Department of Microbiology and Immunology, Faculty of Pharmacy,Zagazig University, Zagazig, Egypt.
Department of Microbiology and Immunology, Faculty of Pharmacy,Zagazig University, Zagazig, Egypt.
Microb Pathog. 2019 Jul;132:266-274. doi: 10.1016/j.micpath.2019.05.022. Epub 2019 May 13.
Carbapenems are widely regarded as the drugs of choice for the treatment of severe infections caused by extended-spectrum beta lactamases producing Enterobacteriaceae. The emergence of carbapenem-resistant organisms is worrisome due to the limited treatment options. Detection of carbapenemase-producing bacteria is critical for the choice of appropriate therapy. However, Inhibition of carbapenemases is an alternative approach to combat resistance to carbapenms. In this study, Escherichia coli and Klebsiella pneumoniae carbapenem resistant isolates were recovered from 300 clinical isolates. They were subjected phenotypically for detection of class B metallo-carbapenemase (MBL) producers (by carbapenem disks with or without EDTA), and were subjected for confirmation genotypically by PCR. In addition, the synergistic activities of MBL-inhibitors in combination with carbapenems were elucidated. Two E. coli and 15 K. pneumoniae isolates were carbapenem resistant. The genes encoding blaNDM-1 carbapenemase were detected in 16/17 isolates solely, or collaboratively with either blaVIM, or blaIMP or both in all carbapenem resistant isolates, by PCR method. The VIM-carbapenemase was encoded by one isolate. In pre-clinical trials for development of MBL-specific inhibitors, Sub-inhibitory concentrations of citric acid, malic acid, ascorbic acid and ciprofloxacin in combination with imipenem or meropenem exerted synergistic activities against metallo-carbapenemases. Their activities are probably attributed to the chelation of zinc ions in the active site of carbapenemase. Conclusively, these promising combined therapies might represent a new strategy for combating such serious infections caused by metallo-B-carbapenemase producers of K. pneumoniae and E. coli isolates.
碳青霉烯类抗生素被广泛认为是治疗产超广谱β-内酰胺酶肠杆菌科细菌引起的严重感染的首选药物。由于治疗选择有限,碳青霉烯类耐药菌的出现令人担忧。检测产碳青霉烯酶细菌对于选择合适的治疗方法至关重要。然而,抑制碳青霉烯酶是对抗碳青霉烯类耐药的一种替代方法。在这项研究中,从 300 株临床分离株中回收了耐碳青霉烯类的大肠杆菌和肺炎克雷伯菌。它们在表型上进行了检测,以检测 B 类金属碳青霉烯酶 (MBL) 产生菌(通过带有或不带有 EDTA 的碳青霉烯类药物纸片进行),并通过 PCR 进行了基因确证。此外,还阐明了 MBL 抑制剂与碳青霉烯类药物联合使用的协同作用。有 2 株大肠杆菌和 15 株肺炎克雷伯菌分离株对碳青霉烯类药物耐药。通过 PCR 方法,在 16/17 株分离株中仅检测到blaNDM-1 碳青霉烯酶基因,或在所有耐碳青霉烯类药物的分离株中与 blaVIM 、blaIMP 或两者共同检测到blaNDM-1 碳青霉烯酶基因。VIM-碳青霉烯酶由一株分离株编码。在开发 MBL 特异性抑制剂的临床前试验中,柠檬酸、苹果酸、抗坏血酸和环丙沙星在亚抑菌浓度下与亚胺培南或美罗培南联合使用对金属碳青霉烯酶具有协同作用。它们的活性可能归因于碳青霉烯酶活性部位锌离子的螯合作用。总之,这些有前途的联合治疗方法可能代表了一种新的策略,可以对抗由肺炎克雷伯菌和大肠杆菌分离株产生的金属β-碳青霉烯酶引起的此类严重感染。