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.     

急性亚稀褶红菇中毒的临床特征分析

目的 分析急性亚稀褶红菇中毒的临床特点。方法 回顾性分析2020年1月至2022年12月云南大学附属医院急诊内科收治的71例急性亚稀褶红菇中毒患者临床资料,根据是否发生横纹肌溶解分为横纹肌溶解组(n=33)和非横纹肌溶解组(n=38),对比分析两组临床特征。结果 (1)横纹肌溶解组年龄、住院时间大于非横纹肌溶解组(P<0.05)。两组性别、食用后就诊时间、潜伏期差异无统计学意义(P>0.05)。(2)几乎所有的急性亚稀褶红菇中毒患者均以胃肠道症状首发,随后出现横纹肌溶解症状。(3)横纹肌溶解组入院白细胞计数(WBC)、中性粒细胞计数(NEU)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、尿酸(UA)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)和心肌肌钙蛋白I(cTnI)高于非横纹肌溶解组,淋巴细胞计数(LYM)低于非横纹肌溶解组(P<0.05)。(4)发生器官/系统功能损害的病例均源于横纹肌溶解组,其中肝、心肌、肾及循环系统受累最常见。(5)急性亚稀褶红菇中毒死亡病例均源于横纹肌溶解组,其病死率为27.27%。结论 亚稀褶红菇是横纹肌溶解型毒...     

一起亚稀褶红菇中毒事件调查及救治情况分析

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35 d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。     

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。     

亚稀褶黑菇中毒的临床表现研究

正近年来亚稀褶黑菇(亚黑红菇)中毒事件发生率较高,王锐等[1]根据中国2004-2011年22个省份通过突发公共卫生事件报告管理信息系统报告毒蕈中毒事件,统计稀褶黑菇、毒红菇、亚稀褶黑菇共发生中毒事件16起、中毒66例、死亡25例,死亡例数构成比16.4%,仅次于致命白毒伞(44.1%)。有关致命白毒伞的中毒机制及临床表现研究较多,故临床也较为重视。而关于亚稀褶黑菇中毒的报道相对较少,故对其中毒后临床表现认识不足,导致临床中不能早期识别,给诊治带来了一定的影响,加之中毒机理尚不完全清楚,因此病死率较高。本文选取了近年来国内外明确的亚稀褶黑     

一起蘑菇致急性中毒事件的现场调查与鉴定

目的 调查分析云南省南华县一起蘑菇中毒事件的处置过程,鉴定引起中毒的毒蘑菇种类,为做好此类中毒事件的处置提供借鉴.方法 收集事件病例资料、流行病学调查、对蘑菇样品进行形态学和分子生物学鉴定并对中毒事件进行分析.结果 流行病学调查发现患者均食用自行采摘并炒制的蘑菇,食量不等,潜伏期2h,出现呕吐、抽搐、意识不清等神经精神型中毒症状,经形态学和分子生物学鉴定为假褐云斑鹅膏和小豹斑鹅膏.结论 本事件是因误食名为假褐云斑鹅膏和小豹斑鹅膏引起的急性中毒.结合流行病学特点和患者临床表现,证实了通过形态学及分子生物学方法对假褐云斑鹅膏和小豹斑鹅膏的物种鉴定具有适用性.     

亚稀褶红菇中毒并横纹肌溶解2例

蘑菇中毒严重危害我国人民公共卫生安全,据报道,因食物中毒而死亡的人数中,蘑菇中毒的人数排在第一位.不同地区发布的蘑菇数量不同,发病率和死亡率也就不同,其中西南地区发病率较高,特别是云南,一年的蘑菇中毒事件将近占全国总数的40％[1,2].其中亚稀褶红菇属于红菇属,是我国常见的、能导致患者死亡的毒蘑菇之一[3,4].     

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.     

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.     

亚稀褶红菇重度中毒的急救与护理

总结3例亚稀褶红菇重度中毒患者的急救与护理经验.护理重点为第一时间清除毒素,严密监测生命体征,做好血液净化治疗的护理,包括血浆置换和血液灌流血管通路的维护、低血压的预防与处理、抗凝护理与出血观察、变态反应与溶血反应的预防与处理;预防呼吸衰竭、肝损伤及肝性脑病、急性肾损伤、胃肠功能损伤等并发症;重视心理护理与健康宣教.经...     

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.     

Toxicity of mushrooms Paxillus involutus and Paxillus atrotomentosus

Thirty-eight patients with mushroom (Paxillus involutus and Paxillus atrotomentosus) poisoning were treated. Slight poisoning (acute gastroenteritis) was diagnosed in 17 patients, medium-severe in 13, severe in 6, and extremely severe in 2 patients. Changes in the LPO-AOD system correlated with the severity of hepatorenal involvement. The treatment included hepatotropic therapy; patients with acute renal failure were treated by hemodialysis. Paxillus mushrooms induced functional evacuatory disorders in the small intestine. Eleven patients with adhesions in the abdominal cavity developed ileus. Two patients died: a man aged 26 years after eating fried (not boiled) mushrooms and a woman aged 76 years with ileus with symptoms of multiple organ dysfunction. The rest patients were discharged from hospital in satisfactory condition. Clinical course of poisoning with Paxillus mushrooms is discussed.     

