Department of Infectious Diseases, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, Zhejiang, China.
J Infect Dev Ctries. 2024 Jan 31;18(1):106-115. doi: 10.3855/jidc.17779.
The spread of carbapenem-resistant Klebsiella pneumoniae (CRKP) is a substantial severe global public health burden. Non-carbapenemase-producing CRKP (non-CP-CRKP) is increasingly recognized as the source of severe infections.
We analyzed the genotypic, and phenotypic profiles of non-CP-CRKP strains with the whole-genome sequences isolated between 2017 and 2019 and the clinical characterization of non-CP-CRKP infection.
A total of 91 CRKP strains were collected, of which 5 (5.49%) strains were non-CP-CRKP. Four strains were from male patients; three strains were isolated from the bile of patients who underwent biliary interventional surgery and four had a history of antibiotic exposure. Three strains were sequence type (ST)11, one was ST1, and one was ST5523. The non-CP-CRKP strains were insusceptible to ertapenem. Three strains were susceptible to amikacin. All the strains were susceptible to imipenem, meropenem, tigecycline, ceftazidime/avibatam and polymyxin B. The β-lactamases of non-CP-CRKP predominantly included blaCTX-M, blaSHV, and blaTEM subtypes. Two site mutations in ompK36 (p.A217S and p.N218H) and four in ompK37 (p.I70M, p.I128M, p.N230G, and m233_None234insQ) were detected accounting for carbapenem resistance. Plasmids IncFI and IncFII were found in most strains. Genes encoding aerobactin, yersiniabactin and allantoin utilization were not detected in several isolates, and all non-CP-CRKP strains did not carry rmpA gene.
Non-CP-CRKP infected patients had a history of previous antibiotic exposure or invasive procedures. Non-CP-CRKP strains were insusceptible to ertapenem. The mechanism of resistance includes β-lactamases production and the site mutations in ompK36 and ompK37. Several virulence genes were not detected in non-CP-CRKP.
碳青霉烯类耐药肺炎克雷伯菌（CRKP）的传播是一个严重的全球公共卫生负担。非产碳青霉烯酶的 CRKP（非 CP-CRKP）越来越被认为是严重感染的源头。
我们分析了 2017 年至 2019 年间分离的非 CP-CRKP 菌株的基因型和表型特征，以及非 CP-CRKP 感染的临床特征。
共收集了 91 株 CRKP 菌株，其中 5 株（5.49%）为非 CP-CRKP。4 株来自男性患者；3 株从接受胆道介入手术的患者胆汁中分离出来，4 株有抗生素暴露史。3 株为 ST11 型，1 株为 ST1 型，1 株为 ST5523 型。非 CP-CRKP 菌株对厄他培南不敏感。3 株对阿米卡星敏感。所有菌株均对亚胺培南、美罗培南、替加环素、头孢他啶/阿维巴坦和多黏菌素 B 敏感。非 CP-CRKP 的β-内酰胺酶主要包括 blaCTX-M、blaSHV 和 blaTEM 亚型。在 ompK36 中检测到 2 个点突变（p.A217S 和 p.N218H）和 ompK37 中的 4 个点突变（p.I70M、p.I128M、p.N230G 和 m233_None234insQ），这些突变导致碳青霉烯类耐药。大多数菌株中发现了 IncFI 和 IncFII 质粒。在一些分离株中未检测到编码aerobactin、yersiniabactin 和尿嘧啶利用的基因，所有非 CP-CRKP 菌株均不携带 rmpA 基因。
感染非 CP-CRKP 的患者有先前抗生素暴露或侵袭性操作史。非 CP-CRKP 菌株对厄他培南不敏感。耐药机制包括β-内酰胺酶的产生以及 ompK36 和 ompK37 中的点突变。在非 CP-CRKP 中未检测到一些毒力基因。
