在治疗产生 GES-5 的铜绿假单胞菌感染过程中导致体内头孢他啶/阿维菌素耐药性产生的机制。

IF 4.1 2区医学 Q2 MICROBIOLOGY

Antimicrobial Agents and Chemotherapy Pub Date : 2024-11-06 Epub Date: 2024-10-21 DOI:10.1128/aac.01164-24

Cristhian Herrera, Maria A Gomis-Font, Carla López-Causapé, María Díez-Aguilar, Pablo A Fraile-Ribot, Laura M Cardeñoso, Antonio Oliver

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引用次数: 0

摘要

研究了四对头孢他啶/阿维巴坦易感/耐药的产GES-5 ST235铜绿假单胞菌临床分离株产生头孢他啶/阿维巴坦耐药性的机制。通过克隆实验证实，其中三个病例的头孢他啶/阿维菌素耐药性是由导致 GES-27 (P162Q)、GES-29 (P162A) 或新型 GES-60 (N136S) 的单个突变驱动的。此外，这些突变与头孢哌酮 MICs 增加有关，但与碳青霉烯类（尤其是亚胺培南/雷帕坦）耐药性降低有关。了解抗伪β-内酰胺类药物耐药性机制的复杂性对于指导优化治疗和抗菌药物管理措施至关重要。

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Mechanisms leading to in vivo ceftazidime/avibactam resistance development during treatment of GES-5-producing Pseudomonas aeruginosa infections.

The mechanisms underlying ceftazidime/avibactam resistance development in four ceftazidime/avibactam susceptible/resistant pairs of GES-5-producing ST235 Pseudomonas aeruginosa clinical isolates were investigated. In three of the cases, ceftazidime/avibactam resistance was driven by a single mutation leading to GES-27 (P162Q), GES-29 (P162A), or the novel GES-60 (N136S), as confirmed through cloning experiments. Moreover, these mutations were associated with increased cefiderocol MICs but reduced carbapenem, particularly imipenem/relebactam, resistance. Understanding the complexity of resistance mechanisms to the growing repertoire of antipseudomonal β-lactams is crucial to guide optimized treatments and antimicrobial stewardship measures.

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来源期刊

Antimicrobial Agents and Chemotherapy 医学-微生物学

CiteScore

10.00

自引率

8.20%

发文量

762

审稿时长

3 months

期刊介绍： Antimicrobial Agents and Chemotherapy (AAC) features interdisciplinary studies that build our understanding of the underlying mechanisms and therapeutic applications of antimicrobial and antiparasitic agents and chemotherapy.