Institute for Hygiene and the National Consulting Laboratory for Haemolytic Uraemic Syndrome, University of Münster, Münster, Germany.
Lancet Infect Dis. 2011 Sep;11(9):671-6. doi: 10.1016/S1473-3099(11)70165-7. Epub 2011 Jun 22.
In an ongoing outbreak of haemolytic uraemic syndrome and bloody diarrhoea caused by a virulent Escherichia coli strain O104:H4 in Germany (with some cases elsewhere in Europe and North America), 810 cases of the syndrome and 39 deaths have occurred since the beginning of May, 2011. We analysed virulence profiles and relevant phenotypes of outbreak isolates recovered in our laboratory.
We analysed stool samples from 80 patients that had been submitted to the National Consulting Laboratory for Haemolytic Uraemic Syndrome in Münster, Germany, between May 23 and June 2, 2011. Isolates were screened with standard PCR for virulence genes of Shiga-toxin-producing E coli and a newly developed multiplex PCR for characteristic features of the outbreak strain (rfb(O104), fliC(H4), stx(2), and terD). Virulence profiles of the isolates were determined with PCR targeting typical virulence genes of Shiga-toxin-producing E coli and of other intestinal pathogenic E coli. We sequenced stx with Sanger sequencing and measured Shiga-toxin production, adherence to epithelial cells, and determined phylogeny and antimicrobial susceptibility.
All isolates were of the HUSEC041 clone (sequence type 678). All shared virulence profiles combining typical Shiga-toxin-producing E coli (stx(2), iha, lpf(O26), lpf(O113)) and enteroaggregative E coli (aggA, aggR, set1, pic, aap) loci and expressed phenotypes that define Shiga-toxin-producing E coli and enteroaggregative E coli, including production of Shiga toxing 2 and aggregative adherence to epithelial cells. Isolates additionally displayed an extended-spectrum β-lactamase phenotype absent in HUSEC041.
Augmented adherence of the strain to intestinal epithelium might facilitate systemic absorption of Shiga toxin and could explain the high progression to haemolytic uraemic syndrome. This outbreak demonstrates that blended virulence profiles in enteric pathogens, introduced into susceptible populations, can have extreme consequences for infected people.
German Federal Ministry of Education and Research, Network Zoonoses.
自 2011 年 5 月初以来，德国爆发了由一种毒力较强的产志贺毒素大肠杆菌 O104：H4 引起的溶血性尿毒综合征和血性腹泻疫情，目前已报告了 810 例溶血性尿毒综合征病例和 39 例死亡病例，疫情还蔓延到了欧洲和北美其他一些地区。我们分析了在本实验室分离的暴发菌株的毒力谱和相关表型。
我们分析了 2011 年 5 月 23 日至 6 月 2 日期间送至德国明斯特国家溶血性尿毒综合征咨询实验室的 80 例患者的粪便样本。采用标准 PCR 对产志贺毒素大肠杆菌的毒力基因和新开发的暴发菌株特征性多重 PCR（rfb（O104）、fliC（H4）、stx（2）和 terD）进行筛查。采用针对产志贺毒素大肠杆菌和其他肠道致病性大肠杆菌典型毒力基因的 PCR 方法确定分离株的毒力谱。采用 Sanger 测序法对 stx 进行测序，测定志贺毒素的产生、对上皮细胞的黏附能力，并确定系统发生和抗菌药物敏感性。
所有分离株均为 HUSEC041 克隆（序列类型 678）。所有分离株均具有结合产志贺毒素大肠杆菌（stx（2）、iha、lpf（O26）、lpf（O113））和肠集聚性大肠杆菌（aggA、aggR、set1、pic、aap）特征的毒力谱，并表达了志贺毒素产生和肠集聚性大肠杆菌的表型，包括志贺毒素 2 的产生和对上皮细胞的集聚黏附。分离株还表现出扩展谱β-内酰胺酶表型，而 HUSEC041 则不存在这种表型。
该菌株对肠上皮细胞的黏附能力增强可能有助于志贺毒素的全身吸收，并可解释其向溶血性尿毒综合征的高进展性。此次暴发表明，进入易感人群的肠病原体的混合毒力谱可能会对感染人群造成严重后果。
德国联邦教育与研究部，传染病网络。
