[From the forest to the ICU and back: an investigative work-up of Amanita phalloides poisoning]. / Vom Wald auf die Intensivstation und zurück: Eine detektivische Aufarbeitung einer Knollenblätterpilzvergiftung.

With over 90% of deaths following mushroom ingestion, poisoning with Amatoxin is one of the most dangerous food intoxications. Despite numerous case reports, treatment recommendations are based on a moderate level of evidence due to a lack of randomized controlled trials.We present the case of a 32-year-old patient who presented with acute liver failure after Amanita phalloides (green death cap mushroom) ingestion and whose therapeutic success was significantly influenced by the administration of activated charcoal, silibinin, and N-acetylcysteine as well as the determined research of an external mycologist.In various retrospective studies, a relevant reduction of mortality could be shown by the mentioned medicinal measures. Despite the high estimated amount of ingestion, we could confirm the effectiveness of this combination therapy in this case.Here, in addition to the drug therapy, attention should also be paid to the extraordinary cooperation of a mycologist, who was able to confirm the suspected diagnosis by his investigative approach and thus contributed to the success of the therapy. Immediate contact with the competent poison centre and the involvement of an expert is therefore recommended in unclear situations.

Loss of Consciousness and Prolonged Convulsions Due to Amanita Pantherina Intoxication.

Loss of consciousness ranks among very common causes for emergency medical service actions and is common occurrence in the emergency department. Its differential diagnosis is very broad and includes many possible causes, not in the least an intoxication. The same applies to convulsive states. Clinical course of mushroom poisoning varies depending on the particular fungal species, with some of the species causing loss of consciousness. One typical representative of such species is panther cap (Amanita pantherina). This case report introduces panther cap poisoning, initially presenting in given patient as coma and protracted generalized convulsions. Complex treatment led to withdrawal of neurologic symptoms, circulatory and metabolic stabilisation and subsequent discharge without signs of permanent organ damage.

Accidental colourful mushroom poisoning - delirium, delusions and dreams.

We report a case of a woman presenting with acute onset of delirium following ingestion of Amanita muscaria mushrooms for anxiolytic effect. Immediate diagnosis was obtained after taking a detailed history and confirmation with online poison database images. She fully recovered with supportive treatment and was discharged 24 hours after presentation. To the best of our knowledge, this is the first case report on A muscaria mushroom poisoning in the UK.

[Acute Kidney Injury Caused by Mushrooms: A Case Report of Amanita Echinocephala Ingestion].

Mushroom poisoning can represent an acute event which the clinical nephrologist must deal with and which often leads to the need for emergency dialysis treatment. Through the exposed clinical case, we describe the secondary clinical manifestations of an acute intoxication sustained by Amanita Echinocephalae, and we will provide an overview of the main fungal intoxications of renal interest, the clinical presentation, the diagnostic strategies, and the subsequent treatment.

[Acute Kidney Injury Caused by Orellanic Syndrome: Case Report].

Orellanic syndrome is caused by fungi of the Cortinarius orellanus and speciosissimus (Europe) species, Cortinarius fluorescens (South America), and Cortinarius rainierensis (North America). Orellanic syndrome is characterized by initially nonspecific symptoms such as muscle and abdominal pain, and a metallic taste sensation in the mouth. After a few days, more specific symptoms appear, such as intense thirst, headache, chills without fever, and anorexia, followed by a phase of polyuria and then of oligoanuria. Renal failure occurs in 70% of cases and is often irreversible. The clinical case involves a 52-year-old man who developed acute renal failure from Orellanic syndrome, necessitating hemodialysis.

[The research of liver failure in Banna miniature pigs caused by amanita exitialis].

