山西河津一起毒蘑菇中毒事件调查分析

目的 分析山西河津一起毒蘑菇中毒事件的现场处置过程,为做好蘑菇中毒事件的应急处置提供借鉴.方法 收集流行病学、临床救治资料和可疑毒蘑菇样本,并对蘑菇样本进行了分子生物学鉴定.结果 流行病学调查发现中毒事件患者均食用炒蘑菇,食量不等,潜伏期0.5～1.5h.主要临床表现为恶心、呕吐、腹痛、腹泻、出汗、流涎、乏力,其中4例出现瞳孔缩小、视物模糊,2例肝功能指标异常.给予洗胃、保肝、利尿和对症支持治疗,8d后全部治愈出院.通过鉴定蘑菇样本为墨汁鬼伞、毛头鬼伞和丝盖伞属.结论 墨汁鬼伞、毛头鬼伞和丝盖伞属均属毒蘑菇,结合流行病学、临床表现及分子生物学鉴定结果判定此事件是一起因食用多个种属毒蘑菇引起的中毒事件.     

江苏溧阳6例急性蘑菇中毒的流行病学临床调查及毒物鉴定研究

目的 回顾性分析常州溧阳城乡6例蘑菇中毒的临床诊疗经过,鉴定引发中毒的蘑菇种类,为该地区此类中毒事件的处理提供借鉴。方法 收集2019年8月、9月江苏省人民医院溧阳分院急诊6例蘑菇中毒患者病例资料、流行病学,并对蘑菇样品进行形态学和分子生物学鉴定。结果 流行病学调查发现所有患者均食用自己采摘的野生蘑菇,中毒潜伏期2-6h,出现恶心、呕吐、腹痛、腹泻,其中头晕、乏力2例,心悸1例,发热1例;3例心肌酶谱升高,1例肾功能异常;蘑菇标本经形态学和分子生物学鉴定为可以引起胃肠炎型中毒的青褶伞。结论 青褶伞在常州溧阳较为常见,主要临床表现为胃肠炎症状,以恶心、呕吐、腹痛、腹泻等为主,早期予以抗感染、维持水电解质平衡、补液等对症处理,预后良好。     

一起亚稀褶红菇中毒事件调查及救治情况分析北大核心CSCD

2020年7月云南省楚雄彝族自治州禄丰市发生一起亚稀褶红菇(Russula subnigricans hongo)中毒事件,4例患者经过35d的治疗后康复出院,动态追踪复查,所有患者均未遗留后遗症。鉴于亚稀褶红菇毒性强,近几年仍有致死事件发生,其致死人数仅次于含鹅膏毒肽蘑菇中毒,而国内鲜有关于亚稀褶红菇中毒的报道,致使此类蘑菇中毒的诊疗困难。为警示公众,预防类似中毒事件发生,本文对该起事件的流行病学调查结果和诊断救治情况进行总结分析,现将结果报道如下。     

青褶伞中毒的物种鉴定、中毒特征及救治

目的 探索褶伞属青褶伞的物种鉴定,总结青褶伞中毒诊断及救治方法,为该蘑菇造成的中毒事件处理和中毒患者救治提供借鉴.方法 结合中毒案例,收集流行病学、临床诊断救治资料和可疑毒蘑菇样本,对毒蘑菇样本进行形态学和分子生物学鉴定,并对青褶伞造成的中毒特征及救治进行梳理.结果 2名中毒患者食用了不等量的,自行采集的白色野生蘑菇;发病潜伏期约4h.主要临床表现为恶心、呕吐、腹痛、腹泻(呈稀水样便),一名患者伴有谷丙转氨酶和谷草转氨酶的升高,另一名患者呕吐少量淡红色液体,并在第2天伴有淡血性稀水便.给予足量补液、激素、保肝、青霉素抗感染等对症支持治疗,3d后全部治愈出院.毒蘑菇样本通过形态学结合分子生物学方法鉴定为青褶伞(chlorophyllum molybdites).结论 该中毒事件是一起由青褶伞引起的经口中毒,青褶伞菌为有毒蘑菇,主要引起消化道刺激性改变,病情较轻,病程短;形态学结合分子生物学方法对青褶伞的物种鉴定是识别青褶伞的有效方法.     

