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.

[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.

Amanita muscaria and Amanita pantherina poisoning: two syndromes.

Amanita muscaria contains more excitatory ibotenic acid and less depressant muscimol compared to Amanita pantherina. In this study A. muscaria poisoned patients were more often confused (26/32, p = 0.01) and agitated (20/32, p = 0.03) compared to those poisoned with A. pantherina (8/17 and 5/17). Patients poisoned with A. pantherina were more commonly comatose (5/17) compared to those poisoned with A. muscaria (2/32) (p = 0.03). In conclusion, the so-called ibotenic or pantherina-muscaria syndrome might be divided into two subtypes.

Dog intoxication by lizard's claw mushroom, Lysurus cruciatus (higher Basidiomycetes) in southern Brazil.

A case of mushroom poisoning of a dog caused by a phalloid fungus is reported for the first time. The phalloid caused gastrointestinal syndrome in a 1-year-old dog, and was identified as Lysurus cruciatus, a common phalloid fungus in southern Brazil.

Mycetism: a review of the recent literature.

Approximately 100 of the known species of mushrooms are poisonous to humans. New toxic mushroom species continue to be identified. Some species initially classified as edible are later reclassified as toxic. This results in a continually expanding list of toxic mushrooms. As new toxic species are identified, some classic teachings about mycetism no longer hold true. As more toxic mushrooms are identified and more toxic syndromes are reported, older classification systems fail to effectively accommodate mycetism. This review provides an update of myscetism and classifies mushroom poisonings by the primary organ system affected, permitting expansion, as new, toxic mushroom species are discovered.

[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.

Tender Nesting Polypore (Hapalopilus rutilans) poisoning: report of two cases.

INTRODUCTION: Only four cases of Hapalopilus rutilans poisoning have been previously published. We report two new cases. CASE REPORTS: A father and his 13-year-old daughter picked mushrooms identified as Fistulina hepatica specimens and ate an unknown quantity (Hour 0). At Hour 12 post-ingestion, both subjects complained of abdominal pain, then nausea, vomiting, anorexia, asthenia, diplopia, and blurred vision. The father also had visual hallucinations. On Day 2 post-ingestion, clinical examination showed multidirectional nystagmus. The father also had balance disorders and both subjects emitted purple urine. Laboratory tests showed elevated serum creatinine and blood urea levels, proteinuria and leukocyturia in both subjects, and mild elevation of hepatic enzymes in the father. Urine color returned to normal on Day 2 and Day 7 post-ingestion in the girl and her father, respectively. Complete clinical and biochemical recovery was obtained within one week in both cases. DISCUSSION: Signs and symptoms are similar to those previously reported after H. rutilans ingestion. This mushroom can be easily confused with F. hepatica. Purple discoloration of the urine after ingestion of a polyporic mushroom is highly suggestive of H. rutilans poisoning. Polyporic acid is probably the active toxin.

[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.

Laboratory confirmation of Amanita smithiana mushroom poisoning.

CONTEXT: Here we present a case of Amanita smithiana poisoning resulting in acute kidney injury requiring dialysis, and highlight laboratory methods used to confirm the diagnosis. Identification of Amanita smithiana toxin using thin-layer chromatography can provide greater diagnostic certainty than history and renal function tests alone. CASE DETAILS: A 63-year-old male presented to hospital with anuria and gastrointestinal symptoms, two days after consuming a soup of wild mushrooms he had picked. He was found to be in acute renal failure, requiring hemodialysis. After nine days of supportive treatment, he recovered renal function, and was discharged in good health 15 days post-ingestion. The patient provided a sample of leftover soup, and examination of cooked mushroom fragments by a mycologist provided preliminary identification of A. smithiana. Thin-layer chromatography revealed the presence of A. smithiana toxin in the soup, confirming this identification. DISCUSSION: A. smithiana is a nephrotoxic mushroom that can be easily mistaken for the edible and highly prized Pine mushroom (Tricholoma magnivelare). It causes initial gastrointestinal symptoms, followed by acute renal failure. Treatment includes dialysis and supportive care until the patient recovers renal function. The chemical structure of the A. smithiana toxin is unknown, but it can be identified as a characteristic spot on thin-layer chromatography.

Hypoglycemia and death in mice following experimental exposure to an extract of Trogia venenata mushrooms.

BACKGROUND: Clusters of sudden unexplained death (SUD) in Yunnan Province, China, have been linked to eating Trogia venenata mushrooms. We evaluated the toxic effect of this mushroom on mice. METHODS: We prepared extracts of fresh T. venenata and Laccaria vinaceoavellanea mushrooms collected from the environs of a village that had SUD. We randomly allocated mice into treatment groups and administered mushroom extracts at doses ranging from 500 to 3500 mg/kg and water (control) via a gavage needle. We observed mice for mortality for 7 days after a 3500 mg/kg dose and for 24 hours after doses from 500 to 3000 mg/kg. We determined biochemical markers from serum two hours after a 2000 mg/kg dose. RESULTS: Ten mice fed T. venenata extract (3500 mg/kg) died by five hours whereas all control mice (L. vinaceoavellanea extract and water) survived the seven-day observation period. All mice died by five hours after exposure to single doses of T. venenata extract ranging from 1500 to 3000 mg/kg, while the four mice exposed to a 500 mg/kg dose all survived. Mice fed 2000 mg/kg of T. venenata extract developed profound hypoglycemia (median= 0.66 mmol/L) two hours after exposure. DISCUSSION: Hypoglycemia and death within hours of exposure, a pattern unique among mushroom toxicity, characterize T. venenata poisoning.