[Forensic medical diagnostics of intoxication with certain poisonous mushrooms in the case of the lethal outcome in a hospital].

The present study was undertaken with a view to improving forensic medical diagnostics of intoxication with poisonous mushrooms in the cases of patients' death in a hospital. A total of 15 protocols of forensic medical examination of the corpses of the people who had died from acute poisoning were available for the analysis. The deathly toxins were amanitin and muscarine contained in various combinations in the death cap (Amanita phalloides) and the early false morels (Gyromitra esculenta and G. gigas). The main poisoning season in the former case was May and in the latter case August and September (93.4%). The mortality rate in the case of group intoxication (such cases accounted for 40% of the total) amounted to 28.6%. 40% of the deceased subjects consumed mushrooms together with alcohol. The poisoning caused the development of either phalloidin- or gyromitrin-intoxication syndromes (after consumption of Amanita phalloides and Gyromitra esculenta respectively). It is emphasized that the forensic medical experts must substantiate the diagnosis of poisoning with mushroom toxins based on the results of the chemical-toxicological and/or forensic chemical investigations. The relevant materials taken from the victim or the corpse should be dispatched for analysis not only within the first day but also on days 2-4 after intoxication. The mycological and genetic analysis must include the detection and identification of mushroom microparticles and spores in the smears from the oral cavity, vomiting matter, wash water, gastric and intestinal contents. In addition, the macro- and microscopic morphological signs, clinical data (major syndromes, results of laboratory studies, methods of treatment) should be taken into consideration as well as the time (season) of mushroom gathering, simultaneous poisoning in a group of people, and other pertinent information.

Russula subnigricans Poisoning: From Gastrointestinal Symptoms to Rhabdomyolysis.

Wild mushroom poisoning is often reported to cause acute liver or renal failure. However, acute rhabdomyolysis caused by wild mushroom poisoning has rarely been reported. We describe 7 patients of 1 family with Russula subnigricans Hongo poisoning. Their clinical manifestations varied from gastrointestinal symptoms to rhabdomyolysis, with 1 fatality. Our report provides supporting evidence that rhabdomyolysis may result from ingestion of R subnigricans mushrooms. A key to survival for patients with rhabdomyolysis caused by R subnigricans poisoning may be early recognition and intensive supportive care.

[Mushroom poisoning]. / Intoxication par les champignons.

Mushroom poisoning is a regular complaint for consultation in emergency facilities. These situations are usually benign and symptomatic treatment is sufficient. However, severe damage can occur, potentially life-threatening. We review the various syndromes associated with the toxins involved, their management and the major signs that are suggestive of serious injury and requiring hospitalization.

[Recent trends of mushroom poisoning in Japan].

The incidence of mushroom poisoning was studied statistically from 2001 to 2010 in Japan. The total incident of mushroom poisoning was 569 cases, which involved 1,920 patients and 10 deaths. The average incident was 56.9 cases per year, involving 192 patients and 1 death. On regional differences, the mushroom poisoning was more frequent in the northeastern part of Japan. The rate of total incidents for each type of poisoning, which were classified according to symptoms caused, 54.6% in the type of gastro-intestinal disorder, 11.6% in the type of neurological symptoms, and 2.4% in the type of intracellular disorder (violent vomiting, diarrhea and dehydration and hepato-nephrosis, or rhabdomyolysis, or erroneous perception, etc.), respectively. Two species of poisonous mushrooms with gastro-intestinal disorder, Lampteromyces japonicus and Rhodophyllus rhodopolius caused the majority (52%) of all poisonings in Japan.

The fungal nephrotoxin orellanine simultaneously increases oxidative stress and down-regulates cellular defenses.

Confusion of various nephrotoxic Cortinarius species with edible mushrooms occurs every year throughout Europe and North America. The toxin, orellanine (OR), accumulates selectively in renal tubular epithelium with ensuing renal failure after several days as the only clinical manifestation. This study was performed to clarify the mechanisms behind the kidney damage. Sprague-Dawley rats, 100 g bw, received various doses of purified OR ip (0-5 mg/kg bw). One week later, renal function (GFR) was determined (51Cr-EDTA), ascorbyl radicals in venous blood were analyzed using electron spin resonance, and oxidative protein damage was evaluated immunohistochemically. One OR-treated group (3.5 mg/kg) simultaneously received superoxide dismutase (SOD) targeted to tubular epithelium (HC-SOD; 10 mg/kg ip daily for 5 days). RT-PCR was used for analysis of mRNA expression of genes related to oxidative stress. OR caused a dose-dependent decrease in GFR, paralleled by increased levels of ascorbyl radicals and oxidative protein damage. Antioxidant treatment with HC-SOD decreased renal function even more and also increased tissue damage and mortality. Renal mRNA levels for key components in the antioxidative defense were strongly decreased, whereas those for several cytokines were increased. The data strongly suggest that OR nephrotoxicity in vivo is mediated by oxidative stress, including a virtual shutdown of important antioxidative enzymes. We interpret the unexpected effect of HC-SOD in terms of unbalanced SOD and catalase levels in the presence of OR, leading to massive generation of *OH and cell death.