中国大陆地区蘑菇中毒事件及危害分析

目的 分析蘑菇中毒事件流行病学特征,阐述其发生规律,为蘑菇中毒预防控制和诊疗提供基础数据.方法 对2004～ 2014年全国突发公共卫生事件管理信息系统报告的蘑菇中毒事件进行时间和空间分布分析,并对2010～2014年蘑菇中毒事件发生原因、场所、人群的职业分布和事件鉴定情况进行描述性分析.结果 2004～2014年,我国(不包括港澳台地区)共报告蘑菇中毒事件576起,中毒3 701例,死亡786例,病死率21.24％.蘑菇中毒事件数排列前五位的省份分别为云南、贵州、四川、广西和湖南,夏季高发,重大和较大级别的事件数占76.56％.2010 ～2014年数据显示,中毒原因为误采、误食或购买了有毒蘑菇,发生场所在家庭的占所有发生场所的87.5％,农民、工人、儿童和学生等活动范围大、好奇心强,不具备分辨可食蘑菇和有毒蘑菇能力,是蘑菇中毒事件的主要发生人群;2010～2014年蘑菇中毒事件未能进行蘑菇鉴定和毒素检测的有200起,占同期蘑菇中毒事件数的92.59％;开展规范鉴定,明确鉴定到种的事件仅有2起.结论 蘑菇中毒引起的死亡是造成食源性中毒事件死亡的主要原因之一,应对高发季节和高发省份进行重点监测和管理,同时加强重点地区医疗卫生人员可疑有毒蘑菇采集、鉴定能力培训,开展预防蘑菇中毒健康宣传.     

亚稀褶红菇中毒的物种鉴定、地理分布、中毒特征及救治

目的 探索亚稀褶红菇的物种鉴定、地理分布、中毒症状及救治措施,为该物种造成的中毒事件应急处置及病患救治提供借鉴.方法 结合中毒案例,开展流行病学、临床救治调查分析,对毒蘑菇样本进行形态学和分子生物学鉴定,并对亚稀褶红菇造成的中毒特征及救治方法进行系统整理.结果 2名中毒患者2015年7月26日晚食用了自己采集的“火炭菌”,潜伏期2～3h.主要临床表现为恶心、呕吐、腹痛,伴有酱油色尿,肌酸激酶急剧上升,并伴有丙氨酸氨基转移酶、天门冬氨酸氨基转移酶、肌酸激酶同工酶和血肌酐等的上升,最终表现为肾功能衰竭和呼吸衰竭,符合以往报道的亚稀褶红菇的中毒表现.2位患者给予血液灌流、连续性静脉-静脉血液滤过、保肝、保肾、抗氧化等对症支持治疗,一名患者于40余天后死亡.另一名患者虽然历经转院治疗,至2016年2月底仍未出院,预后不佳.毒蘑菇样本通过形态学结合分子生物学方法鉴定为亚稀褶红菇(russula subnigricans).结论 亚稀褶红菇是一种毒性高的有毒蘑菇,其在我国分布较广,形态学分类结合分子生物学(使用ITS片段)方法是物种鉴定的有效方法,此蘑菇中毒者潜伏期短,人中毒靶器官主要为横纹肌,重症患者预后差.     