Objective: To explore the characteristics of Banna miniature pig liver failure induced by amanita exitialis. Methods: From September to October 2020, a reverse high performance liquid chromatography (RP-HPLC) method was used to determine the toxin content of amanita exitialis solution, and 2.0 mg/kg amanita exitialis solution (α-amanitins+ß-amanitins) was administered orally to Banna miniature pigs. Toxic symptoms, blood biochemical indexes and histopathological changes of liver, heart and kidney were observed at each time point. Results: All Banna miniature pigs died within 76 h of exposure, and different degrees of digestive tract symptoms such as nausea, vomiting and diarrhea appeared between 6 and 36 h. The biochemical indexes of alanine aminotransferase, aspartate aminotransferase, total bilirubin, lactate dehydrogenase, myoglobin, creatine kinase isoenzyme, blood urea nitrogen and creatinine increased significantly at 52 h after exposure, and the differences were statistically significant compared with 0 h (P<0.05). The bleeding of liver and heart was obvious under macroscopic and microscopic observation, hepatocyte necrosis, renal tubule epithelial cell swelling. Conclusion: Large dose of amanita exitialis can cause acute liver failure of Banna miniature pigs, which is in line with the pathophysiological characteristics of acute liver failure, and lays a foundation for further research on the toxic mechanism and detoxification drugs of amanita exitialis induced liver failure.

Mortality Cases of Mushroom Poisoning with Russula subnigricans.

Mushroom poisoning is increasing worldwide, as well as the incidence of fatal mushroom poisoning. Several new syndromes associated with mushroom poisoning have been described in the literature. Notably, 1 of the newly identified mushroom poisonings is Russula subnigricans poisoning. R subnigricans can be classified as causing a delayed-onset rhabdomyolytic syndrome as patients with this severe poisoning present with severe rhabdomyolysis, acute kidney injury, and cardiomyopathy. However, there are only a few reports on the toxicity of R subnigricans. We recently treated 6 patients with R subnigricans mushroom poisoning, of whom 2 died. The 2 patients showed severe rhabdomyolysis, metabolic acidosis, acute renal failure, electrolyte imbalance, and irreversible shock, which caused their deaths. Mushroom poisoning should be considered in the evaluation of rhabdomyolysis of unknown origin. In addition, in cases of mushroom poisoning with severe rhabdomyolysis, R subnigricans poisoning should be promptly identified.

[A case of liver failure caused by fatal amanita poisoning was successfully treated by open cholecystostomy drainage].

The fatality rate of liver failure caused by fatal amanita poisoning is high, and there are no effective antidote drugs in China. On July 30, 2020, the department of infectious diseases and liver diseases of the First People's Hospital of Yunnan Province admitted a 67-year-old female patient with liver failure caused by fatal amanita poisoning. The patient went to the emergency department for treatment due to abdominal pain, vomiting and diarrhea after eating 350-400 g of amanita mushroom for 2 days, accompanied by fatigue for 1 day. There was no abnormality in physical examination. Laboratory indexes: alanine aminotransferase (ALT) 4 798 U/L, aspartate aminotransferase (AST) 10 030 U/L, activated partial thromboplastin time (APTT) 57.5 s, prothrombin time (PT) 72.1 s, international normalized ratio (INR) 8.66, prothrombinactivity (PA) 10%. Based on the patient's medical history, clinical manifestations and laboratory data, the diagnosis was amanita peptide mushroom poisoning and acute liver failure. According to the mechanism of amanita toxin poisoning as enterohepatic circulation, endoscopic retrograde cholangiopancreatography and ultrasound-guided gallbladder puncture and drainage for drainage of bile to discharge toxins were performed to interrupt the enterohepatic circulation of toxins. However, both methods failed, so open cholecystostomy was performed. Because the patient's coagulation function was very poor, artificial hepatic plasma exchange was given to improve coagulation function before open cholecystostomy, and eventually bile was drained successfully. After a total of 19 days of comprehensive medical treatment, the patient was cured and discharged from the hospital, and no sequelae was found after 1 year of follow-up. For such patients, early identification of the disease is required, and blocking the enterohepatic circulation of toxins as soon as possible according to the characteristics and toxicological mechanism of toxins may be the key treatment for rescuing patients with liver failure poisoned by amanita toxin, and it is necessary to combine comprehensive treatments such as active fluid replacement and blood purification to further improve the survival rate.