Indications of hepatic and cardiac toxicity caused by subchronic Tricholoma flavovirens consumption.

The yellow tricholoma (Tricholoma flavovirens or Tricholoma equestre) is a wild mushroom species that was previously considered edible and tasty. Recently, it caused several cases of delayed rhabdomyolysis in humans and elevated serum creatine kinase (CK) activities in laboratory mice (Mus musculus) in a dose-response study. The present study continued to examine the effects of prolonged T. flavovirens consumption at 12 g freshly frozen mushroom kg(-1)d(-1) on the plasma clinical chemistry and organ histology of mice. The plasma CK and CK-MB activities and the plasma bilirubin concentrations were higher in the exposed mice than in the controls. In addition, pericardial lymphocyte infiltrates were present in the mice that had consumed the mushroom. The results indicate myo-, cardio- and hepatotoxic effects of T. flavovirens.

Cerebellar effects after consumption of edible morels (Morchella conica, Morchella esculenta).

Morchella esculenta and Morchella conica are well known edible morels, which seldom induce clinical symptoms. We report six persons who developed cerebellar effects 6-12 hours after consumption of these mushrooms. The symptoms were self-limited and disappeared after one day.

Mushroom Poisoning Cases in Dogs and Cats: Diagnosis and Treatment of Hepatotoxic, Neurotoxic, Gastroenterotoxic, Nephrotoxic, and Muscarinic Mushrooms.

Ingestion of poisonous mushrooms by small animals can lead to liver failure, neurotoxicity, or gastrointestinal irritation. Although amanita poisoning can be lethal, ingestion of other toxic mushrooms is generally self-limiting and not life threatening. Most cases are undiagnosed, as routine diagnostic tests only exist for amanitins and psilocin. Early detection of amanitin exposure can greatly aid in the therapeutic intervention by allowing veterinarians to make timely decisions regarding patient management. Treatment is generally supportive, but specific therapeutic measures exist for amanitin and psilocin exposures.

Survey of Amanita phalloides poisoning: clinical findings and follow-up evaluation.

The aim of our study was to evaluate the severity of hepatic and kidney damage with a focus on their reversibility, and to analyze the prognostic factors following Amanita phalloides poisoning based on calls made to the Czech Toxicological Information Centre. A variety of clinical and laboratory parameters were collected. Student's t-test and Fisher's test were used for statistical analysis. Amanita phalloides poisoning was verified in 34 cases (5 children, 29 adults). The following findings emerged: vomiting (76%), diarrhea (62%), hepatic failure (24%), and renal failure (11%). Two patients died on the fifth day after mushroom ingestion. In 18 patients, all serum levels normalized by the time of discharge; in 10 patients up to 7.3 months on average after discharge. Five patients did not comply with follow-up. Renal damage persisted in only one patient, 19 months after discharge. In conclusion, the interval to recovery from hepatic and renal damage by the time of discharge depended on a decrease in the prothrombin index and an increase in serum transaminase and bilirubin levels. Recovery was favorable in all subjects who survived the acute phase of poisoning, except in one patient with a solitary kidney.

[Mechanism and protective effect of glossy ganoderma decoction on the activities of RNA polymerase in hepatocyte of rabbits with Amanita mushroom poisoning].

OBJECTIVE: To investigate the mechanism of glossy ganoderma decoction in Amanita mushroom poisoning. METHODS: Twenty male New Zealand white rabbits were randomly divided into 4 groups, including a normal control, a model poison group, and 2 treatment groups (different doses of glossy ganoderma decoction). The activities of hepatocyte RNA polymerase were measured by ultraviolet spectrophotometry and liver function were measured. RESULTS: The activities of hepatocyte RNA polymerase of the model group significantly decreased, and those of the 2 treatment groups were significantly higher than those of the model group. There was a dose-dependent manner between the 2 treatment groups ( all Ps<0.01), and the differences of liver function test including total bilirubin (TBIL), direct bilirubin (DB), total bile acid (TBA), and alanine aminotransferase (ALT) in the 4 groups were significant (P<0.01). CONCLUSION: Glossy ganoderma decoction may protect the liver from Amanita mushroom poisoning. Its mechanism may be related to the increase of the activities of hepatocyte RNA polymerase.