发光类脐菇中毒事件调查分析

目的 分析云南省元谋县一起毒蘑菇中毒事件的流行病学调查结果和实验室毒蘑菇鉴定的实验结果,对中毒病因进行确证.方法 收治中毒患者后,当地医务人员迅速开展中毒救治工作,疾控专业人员对患者携带的可疑毒蘑菇样本进行形态学和分子生物学鉴定,并对调查结果进行分析.结果 2015年8月1日,元谋县某电厂12名男性工人,一起食用了一种野生菌约100～200g,进食后10 min到0.5h出现症状.临床表现为不同程度出现恶心、呕吐、腹痛、腹泻,头晕、胸闷症状.4名症状较轻者门诊给予处理后拒绝治疗,3名患者给予机械洗胃,药用炭胃管注入保留等促进毒物排泄治疗,其他患者给予保肝等对症支持治疗.8名患者3～4d后病愈出院.现场采集的可疑毒蘑菇标本经鉴定确认为发光类脐菇(omphalotus olearius).结论 该中毒是一起由发光类脐菇引起的食物中毒事件.明确为由发光类脐菇导致的中毒在国内尚属首次报道.提示要加强对该种毒蘑菇的研究,并对当地群众开展毒针对性的预防和科普教育.     

致命鹅膏的研究进展

致命鹅膏最早发现于我国广东，是我国蘑菇中毒事件中最常见的剧毒蘑菇之一，因含有鹅膏肽类毒素，可以造成急性肝损害型中毒，引起相关食物中毒事件已有73起。本研究系统分析了致命鹅膏的生物学特征、毒素检测、毒素基因组学、中毒事件流行病学及毒理学等方面的研究历程和最新进展，以期为该种剧毒蘑菇中毒的有效防控和精准救治提供科学依据。     

残托斑鹅膏中毒11例报告

1986年4月,本院收治了某林场民工同餐毒蕈中毒的患者11人,主要表现为神经及胃肠道刺激症状,严重者尚有血管-神经性反应。毒蕈经广东省微生物研究所鉴定为残托斑鹅膏(Amanita kwangsiensis wang)。该蕈是我国广西首次发现的一种毒蘑菇。中毒病例在国内罕见,现将有关情况报告如下。     

一起细菌性食物中毒的调查报告

2003年7月9日，贵定县洛北河乡发生一起85名群众集体中毒事件。根据流行病学调查，中毒患者临床表现，及实验室检验分析，证实为一起由沙门氏菌引起的细菌性食物中毒。现将调查结果报道如下：     

鹅膏肽类毒素的研究进展

本文在阅读国内外鹅膏肽类毒素相关文献的基础上,从鹅膏肽类毒素的种类、来源、毒性及毒作用机制、中毒表现及治疗方面做出归纳整理,以期为今后鹅膏肽类毒素的进一步研究提供一定帮助.     

A Reply to “Carnitine” and “Role of Carnitine in Valproic Acid Toxicity”

Background. Amatoxin‐containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion. Objective. To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning. Methods. All cases of mushroom ingestion referred to a Poison Center during a one‐month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut‐off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard. Results. Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut‐off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific. Conclusions. Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.     

Amanita phalloides poisoning in Austria (author's transl)]

An analysis of 28 cases of amanita phalloides poisoning serves as basis for a discussion of the clinical features and therapeutic problems involved. A critical review of recent experimental investigations in animals points to new possibilities in the treatment of amanita phalloides poisoning.     

Treatment of Amanita phalloides poisoning: I. Retrospective evaluation of plasmapheresis in 21 patients.

Amanita phalloides poisoning is the most common cause of lethal mushroom poisoning (lethality >20% in adults). A specific antidote against the amanitin toxins is not available. This retrospective study reports results in 21 patients (12 males, 9 females; ages 9-59 years) treated for amanita phalloides poisoning between 1984 and 1993. Plasmapheresis was carried out using a commercial plasma protein solution (Biseko, Biotest, Dreieich, Germany) in 17 patients, fresh plasma in 2 patients, and human albumin/Ringer's solution in 2 patients. Ancillary drugs, including penicillin and silibinin, also were used for detoxification, correction of blood-clotting deficiencies, and hepatic protection. One patient died of acute hepatic failure. The results, assessed using mortality (4.8% overall) and frequency of complications, indicate that plasmapheresis is a safe and effective treatment for amanita phalloides poisoning but that further investigations are needed, especially involving measurements of efficacy and the efficiency of toxin removal.     