Cyclopeptide mushroom poisoning: A retrospective series of 204 patients.

Cyclopeptide mushroom poisoning is responsible for 90%-95% of deaths from macrofungi ingestion. The main objectives of this study are to describe cases of cyclopeptide mushroom poisoning and to determine risk factors that may influence the severity/mortality of poisoned patients. We included all cases of amatoxin toxicity reported to two French Poison Centers from 2013 through 2019. We compared the severity with the Poison Severity Score (PSS) and the outcomes of patients using simple logistic regression and multinomial logistic regression. We included 204 cases of amatoxin toxicity. More than three-quarters developed an increase in AST and/or ALT (78.1%), and over half developed a decrease in prothrombin ratio (<70%: 53%) and/or Factor V (<70%: 54%). One-third developed an acute renal injury (AKI). Twelve patients (5.9%) developed post-poisoning sequelae (persistent kidney injury more than 1 month after ingestion and liver transplant). Five patients (2.5%) received a liver transplant, and nine died (4.4%). The mean time to onset of digestive disorders was shorter in PSS2 and PSS3-4 patients (10.9 ± 3.9/11.3 ± 6.3 h) than in PSS1 patients (14 ± 6.5 h; p < 0.05). Patients who died or developed post-poisoning sequelae had more frequent cardiovascular comorbidities compared with recovered patients (60.0% versus 29.5%; p < 0.01).

Electrocardiogram of a patient with mushroom poisoning-induced myocarditis.

A patient presented to our hospital with myocarditis caused by mushroom poisoning. The early ECG changes in this patient were very similar to the ECG of hyperacute ST-segment elevation myocardial infarction or hyperkalemia, but further tests eliminated these options. The patient was fully treated by timely hemodialysis treatment, confirming the diagnosis of mushroom poisoning-induced myocarditis. Although not specific to mushroom poisoning myocarditis, our experience shows that the observed ECG changes. Our findings have the potential to help diagnose and manage this potentially fatal disease in the future.

Possible molecular mechanism for acute encephalopathy by angel-wing mushroom ingestion - Involvement of three constituents in onset.

In Japan in 2004, 59 people who had consumed angel-wing mushroom, Pleurocybella porrigens, experienced acute encephalopathy, and of these 17 died. We purified a lethal protein to mice, pleurocybelline (PC), from P. porrigens. Although PC caused no damage to the brain, PC formed a complex with a lectin (PPL) and showed exo-protease activity, degrading substrates from both N- and C-termini. In addition, the presence of an unstable toxic compound, pleurocybellaziridine (PA), in the mushroom was demonstrated. We hypothesized that the complex and PA are involved in disease development and verified that apoptotic cells in the hippocampus were significantly increased by injection of the mixture of PC, PPL, and PA, indicating that these substances might be involved in acute encephalopathy.

Accidental colourful mushroom poisoning - delirium, delusions and dreams.

We report a case of a woman presenting with acute onset of delirium following ingestion of Amanita muscaria mushrooms for anxiolytic effect. Immediate diagnosis was obtained after taking a detailed history and confirmation with online poison database images. She fully recovered with supportive treatment and was discharged 24 hours after presentation. To the best of our knowledge, this is the first case report on A muscaria mushroom poisoning in the UK.

Mycetism - A report of three cases with review of recent literature.

Wild mushroom grow abundantly in the tropical belts of India, and they form part of the diet among the ethnic tribes. However, wild mushrooms are toxic, and some cause organ failure, namely fulminant hepatitis and kidney injury. Mushroom poisoning is frequently diagnosed based on clinical suspicion, and death has been reported commonly because of the consumption of amatoxin-containing mushrooms. In this article, we discuss three cases of amatoxin-induced mushroom poisoning that resulted in acute kidney and liver failure, requiring intensive medical management and renal replacement therapy. One of these patients died from irreversible fulminant hepatitis.

Amanitin intoxication: effects of therapies on clinical outcomes - a review of 40 years of reported cases.

