenic neurotoxic syndrome due to psilocybin and indole derivatives. (7) Psychotropic syndrome by styrylpirones and gymnopilins of Gymnopilus spectabilis or G. junonius. (8) Rhabdomyolysis acute syndrome due to Russula subnigricans. (9) Cyanogenic syndrome by Marasmius oreades. (10) Immunosuppressive syndrome by macrocyclic trichothecenes of Podostroma cornu-damae. (11) Haemolytic syndrome due to ostreolisine of Pleurotus ostreatus, and related species. The symptoms, toxins involved, mechanisms of action, when known, and the species of mushrooms responsible for the mycetisms are analyzed.

Nesta parte 4 da série de quatro artigos sobre intoxicação por cogumelos são analisadas síndromes que se caracterizam por apresentar um período de latência muito breve, com aparecimento de sintomas complexos em menos de 6 horas após a ingestão dos macromicetos. As seguintes intoxicações com cogumelos são discutidas: (1) Toxíndrome muscarínico ou colinérgico periférico por espécies de Inocybe e Clitocybe. (2) Toxíndrome imuno-hemolítica ou hemolítica por Paxillus. (3) Toxíndrome pneumônica alérgica por Lycoperdon perlatum e por Pholiota nameko. (4) Toxíndrome panterínica ou neurotóxica glutaminérgica por compostos isoxazólicos ou síndrome pantherina/muscaria. (5) Toxíndrome coprínica ou cardiovascular (6) Toxíndrome neurotóxico-alucinogênica por psilocibina e derivados indólicos. (7) Toxíndrome psicotrópica por estirilpironas e gimnopilinas de Gymnopilus spectabilis ou G. junonius. (8) Toxíndrome aguda de rabdomiólise por Russula subnigricans. (9) Toxíndrome cianogênica por Marasmius oreades. (10) Toxíndrome imunossupressora por tricotecenos macrocíclicos de Podostroma cornu-damae. (11) Síndrome hemolítica por ostreolisina de Pleurotus ostreatus e espécies relacionadas. São analisados os sintomas, as toxinas envolvidas, os mecanismos de ação, quando conhecidos, e as espécies de cogumelos responsáveis pelas intoxicações.

Poisoning associated with the use of mushrooms: A review of the global pattern and main characteristics.

Worldwide, special attention has been paid to wild mushrooms-induced poisoning. This review article provides a report on the global pattern and characteristics of mushroom poisoning and identifies the magnitude of mortality induced by mushroom poisoning. In this work, reasons underlying mushrooms-induced poisoning, and contamination of edible mushrooms by heavy metals and radionuclides, are provided. Moreover, a perspective of factors affecting the clinical signs of such toxicities (e.g. consumed species, the amount of eaten mushroom, season, geographical location, method of preparation, and individual response to toxins) as well as mushroom toxins and approaches suggested to protect humans against mushroom poisoning, are presented.

Mushroom poisoning: A proposed new clinical classification.