Early onset muscarinic manifestations after wild mushroom ingestion

Despite being a favorite delicacy, only 200–300 of the 5,000 known mushroom species have been clearly established to be safe for consumption. Cases of mushroom poisoning have been reported with diverse clinical syndromes. A syndromic classification of mushroom poisoning has recently been developed to facilitate early interventions. We present a series of five cases of mushroom poisoning with muscarinic manifestations to highlight the difficulties we faced with exact species and toxin identification and the importance of this syndromic classification. The common symptoms in our case series are blurred vision, diarrhea, vomiting, and abdominal cramps.     

Amatoxin Poisoning: Case Reports and Review of Current Therapies

Background

Diagnosis and management of Amanita mushroom poisoning is a challenging problem for physicians across the United States. With 5902 mushroom exposures and two resultant deaths directly linked to Amanita ingestion in 2009, it is difficult for physicians to determine which patients are at risk for lethal toxicity. Identification of amatoxin poisoning can prove to be difficult due to delay in onset of symptoms and difficulty with identification of mushrooms. Consequently, it is difficult for the Emergency Physician to determine proper disposition. Further, treatment options are controversial.

Objectives

To review current data to help health care providers effectively identify and treat potentially deadly Amanita mushroom ingestions.

Case Reports

We present two cases of Amanita mushroom ingestion in the northeastern United States treated with N-acetylcysteine, high-dose penicillin, cimetidine, and silibinin, a semi-purified fraction of milk thistle-derived silymarin, as part of their treatment regimen. The mushroom species was identified by a consultant as Amanita Ocreata.

Conclusions

We present the successful treatment of 2 patients who ingested what we believe to be an Amanita species never before identified in the northeastern United States.     

毒蕈中毒临床类型及特征分析

目的提高对毒蕈中毒的认识，探讨毒蕈中毒的类型及临床特征。方法对1980-01—2004—12在我院救治的172例毒蕈中毒患者进行回顾性临床分析。结果胃肠炎型17例，全部治愈；急性肾功能衰竭型136例，治愈135例（99．3％），死亡1例（0．7％）；中毒性肝炎型19例，治愈13例（68．4％），死亡6例（31．6％）。结论毒蕈中毒的临床表现和毒理机制复杂，毒蕈中毒类型及分型应符合临床病例资料及特征，据本组172例临床资料及文献报道分为四型：①胃肠炎型；②急性肾功能衰竭型；③中毒性肝炎型；④混合型，虽本组172例中没有符合此型病例，但还是作为临床一个类型提出，供同道们商榷。     

Three New Herbal Hepatotoxic Syndromes

Background: Amatoxin poisoning is a medical emergency characterized by a long incubation time lag, gastrointestinal and hepatotoxic phases, coma, and death. This mushroom intoxication is ascribed to 35 amatoxin-containing species belonging to three genera: Amanita, Galerina, and Lepiota. The major amatoxins, the α-, β-, and γ-amanitins, are bicyclic octapeptide derivatives that damage the liver and kidney via irreversible binding to RNA polymerase II. Methods: The mycology and clinical syndrome of amatoxin poisoning are reviewed. Clinical data from 2108 hospitalized amatoxin poisoning exposures as reported in the medical literature from North America and Europe over the last 20 years were compiled. Preliminary medical care, supportive measures, specific treatments used singly or in combination, and liver transplantation were characterized. Specific treatments consisted of detoxication procedures (e.g., toxin removal from bile and urine, and extra-corporeal purification) and administration of drugs. Chemotherapy included benzylpenicillin or other β-lactam antibiotics, silymarin complex, thioctic acid, antioxidant drugs, hormones and steroids administered singly, or more usually, in combination. Supportive measures alone and 10 specific treatment regimens were analyzed relative to mortality. Results: Benzylpenicillin (Penicillin G) alone and in association was the most frequently utilized chemotherapy but showed little efficacy. No benefit was found for the use of thioctic acid or steroids. Chi-square statistical comparison of survivors and dead vs. treated individuals supported silybin, administered either as mono-chemotherapy or in drug combination and N-acetylcysteine as mono-chemotherapy as the most effective therapeutic modes. Future clinical research should focus on confirming the efficacy of silybin, N-acetylcysteine, and detoxication procedures.