Suppr超能文献

恶臭假单胞菌对氟喹诺酮类和碳青霉烯类抗生素的耐药机制

Mechanisms of resistance to fluoroquinolones and carbapenems in Pseudomonas putida.

作者信息

Horii Toshinobu, Muramatsu Hideaki, Iinuma Yoshitsugu

机构信息

Department of Laboratory Medicine, Hamamatsu University School of Medicine, 1-20-1 Handa-yama, Hamamatsu 431-3192, Japan.

出版信息

J Antimicrob Chemother. 2005 Oct;56(4):643-7. doi: 10.1093/jac/dki254. Epub 2005 Jul 26.

Abstract

OBJECTIVES

Pseudomonas putida is an uncommon opportunistic pathogen, usually susceptible to antimicrobial agents. Data concerning resistance to antimicrobial agents in clinical P. putida isolates are limited.

PATIENTS AND METHODS

Susceptibilities to fluoroquinolones, carbapenems and other antibiotics were characterized in five clinical isolates of P. putida recovered from different patients with urinary tract infections as causative pathogens. Fluoroquinolone and carbapenem resistance were characterized genetically by the methods of PCR and DNA sequencing. Outer membrane protein (OMP) profiles were characterized by SDS-PAGE.

RESULTS

Four of five isolates were resistant or intermediate to both fluoroquinolones and carbapenems. Nucleotide sequences in the quinolone resistance-determining regions suggested that amino acid mutations such as Thr-83-->Ile in GyrA and Glu-469-->Asp in GyrB may contribute to high resistance to fluoroquinolones. Four metallo-beta-lactamase-producing isolates that showed resistance to carbapenems carried the IMP-type metallo-beta-lactamase genes. A combined effect of reduced production of 46 kDa OMP and metallo-beta-lactamase production was shown by a P. putida isolate exhibiting the highest MICs of carbapenems.

CONCLUSIONS

This study identified mechanisms of resistance to fluoroquinolones and carbapenems in clinical P. putida isolates.

摘要

目的

恶臭假单胞菌是一种不常见的机会致病菌,通常对抗菌药物敏感。关于临床分离的恶臭假单胞菌对抗菌药物耐药性的数据有限。

患者和方法

对从不同尿路感染患者中分离出的5株恶臭假单胞菌临床分离株进行了氟喹诺酮类、碳青霉烯类和其他抗生素的药敏试验,这些菌株为尿路感染的致病病原体。采用PCR和DNA测序方法对氟喹诺酮类和碳青霉烯类耐药性进行基因特征分析。通过SDS-PAGE对外膜蛋白(OMP)图谱进行特征分析。

结果

5株分离株中有4株对氟喹诺酮类和碳青霉烯类均耐药或中介。喹诺酮耐药决定区的核苷酸序列表明,GyrA中Thr-83→Ile和GyrB中Glu-469→Asp等氨基酸突变可能导致对氟喹诺酮类的高耐药性。4株产金属β-内酰胺酶且对碳青霉烯类耐药的分离株携带IMP型金属β-内酰胺酶基因。一株恶臭假单胞菌分离株对碳青霉烯类的最低抑菌浓度最高,显示出46 kDa OMP产量降低和金属β-内酰胺酶产生的联合作用。

结论

本研究确定了临床恶臭假单胞菌分离株对氟喹诺酮类和碳青霉烯类的耐药机制。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验