Inhibitory effects of reserpine and carbonyl cyanide m-chloro-phenylhydrazone on fluoroquinolone resistance of Acinetobacter baumannii

Mechanisms of bacterial resistance to fluoroquinolones may be grouped into three principal categories: gene mutations of DNA topoisomerase II (GyrA or GyrB), DNA topoisomerase IV (ParC or ParE), decrease of outer membrane permeation and upregulation of multi-drug efflux pump (active efflux system).(...

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Published inChinese medical journal Vol. 118; no. 4; pp. 340 - 343
Main Authors Shi, Wei-feng, Jiang, Jian-ping, Xu, Ning, Huang, Zhi-mi, Wang, Yu-yue
Format Journal Article
LanguageEnglish
Published China Department of Clinical Laboratory, Third Affiliated Hospital of Suzhou University, Changzhou 213003, China%Department of Clinical Chemistry, University Hospital of Lund, Lund S-221 85, Sweden%Department of Clinical Laboratory, 98th PLA Hospital, Huzhou 313000, China 20.02.2005
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Summary:Mechanisms of bacterial resistance to fluoroquinolones may be grouped into three principal categories: gene mutations of DNA topoisomerase II (GyrA or GyrB), DNA topoisomerase IV (ParC or ParE), decrease of outer membrane permeation and upregulation of multi-drug efflux pump (active efflux system).(1) Efflux pumps are transport proteins removing toxic substrates ( including virtually all classes of clinically relevant antibiotics) from cells to the external environment. These proteins exist in both Gram positive bacteria and Gram negative bacteria as well as in fungi and mammalian (tumour) cells.(2-4) It has been reported that alkaloid reserpine and carbonyl cyanide m-chlorophenylhydrazone (CCCP) can inhibit NorA multi-drug efflux.(5,6) In order to explore the universality of drug efflux in microorganisms, 85 strains of Acinetobacter baumannii (A. baumannii) were tested using reserpine and CCCP. The quinolone-resistant-determining region (QRDR) of gyrA and parC genes in 35 isolates of A. baumannii were amplified by polymerase chain reaction (PCR) and sequenced by DNA sequencer. The correlation between resistant mutation regularity and bacterial drug efflux were analysed.
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ISSN:0366-6999