A Large, Refractory Nosocomial Outbreak of Klebsiella pneumoniae Carbapenemase-Producing Escherichia coli Demonstrates Carbapenemase Gene Outbreaks Involving Sink Sites Require Novel Approaches to Infection Control
A Large, Refractory Nosocomial Outbreak of Klebsiella pneumoniae Carbapenemase-Producing Escherichia coli Demonstrates Carbapenemase Gene Outbreaks Involving Sink Sites Require Novel Approaches to Infection Control
复制标题
DOI：
10.1128/aac.01689-18
复制
发表时间：
2018-12-01
影响因子：
4.9
通讯作者：
Cawthorne, J.
中科院分区：
文献类型：
--
作者：
Decraene, V.;Phan, H. T. T.;Cawthorne, J.
碳青霉烯类耐药肠杆菌（CRE）对健康构成威胁，但有效的控制干预措施仍不清楚。医院废水场越来越被视为重要的潜在水库。我们调查了中央曼彻斯特大学医院 NHS 基金会信托基金 (CMFT)（英国）过去 8 年的大规模产肺炎克雷伯菌碳青霉烯酶 (KPC) 大肠杆菌疫情和更广泛的 CRE 发病趋势，以确定感染预防和控制措施的影响。将细菌学和患者管理数据（2009 年至 2017 年）联系起来，并对 CMFT 或地区医院 KPC 产生的大肠杆菌分离株 (n = 268) 的子集进行了测序。控制干预措施遵循国际指南，包括分组、直肠筛查（n = 184,539 次筛查）、环境采样、加强清洁、关闭病房和更换管道。 CRE 检测时间趋势的分段回归用于评估干预措施对 CRE 发生率的影响。基因组分析（n = 268 个分离株）确定了产 KPC 的大肠杆菌爆发克隆（菌株 A，序列类型 216 [ST216]；n = 125）在患者和环境中的传播，特别是在 2 个心脏病房（病房 3 和 4）中，尽管采取了控制措施。 ST216 A 株曾引起过一次爆发，并与其他大肠杆菌谱系和肠杆菌科物种共享其 KPC 质粒。在关闭 3 号和 4 号病房并更换管道后，CRE 感染发生率下降，表明对环境有贡献。然而，第 3 病区/第 4 病区废水处理场很快就被 CRE 重新定殖，并且患者 CRE 的收购再次出现，尽管速度较低。患者搬迁和管道更换与控制产生 KPC 的克隆性大肠杆菌爆发有关；然而，在这种干预措施之后，CRE 和患者 CRE 采集造成的环境污染很快再次出现。大量病例和 bla(KPC) 在大肠杆菌（包括致病谱系）中的持续存在令人担忧。
Carbapenem-resistant Enterobacteriaceae (CRE) represent a health threat, but effective control interventions remain unclear. Hospital wastewater sites are increasingly being highlighted as important potential reservoirs. We investigated a large Klebsiella pneumoniae carbapenemase (KPC)-producing Escherichia coli outbreak and wider CRE incidence trends in the Central Manchester University Hospital NHS Foundation Trust (CMFT) (United Kingdom) over 8 years, to determine the impact of infection prevention and control measures. Bacteriology and patient administration data (2009 to 2017) were linked, and a subset of CMFT or regional hospital KPCproducing E. coli isolates (n = 268) were sequenced. Control interventions followed international guidelines and included cohorting, rectal screening (n = 184,539 screens), environmental sampling, enhanced cleaning, and ward closure and plumbing replacement. Segmented regression of time trends for CRE detections was used to evaluate the impact of interventions on CRE incidence. Genomic analysis (n = 268 isolates) identified the spread of a KPC-producing E. coli outbreak clone (strain A, sequence type 216 [ST216]; n = 125) among patients and in the environment, particularly on 2 cardiac wards (wards 3 and 4), despite control measures. ST216 strain A had caused an antecedent outbreak and shared its KPC plasmids with other E. coli lineages and Enterobacteriaceae species. CRE acquisition incidence declined after closure of wards 3 and 4 and plumbing replacement, suggesting an environmental contribution. However, ward 3/ward 4 wastewater sites were rapidly recolonized with CRE and patient CRE acquisitions recurred, albeit at lower rates. Patient relocation and plumbing replacement were associated with control of a clonal KPC-producing E. coli outbreak; however, environmental contamination with CRE and patient CRE acquisitions recurred rapidly following this intervention. The large numbers of cases and the persistence of bla(KPC) in E. coli, including pathogenic lineages, are of concern.