BACKGROUND AND AIMS: Amanita phalloides poisoning causes severe liver damage which may be potentially fatal. Several treatments are available, but their effectiveness has not been systematically evaluated. We performed a systematic review to investigate the effect of the most commonly used therapies: N-acetylcysteine (NAC), benzylpenicillin (PEN), and silibinin (SIL) on patient outcomes. In addition, other factors contributing to patient outcomes are identified. METHODS: We searched MEDLINE and Embase for case series and case reports that described patient outcomes after poisoning with amanitin-containing Amanita mushrooms. We extracted clinical characteristics, treatment details, and outcomes. We used the liver item from the Poisoning Severity Score (PSS) to categorize intoxication severity. RESULTS: We included 131 publications describing a total of 877 unique cases. The overall survival rate of all patients was 84%. Patients receiving only supportive care had a survival rate of 59%. The use of SIL or PEN was associated with a 90% (OR 6.40 [3.14-13.04]) and 89% (OR 5.24 [2.87-9.56]) survival rate, respectively. NAC/SIL combination therapy was associated with 85% survival rate (OR 3.85 [2.04, 7.25]). NAC/PEN/SIL treatment group had a survival rate of 76% (OR 2.11 [1.25, 3.57]). Due to the limited number of cases, the use of NAC alone could not be evaluated. Additional analyses in 'proven cases' (amanitin detected), 'probable cases' (mushroom identified by mycologist), and 'possible cases' (neither amanitin detected nor mushroom identified) showed comparable results, but the results did not reach statistical significance. Transplantation-free survivors had significantly lower peak values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total serum bilirubin (TSB), and international normalized ratio (INR) compared to liver transplantation survivors and patients with fatal outcomes. Higher peak PSS was associated with increased mortality. CONCLUSION: Based on data available, no statistical differences could be observed for the effects of NAC, PEN or SIL in proven poisonings with amanitin-containing mushrooms. However, monotherapy with SIL or PEN and combination therapy with NAC/SIL appear to be associated with higher survival rates compared to supportive care alone. AST, ALT, TSB, and INR values are possible predictors of potentially fatal outcomes.

Russula subnigricans Poisoning Causes Severe Rhabdomyolysis That Could be Misdiagnosed as Non-ST Segment Elevation Myocardial Infarction.

Mushroom poisoning and subsequently the number of patients visiting emergency rooms are increasing, as well as the proportion of fatal mushroom poisonings. Myocytic mushroom poisoning is one of the new clinical classifications. This report documents the course of a family with Russula subnigricans poisoning complicated by severe rhabdomyolysis, including a case that was misdiagnosed as myocardial infarction. A 64-y-old man visited our hospital with symptoms including substernal chest discomfort, nausea, vomiting, and myalgia, lasting for 12 h. His laboratory tests showed elevated serum high-sensitive troponin I. He was diagnosed with non-ST segment elevation myocardial infarction. After that, 2 family members who ate mushrooms together were transferred from a local emergency room with the diagnosis of rhabdomyolysis. Consequently, rhabdomyolysis due to mushroom poisoning was diagnosed. They were hospitalized in the intensive care unit. After admission, conservative management, including primary fluid resuscitation, was performed, and the patients were discharged without complications. R subnigricans poisoning was revealed after investigation and should be considered in mushroom poisoning with rhabdomyolysis. Early recognition and intensive supportive care are important for mushroom poisoning patients.

The characteristics of liver injury induced by Amanita and clinical value of α-amanitin detection.