Mushroom poisoning is a significant and increasing form of toxin-induced-disease. Existing classifications of mushroom poisoning do not include more recently described new syndromes of mushroom poisoning and this can impede the diagnostic process. We reviewed the literature on mushroom poisoning, concentrating on the period since the current major classification published in 1994, to identify all new syndromes of poisoning and organise them into a new integrated classification, supported by a new diagnostic algorithm. New syndromes were eligible for inclusion if there was sufficient detail about both causation and clinical descriptions. Criteria included: identity of mushrooms, clinical profile, epidemiology, and the distinctive features of poisoning in comparison with previously documented syndromes. We propose 6 major groups based on key clinical features relevant in distinguishing between poisoning syndromes. Some clinical features, notably gastrointestinal symptoms, are common to many mushroom poisoning syndromes. Group 1 - Cytotoxic mushroom poisoning. Syndromes with specific major internal organ pathology: (Subgroup 1.1; Primary hepatotoxicity); 1A, primary hepatotoxicity (amatoxins); (Subgroup 1.2; Primary nephrotoxicity); 1B, early primary nephrotoxicity (amino hexadienoic acid; AHDA); 1C, delayed primary nephrotoxicity (orellanines). Group 2 - Neurotoxic mushroom poisoning. Syndromes with primary neurotoxicity: 2A, hallucinogenic mushrooms (psilocybins and related toxins); 2B, autonomic-toxicity mushrooms (muscarines); 2C, CNS-toxicity mushrooms (ibotenic acid/muscimol); 2D, morel neurologic syndrome (Morchella spp.). Group 3 - Myotoxic mushroom poisoning. Syndromes with rhabdomyolysis as the primary feature: 3A, rapid onset (Russula spp.); 3B, delayed onset (Tricholoma spp.). Group 4 - Metabolic, endocrine and related toxicity mushroom poisoning. Syndromes with a variety of clinical presentations affecting metabolic and/or endocrine processes: 4A, GABA-blocking mushroom poisoning (gyromitrins); 4B, disulfiram-like (coprines); 4C, polyporic mushroom poisoning (polyporic acid); 4D, trichothecene mushroom poisoning (Podostroma spp.); 4E, hypoglycaemic mushroom poisoning (Trogia venenata); 4F, hyperprocalcitoninemia mushroom poisoning (Boletus satanas); 4G, pancytopenic mushroom poisoning (Ganoderma neojaponicum). Group 5 - Gastrointestinal irritant mushroom poisoning. This group includes a wide variety of mushrooms that cause gastrointestinal effects without causing other clinically significant effects. Group 6 - Miscellaneous adverse reactions to mushrooms. Syndromes which do not fit within the previous 5 groups: 6A, Shiitake mushroom dermatitis; 6B, erythromelagic mushrooms (Clitocybe acromelagia); 6C, Paxillus syndrome (Paxillus involutus); 6D, encephalopathy syndrome (Pleurocybella porrigens).

Intoxicación por Amanita phalloides / Amanita phalloides poisoning

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[A study of the clinical classification of 3638 cases of mushroom poisoning].

OBJECTIVE: To study the clinical classification and characteristics as well as prognosis of mushroom poisoning. METHODS: We retrospectively analyzed 191 papers published domestically for 3466 cases of mushroom poisoning from 1995 to 2004 and studied the Xinqiao Hospital data of 172 cases of mushroom poisoning treated from 1980 through 2004. We made a retrospective investigation and clinical classification of all the 3638 cases of mushroom poisoning. RESULTS: Among the 3638 patients, clinical manifestations as gastroenteritis were found in 571, all of them were cured. The most common symptoms were those of acute renal failure being found in 1450 cases; 1414 were cases (97.5%) and 36 died (2.5%). Symptoms of toxic hepatitis were found in 1010 cases, 841 were cases (83.3%) and 169 died (16.7%). Psychoneurological disorder was manifested in 214 cases; 197 were cases (92.1%) and 17 died (7.9%). Erythrolysis was found in 73 cases; 71 were cases (97.3%) and 2 died (2.7%). The therapeutic effect and prognosis of mushroom poisoning with different clinical manifestation varied very significantly (P < 0.001). Of the 320 cases clinically unclassified, multiple organ dysfunction syndrome was found in 222 cases; 98 were cases (44.1%) and 124 died (55.9%). Definite classification could not be made in 98 cases; 90 were cases (91.8%) and 8 died (8.2%). CONCLUSIONS: The clinical classification of mushroom poisoning was usually of four types as described in the textbooks or special articles, but it should be of five types according to the analysis of the data of the present study, i.e. gastroenteritis type, acute renal failure type, toxic hepatitis type, psychoneurological disorder type and erythrolysis type. It is not clear whether there is a mixed type or not. Further investigation is needed in this respect.

Evolving global epidemiology, syndromic classification, general management, and prevention of unknown mushroom poisonings.

