新生儿感染 KPC2 生产型高病毒卡巴培南耐药肺炎克雷伯氏菌后对考利司汀快速产生耐药性的调查。

IF 3.7 3区 医学 Q2 INFECTIOUS DISEASES Journal of global antimicrobial resistance Pub Date : 2024-06-06 DOI:10.1016/j.jgar.2024.05.021
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引用次数: 0

摘要

目的:高病毒性耐碳青霉烯类肺炎克雷伯氏菌(hv-CRKp)对公共卫生构成重大威胁。本研究报告了早产儿感染 hv-CRKp 的情况,并揭示了其对可乐定的耐药性以及在宿主体内的进化机制:方法:从一名患有败血症和 CRKp 骨关节炎并一直接受可乐定抗菌治疗的患者体内分离出三株产 KPC 的 CRKp 菌株。头孢他啶、头孢他啶-阿维巴坦(CAZ-AVI)、美罗培南、亚胺培南、替加环素、阿米卡星、米诺环素、磺胺甲噁唑/三甲氧苄青霉素、环丙沙星、阿米卡星、阿米卡星的最低抑菌浓度(MICs)分别为 1.0、1.0、1.0、1.0、1.0、1.0、1.0、1.0、采用微流稀释法测定环丙沙星、左氧氟沙星、氨曲南、头孢吡肟、头孢哌酮/舒巴坦、哌拉西林/他唑巴坦和秋水仙碱。通过全基因组测序分析,确定了 3 株 CRKp 菌株的 STs、毒力基因和抗生素耐药基因:结果:全基因组测序显示,三株CRKp菌株均属于序列类型(ST)11克隆,并携带有编码blaKPC-2的质粒。这三个菌株都具有 iucABCDiutA 毒力簇、peg-344 基因和 rmpA/rmpA2 基因,因此被定义为 hv-CRKp。进一步的实验和全基因组分析表明,一株 Kp 对可乐定产生了抗药性。发现对可乐定产生耐药性的机制是包括 mgrB 基因在内的约 9000 bp 的缺失突变:本研究揭示了 ST11 克隆 hv-CRKp 在秋水仙素治疗期间对秋水仙素产生耐药性及其在宿主体内快速进化的特点。
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Investigation of the Rapid Emergence of Colistin Resistance in a Newborn Infected with KPC-2–Producing Hypervirulent Carbapenem-Resistant Klebsiella pneumoniae

Objectives

Hypervirulent carbapenem-resistant Klebsiella pneumoniae (hv-CRKp) poses a significant threat to public health. This study reports an infection related to hv-CRKp in a premature infant and reveals its colistin resistance and evolutionary mechanisms within the host.

Methods

Three KPC-producing CRKp strains were isolated from a patient with sepsis and CRKp osteoarthritis who had been receiving colistin antimicrobial therapy. The minimum inhibitory concentrations (MICs) of ceftazidime, ceftazidime-avibactam (CAZ-AVI), meropenem, imipenem, tigecycline, amikacin, minocycline, sulfamethoxazole/trimethoprim, ciprofloxacin, levofloxacin, aztreonam, cefepime, cefoperazone/sulbactam, piperacillin/tazobactam, and colistin were determined using the microbroth dilution method. The whole-genome sequencing analysis was conducted to determine the sequence types (STs), virulence genes, and antibiotic resistance genes of the three CRKp strains.

Results

Whole-genome sequencing revealed that all three CRKp strains belonged to the ST11 clone and carried a plasmid encoding blaKPC-2. The three strains all possessed the iucABCDiutA virulence cluster, peg-344 gene, and rmpA/rmpA2 genes, defining them as hv-CRKp. Further experiments and whole-genome analysis revealed that a strain of K. pneuomniae had developed resistance to colistin. The mechanism found to be responsible for colistin resistance was a deletion mutation of approximately 9000 bp including the mgrB gene.

Conclusion

This study characterizes colistin resistance of the ST11 clone hv-CRKp during colistin treatment and its rapid evolution within the host.

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来源期刊
Journal of global antimicrobial resistance
Journal of global antimicrobial resistance INFECTIOUS DISEASES-PHARMACOLOGY & PHARMACY
CiteScore
8.70
自引率
2.20%
发文量
285
审稿时长
34 weeks
期刊介绍: The Journal of Global Antimicrobial Resistance (JGAR) is a quarterly online journal run by an international Editorial Board that focuses on the global spread of antibiotic-resistant microbes. JGAR is a dedicated journal for all professionals working in research, health care, the environment and animal infection control, aiming to track the resistance threat worldwide and provides a single voice devoted to antimicrobial resistance (AMR). Featuring peer-reviewed and up to date research articles, reviews, short notes and hot topics JGAR covers the key topics related to antibacterial, antiviral, antifungal and antiparasitic resistance.
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