BACKGROUND: Amanita poisoning as a foodborne disease has raised concerning mortality issues. Reducing the interval between mushroom ingestion and medical intervention could greatly influence the outcomes of Amanita poisoning patients, while treatment is highly dependent on a confirmed diagnosis. To this end, we developed an early detection-guided intervention strategy by optimizing diagnostic process with performing α-amanitin detection, and further explored whether this strategy influenced the progression of Amanita poisoning. METHODS: This study was a retrospective analysis of 25 Amanita poisoning patients. Thirteen patients in the detection group were diagnosed mainly based on α-amanitin detection, and 12 patients were diagnosed essentially on the basis of mushroom consumption history, typical clinical patterns and mushroom identification (conventional group). Amanita poisoning patients received uniform therapy, in which plasmapheresis was executed once confirming the diagnosis of Amanita poisoning. We compared the demographic baseline, clinical and laboratory data, treatment and outcomes between the two groups, and further explored the predictive value of α-amanitin concentration in serum. RESULTS: Liver injury induced by Amanita appeared worst at the fourth day and alanine aminotransferase (ALT) rose higher than aspartate aminotransferase (AST). The mortality rate was 7.7% (1/13) in the detection group and 50.0% (6/12) in the conventional group (P = 0.030), since patients in the detection group arrived hospital much earlier and received plasmapheresis at the early stage of disease. The early detection-guided intervention helped alleviate liver impairment caused by Amanita and decreased the peak AST as well as ALT. However, the predictive value of α-amanitin concentration in serum was still considered limited. CONCLUSIONS: In the management of mushroom poisoning, consideration should be given to the rapid detection of α-amanitin in suspected Amanita poisoning patients and the immediate initiation of medical treatment upon a positive toxin screening result.

Reversible sub-acute motor neuron syndrome after mushroom intoxication masquerading as amyotrophic lateral sclerosis.

A 56-year-old man presented with rapidly evolving/sub-acute upper and lower motor neuron syndrome in 2015 with significant weakness in the four limbs and the bulbar region. Amyotrophic lateral sclerosis functional rating scale-revised (ALSFRS-r) was rated 34/48. On electromyography, there was a diffuse and active denervation in the four limbs and the tongue. A diagnosis of definite ALS according to international criteria was made. Six months later the patient stopped worsening. In the following years he progressively recovered. ALSFRS-r score improved to reach 48/48 in 2021. His neurological examination is normal and electromyography shows no denervation. Inquiry revealed that he presented a few months and, again a few days before onset, a mushroom poisoning. He was used to eating false morels either crude or undercooked and developed muscles cramps, nausea and vertigo. The relationships between this reversible sub-acute motor neuron syndrome and mushroom intoxication are discussed in the light of the recently described cluster in the Alps with a high incidence of ALS cases. Epidemiological investigations showed that all patients, but not their spouses, used to eat crude or undercooked false morels. Such a mushroom contains hydrazines, a known neurotoxic agent. We are not aware of another case of ALS reversal in that cluster area. We propose that a potential mushroom poisoning be thoroughly searched for when facing with a patient with sub-acute or rapidly worsening ALS syndrome.

Acute liver failure caused by Amanita verna: a case series and review of the literature.

BACKGROUND: Amanita verna is one of the most harmful wild fungi in China. Amanita verna poisoning occurs every year, and the mortality is as high as 50%. However, its clinical manifestations are complex and diverse. CASE PRESENTATION: In March 2019, three patients took a large amount of Amanita, and one of them received liver transplantation in Zhongshan hospital, Sun Yat-sen University. All patients had vomiting and diarrhea 8-12 h after eating wild mushrooms (Amanita). The patients were initially diagnosed with Amanita poisoning. One case (case 3) was complicated and diagnosed as mushroom poisoning (fatal Amanita), toxic hepatitis, acute liver failure, toxic encephalopathy, hemorrhagic colitis, toxic myocarditis, disseminated intravascular coagulation (DIC) and pregnancy. The general clinical data of all patients were recorded, who received early treatment such as hemodialysis, artificial liver plasma exchange, hormone shock and anti-infection. One case (case 1) recovered smoothly after liver transplantation, and the indexes of liver, kidney, coagulation function and infection were improved. The other two cases died of intracerebral hemorrhage. CONCLUSION: Liver transplantation is an effective method for the treatment of acute liver failure caused by mushroom poisoning and can improve the survival rate of patients with toxic liver failure.