Wild mushroom poisoning is a global public health concern, with mushrooms containing amatoxins being the main cause of fatalities. Mushrooms from the genus Amanita and Galerina contain amatoxins. Here we present a case of wild mushroom poisoning that affected three individuals, resulting in two fatalities. Within 10-15 hours after consumption, they experienced symptoms of gastroenteritis such as vomiting, abdominal pain, and diarrhea. One individual sought medical attention promptly and recovered, while the other two sought medical help nearly two or three days after the onset of symptoms, by which time their conditions had already worsened and led to their deaths. The mushrooms were identified belonging to genus Galerina, and laboratory test revealed variations in toxin levels among mushrooms collected from different parts of the decaying stump. The higher levels of α-amanitin, β-amanitin, and γ-amanitin were detected near the base of the tree stump, but trace levels of α-amanitin were found near the top of the stump, while β-amanitin and γ-amanitin were undetectable. This case emphasizes the importance of seeking immediate medical attention when experiencing delayed-onset gastrointestinal symptoms, as it may indicate more severe mushroom poisoning, particularly amatoxin poisoning. Timely and appropriate treatment is equally important. Additionally, consuming different units of the mushrooms in the same incident can lead to varying prognoses due to differences in toxin levels.

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.

OBJECTIVE: To explore the cytotoxicity of four wild mushrooms involved in a case of Yunnan sudden unexplained death (YNSUD), to provide the experimental basis for prevention and treatment of YNSUD.
METHODS: Four kinds of wild mushrooms that were eaten by family members in this YNSUD incident were collected and identified by expert identification and gene sequencing. Raw extracts from four wild mushrooms were extracted by ultrasonic extraction to intervene HEK293 cells, and the mushrooms with obvious cytotoxicity were screened by Cell Counting Kit-8 (CCK-8). The selected wild mushrooms were prepared into three kinds of extracts, which were raw, boiled, and boiled followed by enzymolysis. HEK293 cells were intervened with these three extracts at different concentrations. The cytotoxicity was detected by CCK-8 combined with lactate dehydrogenase (LDH) Assay Kit, and the morphological changes of HEK293 cells were observed under an inverted phase contrast microscope.
RESULTS: Species identification indicated that the four wild mushrooms were Butyriboletus roseoflavus, Boletus edulis, Russula virescens and Amanita manginiana. Cytotoxicity was found only in Amanita manginiana. The raw extracts showed cytotoxicity at the mass concentration of 0.1 mg/mL, while the boiled extracts and the boiled followed by enzymolysis extracts showed obvious cytotoxicity at the mass concentration of 0.4 mg/mL and 0.7 mg/mL, respectively. In addition to the obvious decrease in the number of HEK293 cells, the number of synapses increased and the refraction of HEK293 cells was poor after the intervention of Amanita manginiana extracts.
CONCLUSIONS: The extracts of Amanita manginiana involved in this YNSUD case has obvious cytotoxicity, and some of its toxicity can be reduced by boiled and enzymolysis, but cannot be completely detoxicated. Therefore, the consumption of Amanita manginiana is potentially dangerous, and it may be one of the causes of the YNSUD.
目的: 探究一起云南不明原因猝死（Yunnan sudden unexplained death，YNSUD）案件中涉及的4种野生菌的细胞毒性，为YNSUD的防治提供实验依据。方法: 采集事件发生家庭食用过的4种野生菌，通过专家辨认和基因测序鉴定种属。运用超声波萃取法提取4种野生菌的生品浸膏干预HEK293细胞，然后用细胞计数试剂盒-8（Cell Counting Kit-8，CCK-8）筛选出有明显细胞毒性的野生菌。将筛选出的野生菌再分别制成生品、熬煮和熬煮后酶解3种浸膏，所得3种浸膏以不同浓度干预HEK293细胞，用CCK-8与乳酸脱氢酶（lactate dehydrogenase，LDH）检测法联合检测细胞毒性，并用倒置相差显微镜观察细胞形态。结果: 4种野生菌分别为粉黄黄肉牛肝菌（Butyriboletus roseoflavus）、美味牛肝菌（Boletus edulis）、变绿红菇（Russula virescens）和隐花青鹅膏（Amanita manginiana）。仅在隐花青鹅膏中发现细胞毒性，其生品浸膏在质量浓度为0.1 mg/mL时显示出细胞毒性，熬煮浸膏和熬煮后酶解浸膏分别在质量浓度为0.4 mg/mL和0.7 mg/mL时有明显细胞毒性。除数量明显减少外，隐花青鹅膏提取物干预后的HEK293细胞还表现出突触增多及折光性差等改变。结论: 该起YNSUD案件涉及的野生菌中，隐花青鹅膏的提取物具有明显细胞毒性，通过熬煮和酶解两种工艺可以降低其部分毒性，但不能完全灭毒，食用该菌具有一定的安全隐患，隐花青鹅膏可能是导致该起YNSUD案件的原因之一。.

