Chromosomal Mutations in oprD, gyrA, and parC in Carbapenem Resistant Pseudomonas aeruginosa.
10.5145/KJCM.2011.14.4.131
- Author:
Ji Youn SUNG
1
;
Hye Hyun CHO
;
Kye Chul KWON
;
Sun Hoe KOO
Author Information
1. Department of Biomedical Laboratory Science, Far East University, Eumseong, Korea.
- Publication Type:Original Article
- Keywords:
Carbapenem resistant P. aeruginosa;
OprD;
Efflux system regulatory proteins;
QRDR
- MeSH:
Bacterial Proteins;
beta-Lactamases;
Ciprofloxacin;
Cross Infection;
Disease Outbreaks;
Genes, Regulator;
Imipenem;
Point Mutation;
Polymerase Chain Reaction;
Proteins;
Pseudomonas;
Pseudomonas aeruginosa;
Sequence Analysis, DNA
- From:Korean Journal of Clinical Microbiology
2011;14(4):131-137
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Outbreaks of carbapenem resistant P. aeruginosa give rise to significant therapeutic challenges for treating nosocomial infections. In this study, we analyzed carbapenem resistance mechanisms in carbapenem resistant and clonally different P. aeruginosa strains. We analyzed chromosomal alterations in the genes of OprD and efflux system regulatory proteins (MexR, NalC, NalD, MexT, and MexZ). We also investigated chromosomal alterations in the quinolone resistance-determining region (QRDR) for quinolone resistance mechanisms. METHODS: Twenty-one clonally different P. aeruginosa strains were isolated by repetitive extragenic palindromic sequence-based PCR (rep-PCR). PCR and DNA sequencing were conducted for the detection of beta-lactamase genes and chromosomal alterations of efflux pump regulatory genes, oprD, and QRDR in gyrA, gyrB, parC, and parE. RESULTS: Only one (P28) of the 21 strains harbored bla VIM-2. Two isolates had mutations in nalD or mexZ that were associated with efflux pump overexpression. Chromosomal alterations causing loss of OprD were found in 4 out of 21 carbapenem resistant P. aeruginosa strains. Nine of 10 imipenem and ciprofloxacin resistant strains had alterations in gyrA and/or parC. CONCLUSION: Carbapenem resistance in P. aeruginosa was mediated by several mechanisms, including loss of the OprD, overexpression of efflux systems, and production of carbapenemase. Resistance to quinolone is frequently caused by point mutations in gyrA and/or parC.