OBJECTIVE: To assess the evolving global epidemiology of mushroom poisoning and to identify new and emerging mushroom poisonings and their treatments, a descriptive analysis and review of the world's salient scientific literature on mushroom poisoning was conducted. DATA SOURCE: Data sources from observation studies conducted over the period 1959-2002 and describing 28,018 mushroom poisonings since 1951 were collected from case reports, case series, regional descriptive studies, meta-analyses, and laboratory studies of mushroom poisonings and the toxicokinetics of mycotoxins. STUDY SELECTION: Studies included in the review were selected by a MEDLINE search, 1966-2004, an Ovid OLDMEDLINE search, 1951-1965, and a medical library search for sources published before 1951. DATA EXTRACTION: To better guide clinicians in establishing diagnoses and implementing therapies, despite confusing ingestion histories, data were extracted to permit an expanded syndromic classification of mushroom poisoning based on presentation timing and target organ systemic toxicity. DATA SYNTHESIS: The final 14 major syndromes of mushroom poisoning were stratified first by presentation timing and then by target organ systemic toxicity and included early (<6 hrs), late (6-24 hrs), and delayed syndromes (> or =1 day). There were eight early syndromes (four neurotoxic, two gastrointestinal, two allergic); three late syndromes (hepatotoxic, accelerated nephrotoxic, erythromelalgia); and three delayed syndromes (delayed nephrotoxic, delayed neurotoxic, rhabdomyolysis). Four new mushroom poisoning syndromes were classified including accelerated nephrotoxicity (Amanita proxima, Amanita smithiana), rhabdomyolysis (Tricholoma equestre, Russula subnigricans), erythromelalgia (Clitocybe amoenolens, Clitocybe acromelalgia), and delayed neurotoxicity (Hapalopilus rutilans). In addition, data sources were stratified by three chronological time periods with >1,000 confirmed mushroom ingestions reported and tested for any statistically significant secular trends in case fatalities from mushroom ingestions over the entire study period, 1951-2002. CONCLUSIONS: Since the 1950s, reports of severe and fatal mushroom poisonings have increased worldwide. Clinicians must consider mushroom poisoning in the evaluation of all patients who may be intoxicated by natural substances. Since information on natural exposures is often insufficient and incorrect, a new syndromic classification of mushroom poisoning is recommended to guide clinicians in making earlier diagnoses, especially in cases where only advanced critical care, including organ transplantation, may be life saving.

The epidemiology, toxidromic classification, general management, and prevention of mushroom poisoning in the United States.

Since the 1950s, reports of severe and fatal mushroom poisonings have increased worldwide. Clinicians must consider mushroom poisoning in the evaluation of all patients who may be intoxicated by natural substances. Because information on natural exposures is often incorrect or insufficient, a new syndromic classification of mushroom poisoning is proposed to guide clinicians in making earlier diagnoses, especially in cases where only advanced critical care, including kidney or liver transplantation, may be life saving.

[Acute higher funghi mushroom poisoning and its treatment]. / Intoxications aiguës par les champignons supérieurs et leur traitement.

PRINCIPLE: The various mushroom poisoning syndromes are summarised together with elements underlining uncertainty and lack of knowledge. For each of the classical syndromes concerned, classified in delays inferior or superior to 6 hours, the toxins and their mechanisms of action, the main mushrooms responsible, the symptoms and their treatment are all presented. EARLY SYNDROMES: Characterised by early onset within 6 hours, these represent the majority of intoxications. There are 6 syndromes: gastro-intestinal (resinoid), muscarine (sudorien, cholinergic), pantherine (myco-atropine, anticholinergic), coprine (similar to the antabuse syndrome), narcotine (psilocybin, hallucinatory) and paxillus syndrome (exceptional). LATE SYNDROMES: Characterised by an onset after six hours, they regroup the phalloid syndrome that is responsible for 90 to 95% of deaths due to higher funghi mushrooms, the orellanine and gyromitrin syndrome and new syndromes identified over the past decade concerning acute renal failure with shorter onset than during the orellanine syndrome (Amanita proxima), erythermalgia (Clitocybe amoenolens), rhabdomyolysis (Tricholoma equestre) and central nervous system failure (Hapalopilus rutilans).

[Clinical importance of the Gavornik classification of mushroom poisoning]. / Klinický význam Gavorníkovej klasifikácie otráv hubami.

The lack of experience and fundamental knowledge about mycology by some mushroomers is one of the leading causes of increasing occurrence of fatal mushroom poisonings. Mushroom intoxications are caused not only by poisonous mushrooms (true primary intoxications), but under certain conditions also by edible mushrooms (secondary intoxications, false intoxications, pseudo-intoxications). Apart from fresh mushrooms intoxications may result also from preserved mushrooms (sterilized in pickles, soured, dried, used for preparation of mushroom extracts, powders, etc.), which are used as garnish. (Tab. 1, Ref. 44.)

[Mushroom poisoning--classification, symptoms and therapy]. / Otrava hubami--klasifikácia, symptomatóza a liecba.