New syndromes in mushroom poisoning.

Several new mushroom poisoning syndromes have been described since the early 1990s. In these syndromes, the onset of symptoms generally occurs >6 hours after ingestion. Treatment is mainly supportive. The syndrome induced by Amanita smithiana/proxima consists of acute tubulopathy, which appears earlier and does not have the same poor prognosis as the orellanine-induced syndrome. It has been described since 1992 in the US and Canada with A. smithiana; in France, Spain and Italy with A. proxima; and in Japan with A. pseudoporphyria. The responsible toxin is probably 2-amino-4,5-hexadienoic acid. The erythromelalgia syndrome has been described as early as the late 19th century in Japan and South Korea with Clitocybe acromelalga, and since 1996 in France and then Italy with C. amoenolens. Responsible toxins are probably acromelic acids identified in both species. Several cases of massive rhabdomyolysis have been reported since 1993 in France and 2001 in Poland after ingestion of large amounts of an edible and, until then, valuable species called Tricholoma equestre. These cases of rhabdomyolysis are associated with respiratory and cardiac (myocarditis) complications leading to death. Rhabdomyolysis with an apparently different mechanism was described in Taiwan in 2001 with Russula subnigricans. Finally, cases of encephalopathy were observed twice after ingestion of Hapalopilus rutilans in Germany in 1992 and Pleurocybella porrigens in Japan in 2004, where a convulsive encephalopathy outbreak was reported in patients with history of chronic renal failure.

Amanita bisporigera ingestion: mistaken identity, dose-related toxicity, and improvement despite severe hepatotoxicity.

Ingestion of wild mushrooms has led to unintentional poisonings caused by mistaken identity. We report 3 cases of exposure to Amanita bisporigera, demonstrating dose-related toxicity. The use of nasobiliary drainage as a novel approach to interrupting the enterohepatic circulation of amatoxins is illustrated. Pathophysiology and treatment of Amanita poisoning are reviewed.

A retrospective study of mushroom poisoning in Iran.

The objective of this study was to describe the pattern of mushroom poisoning in adults admitted to the Loghman-Hakim Hospital Poison Center from 1992 to 2002. All patients > or = 12 years of age were included in the study. The frequency of mushroom poisoning with respect to age, sex, season, reason, place of residence, latent phase, clinical and laboratory findings, treatment, and outcome of patients was investigated. Of the 72421 poisoning cases admitted to Loghman-Hakim Hospital Poison Center from 1992 to 2002, only 37 were poisoned by consumption of toxic mushrooms. As some of the patients' files were incomplete, only 25 files were included in the study. Of this number, 68% were male. The patients' age ranged between 12 and 65 years, with a mean of 31 years of age. All cases were accidental and mostly from Tehran (36%) and the northern provinces (rainy woodlands) of Iran (32%). Autumn was the most common season for poisoning with a frequency of 80%. The latent phase of poisonings was between 0.5 and 12 hours. The most frequently reported symptoms were vomiting (84%), nausea (60%), abdominal pain (60%) and diarrhea (40%). Jaundice was observed in 44% of cases, with a 50% rate of hepatic encephalopathy. A total of 66% of patients were discharged and the duration range of hospitalization was 1-12 days. In conclusion, people should be more informed of the dangers posed by wild mushrooms. Training of physicians and nurses in the accurate diagnosis and management of patients poisoned with poisonous mushrooms would improve the rate of survival.

Severe rhabdomyolysis, acute renal failure and posterior encephalopathy after 'magic mushroom' abuse.

We report the case of a 25-year-old, hepatitis C-infected man, who presented with severe rhabdomyolysis and acute renal failure, and later developed posterior encephalopathy with cortical blindness after the ingestion of magic mushrooms. Conventional respiratory and cardiovascular support including mechanical ventilation, continuous veno-venous hemodialysis and corticosteroids led to improvement and the patient recovered completely over the following months. Magic mushrooms are becoming increasingly fashionable among drug users, as they are believed to be more harmless than other hallucinogenic designer drugs. So far, little is known about their possible severe side effects.