Laboratoire de Microbiologie, Hôpital Robert Debré, Assistance Publique des Hôpitaux de Paris, Paris, France.
J Clin Microbiol. 2012 Apr;50(4):1295-302. doi: 10.1128/JCM.06131-11. Epub 2012 Jan 18.
Dissemination of carbapenem resistance among Enterobacteriaceae poses a considerable threat to public health. Carbapenemase gene detection by molecular methods is the gold standard but is available in only a few laboratories. The aim of this study was to test phenotypic methods for the detection of metallo-β-lactamase (MBL)- or Klebsiella pneumoniae carbapenemase (KPC)-producing Enterobacteriaceae and associated mechanisms of β-lactam resistance against a panel of 30 genotypically characterized carbapenem-resistant Enterobacteriaceae : 9 MBL, 7 KPC, 6 OXA-48, and 8 extended-spectrum β-lactamase (ESBL) or AmpC β-lactamases associated with decreased permeability. We used carbapenemase inhibitor-impregnated agar to test for carbapenem-resistant strains. Differences in the inhibition zone sizes of the meropenem, imipenem, ertapenem, and doripenem disks were measured between control and inhibitor (EDTA or phenylboronic acid [PBA] with or without cloxacillin)-impregnated Mueller-Hinton agar with a cutoff of 10 mm. All 9 MBL- and 7 KPC-producing Enterobacteriaceae were identified from the differences in zone size in the presence and absence of specific inhibitors, regardless of the carbapenem MICs and including isolates with low-level resistance to carbapenems. We also detected their associated β-lactam resistance mechanisms (11 ESBL-type and 5 class A β-lactamase 2b). No differences in zone size were observed for OXA-48-producing strains or other carbapenem resistance mechanisms such as ESBL and decreased permeability. We propose a new strategy to detect carbapenemases (MBL- and KPC-type) and associated mechanisms of β-lactam resistance (ESBL or class A β-lactamase 2b) by the use of inhibitor-impregnated agar. A rapid phenotypic detection of resistance mechanisms is important for epidemiological purposes and for limiting the spread of resistant strains by implementing specific infection control measures.
肠杆菌科碳青霉烯类耐药的传播对公共健康构成了重大威胁。通过分子方法检测碳青霉烯酶基因是金标准,但仅在少数实验室可用。本研究的目的是测试表型方法检测产金属β-内酰胺酶(MBL)或肺炎克雷伯菌碳青霉烯酶(KPC)的肠杆菌科和相关β-内酰胺耐药机制,针对 30 种经基因分型鉴定的碳青霉烯类耐药肠杆菌科:9 种 MBL、7 种 KPC、6 种 OXA-48 和 8 种与通透性降低相关的扩展谱β-内酰胺酶(ESBL)或 AmpCβ-内酰胺酶。我们使用碳青霉烯酶抑制剂浸渍琼脂来检测碳青霉烯类耐药菌株。在含有或不含有苯唑西林的美罗培南、亚胺培南、厄他培南和多利培南药敏纸片的 EDTA 或苯硼酸(PBA)抑制剂浸渍 Mueller-Hinton 琼脂中,通过测量抑制环的大小来测量美罗培南、亚胺培南、厄他培南和多利培南药敏纸片的差异,抑制环大小的截断值为 10 毫米。所有 9 种 MBL 和 7 种 KPC 产肠杆菌科都可以通过在有无特定抑制剂存在时的抑菌环大小差异来识别,而与碳青霉烯类 MIC 无关,包括对碳青霉烯类具有低水平耐药的分离株。我们还检测了它们相关的β-内酰胺耐药机制(11 种 ESBL 型和 5 种 A 类β-内酰胺酶 2b)。产 OXA-48 的菌株或其他如 ESBL 和通透性降低的碳青霉烯类耐药机制之间没有观察到抑菌环大小的差异。我们提出了一种新的策略,通过使用抑制剂浸渍琼脂来检测碳青霉烯酶(MBL 和 KPC 型)和相关的β-内酰胺耐药机制(ESBL 或 A 类β-内酰胺酶 2b)。快速表型检测耐药机制对于流行病学目的和通过实施特定的感染控制措施限制耐药菌株的传播非常重要。