Mushroom poisoning: an analysis of the data between 1996 and 2000.

One hundred and forty-three cases (89 women and 54 men) of mushroom poisoning recorded at the emergency service of Osmangazi University Hospital, Faculty of Medicine, between 1996 and 2000 were evaluated. The first symptoms seen were loss of consciousness, fatigue, dizziness, severe headaches, abdominal discomfort and vomiting. The symptoms characteristically appeared suddenly. Eight patients suffering from poisoning caused by cultivated mushrooms, and four patients suffering from poisoning caused by wild mushrooms died from fulminant hepatic failure. The other patients were discharged within a period of 1-10 days. It is suggested that people should be informed of the possibility of mushroom poisoning, which has been increasing recently in Turkey.     

Investigation and analysis of Galerina sulciceps poisoning in a canteen

Introduction: Guizhou Province in China has an abundant resource of wild mushrooms, including numerous poisonous species which contain various toxins. The mortality rate from wild mushroom poisoning has been high in this area in recent years. Galerina sulciceps is a dangerously toxic mushroom which can be fatal if ingested.

Methods: we report on an epidemiological investigation of G. sulciceps poisoning which occurred in Duyun City of Guizhou Province. The characteristics of this species, its toxicity, observed clinical features, laboratory data, treatment modality, and prognosis were investigated in order to provide a reference point for the prevention and treatment of this kind of mushroom poisoning.

Results: Thirteen employees showed toxic symptoms after ingesting wild mushrooms the previous day in a company canteen. Clinical manifestation varied from gastroenteritis to hepatic and renal dysfunction. Most of the 13 patients presented with nausea, vomiting, abdominal pain, diarrhea, and elevated levels of biochemical indices of hepatic and renal function, during which transaminase concentration peaked within 48–72?h. At 48?hours post-ingestion, all patients had hemodialysis, in addition to supportive care for hepatic and renal injury with oral Silibinin and Shenshuaining. All acute renal injury had resolved by day 10, and liver transaminases had trended toward normal in all patients and they were discharged. At follow-up in 30 days, both liver and renal function had completely recovered in all.

Conclusion: This poisoning occurs as a result of unintentional consumption of G. sulciceps, which is relatively rare in mushroom poisonings. All patients recovered fully after timely diagnosis and treatment. To prevent wild mushroom poisoning, the best preventive measure is to educate the public not to gather and eat any unidentified wild mushrooms.     

Mycotoxins revisited: Part II

Mushrooms are ubiquitous in nature. They are an important source of nutrition, however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, whereas foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I reviewed the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and presented an overview of the cyclopeptide-containing mushroom class. Part II is focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.     

Intoxication par les champignons sauvages

Poisoning by ingestion of toxic mushrooms often is a diagnostic and therapeutic challenge for the emergency physician. The delayed symptoms and the ingestion of different mushrooms may render the interpretation of the symptomatology equivocal and the identification of the type of ingested mushroom difficult. Moreover, the result of the toxic dosage is sometimes delayed as for example, for alpha-amanitin, in the case of Amanita phalloides poisoning. In summary, the therapeutic options remain controversial in several types of mushroom poisoning.     

Mycotoxins revisited: Part I

Mushrooms are ubiquitous in nature. They are an important source of nutrition; however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, but foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I, presented in this issue of the Journal, reviews the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and an overview of the cyclopeptide-containing mushroom class. Part II, to be published in the next issue of the Journal, will be focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.     

Poisoning due to amatoxin-containing Lepiota species

Twenty-seven consecutive mushroom poisoning cases were followed up over a period of 14 days. Fourteen out of 27 died of liver failure. There were no deaths from renal failure. The mushrooms were identified as the amatoxin-containing Lepiota species. Therapeutic measures included nasogastric lavage, charcoal, vitamin C, vitamin B, penicillin G, corticosteroids, oral streptomycin and, in the case of a few patients, limited amounts of thioctic acid. Of the ten haemodialysed, nine died. Unfortunately charcoal haemoperfusion was not available. It appeared that therapeutic measures were ineffective and it also seemed that the amount of mushroom ingested was the determining factor for the prognosis. An important point to make is that renal failure does not occur and liver failure is always delayed (group II). For this reason all suspected cases of mushroom poisoning, regardless of absence of clinical signs and symptoms, must be hospitalised for a period of at least one week. The poisonous properties of wild mushrooms have been recognized since ancient times. However, despite awareness of their inherent dangers, serious poisoning continues to occur. Fatal intoxications can be attributed almost entirely to the amtoxin-containing species. Amanita phalloides have been blamed for over 90% of poisoning deaths in North America. There are reports of intoxications of other amatoxin-containing species in Europe, but fatalities due to Lepiota species are reported only rarely. It was previously acknowledged that the interval between ingestion of mushrooms and the onset of symptoms is longer than expected in serious poisonings.(ABSTRACT TRUNCATED AT 250 WORDS)