Goodman K E, Simner P J, Tamma P D, Milstone A M
a Department of Epidemiology , The Johns Hopkins Bloomberg School of Public Health , Baltimore , MD , USA.
b Department of Pathology, Division of Medical Microbiology , Johns Hopkins University School of Medicine , Baltimore , MD , USA.
Expert Rev Anti Infect Ther. 2016;14(1):95-108. doi: 10.1586/14787210.2016.1106940. Epub 2015 Nov 4.
The Centers for Disease Control and Prevention (CDC) defines carbapenem-resistant Enterobacteriaceae (CRE) based upon a phenotypic demonstration of carbapenem resistance. However, considerable heterogeneity exists within this definitional umbrella. CRE may mechanistically differ by whether they do or do not produce carbapenemases. Moreover, patients can acquire CRE through multiple pathways: endogenously through antibiotic selective pressure on intestinal microbiota, exogenously through horizontal transmission or through a combination of these factors. Some evidence suggests that non-carbapenemase-producing CRE may be more frequently acquired by antibiotic exposure and carbapenemase-producing CRE via horizontal transmission, but definitive data are lacking. This review examines types of CRE resistance mechanisms, antibiotic exposure and horizontal transmission pathways of CRE acquisition, and the implications of these heterogeneities to the development of evidence-based CRE healthcare epidemiology policies. In our Expert Commentary & Five-Year View, we outline specific nosocomial CRE knowledge gaps and potential methodological approaches for their resolution.
美国疾病控制与预防中心（CDC）基于碳青霉烯耐药性的表型表现来定义耐碳青霉烯类肠杆菌科细菌（CRE）。然而，在这个定义范畴内存在相当大的异质性。CRE在机制上可能因是否产生碳青霉烯酶而有所不同。此外，患者可通过多种途径感染CRE：内源性途径是通过抗生素对肠道微生物群的选择性压力，外源性途径是通过水平传播或这些因素的综合作用。一些证据表明，非碳青霉烯酶产生型CRE可能更常通过抗生素暴露获得，而碳青霉烯酶产生型CRE则通过水平传播获得，但缺乏确凿数据。本综述探讨了CRE耐药机制的类型、CRE获得的抗生素暴露和水平传播途径，以及这些异质性对制定基于证据的CRE医疗保健流行病学政策的影响。在我们的专家评论和五年展望中，我们概述了医院内CRE的具体知识空白以及解决这些空白的潜在方法。
