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产志贺毒素大肠杆菌 O104:H4:微生物学的新挑战。

Shiga toxin-producing Escherichia coli O104:H4: a new challenge for microbiology.

机构信息

Department of Microbiology, University of Barcelona, Barcelona, Spain.

出版信息

Appl Environ Microbiol. 2012 Jun;78(12):4065-73. doi: 10.1128/AEM.00217-12. Epub 2012 Apr 13.

DOI:10.1128/AEM.00217-12
PMID:22504816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3370534/
Abstract

In 2011, Germany experienced the largest outbreak with a Shiga toxin-producing Escherichia coli (STEC) strain ever recorded. A series of environmental and trace-back and trace-forward investigations linked sprout consumption with the disease, but fecal-oral transmission was also documented. The genome sequences of the pathogen revealed a clonal outbreak with enteroaggregative E. coli (EAEC). Some EAEC virulence factors are carried on the virulence plasmid pAA. From an unknown source, the epidemic strains acquired a lambdoid prophage carrying the gene for the Shiga toxin. The resulting strains therefore possess two different mobile elements, a phage and a plasmid, contributing essential virulence genes. Shiga toxin is released by decaying bacteria in the gut, migrates through the intestinal barrier, and is transported via the blood to target organs, like the kidney. In a mouse model, probiotic bifidobacteria interfered with transport of the toxin through the gut mucosa. Researchers explored bacteriophages, bacteriocins, and low-molecular-weight inhibitors against STEC. Randomized controlled clinical trials of enterohemorrhagic E. coli (EHEC)-associated hemolytic uremic syndrome (HUS) patients found none of the interventions superior to supportive therapy alone. Antibodies against one subtype of Shiga toxin protected pigs against fatal neurological infection, while treatment with a toxin receptor decoy showed no effect in a clinical trial. Likewise, a monoclonal antibody directed against a complement protein led to mixed results. Plasma exchange and IgG immunoadsoprtion ameliorated the condition in small uncontrolled trials. The epidemic O104:H4 strains were resistant to all penicillins and cephalosporins but susceptible to carbapenems, which were recommended for treatment.

摘要

2011 年,德国经历了有史以来最大的一次肠出血性大肠杆菌(STEC)疫情。一系列环境和追溯调查将豆芽消费与疾病联系起来,但也有粪口传播的记录。病原体的基因组序列显示了一次克隆性爆发,与聚集性大肠杆菌(EAEC)有关。一些 EAEC 毒力因子携带在毒力质粒 pAA 上。从一个未知的来源,流行菌株获得了一个携带志贺毒素基因的λ类噬菌体。因此,这些菌株拥有两种不同的移动元件,一个噬菌体和一个质粒,携带重要的毒力基因。志贺毒素由肠道中腐烂的细菌释放,穿过肠壁迁移,并通过血液运输到靶器官,如肾脏。在小鼠模型中,益生菌双歧杆菌干扰了毒素通过肠黏膜的运输。研究人员探索了针对 STEC 的噬菌体、细菌素和低分子量抑制剂。针对肠出血性大肠杆菌(EHEC)相关溶血性尿毒综合征(HUS)患者的随机对照临床试验发现,没有一种干预措施比单独支持治疗更有效。针对一种志贺毒素亚型的抗体可保护猪免受致命的神经感染,而在临床试验中,毒素受体诱饵的治疗没有效果。同样,一种针对补体蛋白的单克隆抗体也有不同的结果。血浆置换和 IgG 免疫吸附在小规模非对照试验中改善了病情。流行的 O104:H4 菌株对所有青霉素和头孢菌素都有耐药性,但对碳青霉烯类敏感,因此被推荐用于治疗。

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No evidence of the Shiga toxin-producing E. coli O104:H4 outbreak strain or enteroaggregative E. coli (EAEC) found in cattle faeces in northern Germany, the hotspot of the 2011 HUS outbreak area.在德国北部(2011 年出血性大肠杆菌 O104:H4 暴发疫情的热点地区),未在牛粪便中发现产志贺毒素大肠埃希氏菌 O104:H4 暴发菌株或聚集性大肠埃希氏菌(EAEC)。
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German outbreak of Escherichia coli O104:H4 associated with sprouts.德国暴发与豆芽相关的肠出血性大肠杆菌 O104:H4 疫情。
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Timeliness of surveillance during outbreak of Shiga Toxin-producing Escherichia coli infection, Germany, 2011.2011 年德国产志贺毒素大肠杆菌感染爆发期间的监测及时性。
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