The most serious poisonings are the hepatotoxic ones which are caused above all by Amanita phalloides, virosa, verna, Lepiota helveola, Galerina marginata, Gyromitra esculenta, Hypholoma fasciculare, and nephroptoxic intoxications which are caused above all by Cortinarius orrelanus and Paxillus involutus. Neurotoxic and psychotropic intoxications develop after ingestion of Inocybe, Clitocybe, Amanita-panterina, muscaria and Psilocybe. Most frequently the gastroenteric type of mushroom poisoning is encountered which is caused by many species e.g. Boletus satanas, Entoloma sinuatum and others. In the diagnosis anamnestic data are used, the clinical picture, mycological and toxicological examinations of residues of mushrooms, their spores and toxins. Therapeutic strategy comprises elimination methods gastric lavage, intestinal lavage and administration of large amounts of animal charcoal, forced diuresis, haemoperfusion, haemodialysis or peritoneal dialysis, administration of antidotes and symptomatic treatment, i.e. mainly rehydration and restoration of the mineral balance. Early and comprehensive treatment are important.

Intensive hemodialysis and hemoperfusion treatment of Amanita mushroom poisoning.

Over a period of fifteen years, 41 patients including 23 males and 18 females with Amanita mushroom poisoning were treated at the University Hospital of Lund, Sweden. The intensity of poisoning was graded according to serum transaminase elevations and prothrombin time reductions. Severity was mild in 16 patients (Group A), moderate in 14 (Group B) and severe in 11 (Group C). Members of Group C reported shorter latency periods before the onset of symptoms, (10 +/- 1 hours, P < 0.05) and longer delays in treatment, (34 +/- 4 hours), than did the other patients. Intensive treatment was begun before the results of urine amatoxin assay were reported. Treatment consisted of: fluid and electrolyte replacement, oral activated charcoal and lactulose, i.v. penicillin, combined hemodialysis and hemoperfusion in two 8 hour sessions, some received i.v. thioctic acid, other i.v. silibinin, all received a special diet. This combination of treatment modalities was used to accelerate the elimination of amatoxin from the patients' bodies. The longest period of hospitalization, 13 +/- 2 days, was required by the patients of Group C (p < 0.01). All patients improved and were discharged from the hospital asymptomatic. No sequelae were later reported for the majority of those moderately and severely poisoned. We have concluded that intensive combined treatment applied in these cases is effective in relieving patients with both moderate and severe amanitin poisoning.

Clinical approach to toxic mushroom ingestion.

BACKGROUND: This review provides the physician with a clinical approach to the diagnosis and management of toxic mushroom ingestion. It reviews the recent literature concerning proper management of seven clinical profiles. METHODS: Using the key words "mushroom poisoning," "mushroom toxicology," "mycetism," "hallucinogenic mushroom ingestion," and "Amanita poisoning," the MEDLINE files were searched for articles pertinent to the practicing physician. Much of the original data were gathered at the Aspen Mushroom Conference held each summer throughout the 1970s at Aspen, Colorado, sponsored by Beth Israel Hospital and the Rocky Mountain Poison Center. Texts related to poisonous plants and specific writings concerning mushroom poisoning were also consulted; many of these texts are now out of print. RESULTS AND CONCLUSIONS: The 100 or so toxic mushroom groups can be divided into seven clinical profiles, each of which requires a specific clinical approach. Two of the seven groups (amanitin and gyromitrin) have a delay in onset of symptoms of up to 6 hours following ingestion and provide essentially all the major mobility and mortality associated with toxic mushroom ingestion. These two groups are the major focus of this review. Treatment of the potential mushroom ingestion, as well as guidelines for asking clinical questions, are included. These questions serve as a form of algorithm to assist the clinician in arriving at the correct toxic group.

Poisoning from accidental ingestion of mushrooms.

Poisoning from the accidental ingestion of mushrooms is an uncommon cause of morbidity within Australia and unlike many other countries no deaths have yet been recorded. This review seeks to draw attention to the various syndromes associated with mushroom poisoning and their management, thereby helping to keep our good record intact. Although the number of toxic species is relatively small, the collection and ingestion of field varieties should be left to those absolutely certain of their quest. In cases of poisoning, identification of the offending mushroom is of paramount importance in the management. In suspected or known amatoxin poisoning prompt treatment favourably influences outcome.