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.

This paper reported a case of poisoning caused by ingestion of Amanita neoovoidea. The patient experienced nausea, vomiting, oliguria, acute renal function injury, and was discharged after symptomatic support treatment and blood purification treatment. Given the different toxicity of different mushrooms, species identification of poisonous mushrooms can help clinicians in diagnosis and treatment.
本文报道1例误食拟卵盖鹅膏中毒病例。患者出现恶心、呕吐、少尿、急性肾功能损伤伴轻度肝损伤，经过对症支持治疗及血液净化治疗后痊愈出院。鉴于不同蘑菇毒性不同，对毒蘑菇的物种鉴定有助于临床医生的诊断与治疗。.

Mushroom poisoning is a deeply concerning food safety problem that affects the public in China every year. Although there are statistics on the number of poisonings and incidents, there is a lack of data on the types of toxic mushrooms, clinical manifestations and toxins. A case of wild mushroom poisoning occurred in Xiamen. Descriptive epidemiological investigation, toxins detection, and morphological and phylogenetic identification were immediately performed. The patients exhibited typical neurotoxic symptoms after consuming wild mushrooms, including chills, vertigo, drowsiness, salivation and coma. The average incubation period was 30 min. Treatments that were adopted included fluid infusion, gastric lavage, catharsis, and liver protection treatment. All patients recovered within 10 days. The species was identified as Amanita pseudosychnopyramis, and its contents of muscarine, muscimol and ibotenic acid were 170.3 ± 5.9 mg/kg, 835.4 ± 43.1 mg/kg and 637.9 ± 54.8 mg/kg in dry weight, respectively, as detected by ultrahigh-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). To our knowledge, this is the first report of Amanita pseudosychnopyramis poisoning worldwide.

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.
METHODS: 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.
CONCLUSIONS: 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.

Amanita fuliginea (A. fuliginea) poisoning is an uncommon and potentially fatal amatoxin exposure. We present 3 cases of severe A. fuliginea poisoning associated with thrombocytopenia in China. Three patients consumed foraged A. fuliginea and developed nausea, vomiting, abdominal pain, and diarrhea. They were transferred from primary clinics to our hospital 19-39 h after mushroom ingestion. They all presented with acute hepatic injury, coagulopathy, thrombocytopenia (6-41 × 109/L), and positive fecal occult blood. Intravenous fluids and antioxidants were administered immediately after admission. Fibrinogen and platelets were given to patients A, B and C. Patient A developed fulminant liver failure and died on day 5 after mushroom exposure. Patients B and C recovered and were discharged on days 11 and 9, respectively. The main targets of A. fuliginea poisoning are the liver and digestive tract. To our knowledge this is the first report of thrombocytopenia associated with A. fuliginea ingestion.

Amanita neoovoidea (genus Amanita Pers.) poisoning leads to acute renal failure. Here, we present seven case reports of acute renal failure with acute hepatic failure due to ingestion of A. neoovoidea. Clinical manifestations included gastrointestinal symptoms 1-72 h after ingestion; elevation of renal parameters and blood uric acid, blood urea nitrogen, and creatinine levels; a few abnormal hepatic parameters, primarily albumin decrease and alanine aminotransferase increase; and elevation of zymogram parameters such as cholinesterase and lactate dehydrogenase. To determine whether the hepatic/renal lesions were caused by amanitins, we analyzed the blood and urine samples of patients and specimens of poisonous mushrooms. Morphological and molecular biological analyses indicated that the mushroom was A. neoovoidea. However, no amatoxins and phallotoxins were detected in its basidiomata.

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