| Title | Mutational inactivation of OprD in carbapenem-resistant Pseudomonas aeruginosa isolates from Korean hospitals |
|---|---|
| Author | Chi Hyun Kim1, Hee Young Kang1, Bo Ra Kim1, Hyejin Jeon1, Yoo Chul Lee1, Sang Hwa Lee2, and Je Chul Lee1* |
| Address | 1Department of Microbiology, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea, 2Department of Microbiology, Dong-A University, College of Medicine, Busan 602-714, Republic of Korea |
| Bibliography | Journal of Microbiology, 54(1),44-49, 2016, |
| DOI | 10.1007/s12275-016-5562-5 |
| Key Words | carbapenem, OprD protein, efflux pump, sequence type, international clone |
| Abstract | This study investigated the mechanisms underlying the carbapenem resistance of bloodstream isolates of Pseudomonas aeruginosa obtained from two Korean hospitals. Of the 79 P. aeruginosa isolates, 22 and 21 were resistant to imipenem and meropenem, respectively. The 22 imipenem-resistant P. aeruginosa isolates were classified into 7 sequence types (STs) and 13 pulsotypes. Twelve imipenem-resistant isolates from one hospital were found to belong to the international clone ST111. Two imipenem-resistant P. aeruginosa ST235 isolates carried the blaIMP-6 gene, but the remaining 20 isolates did not produce carbapenemases. Mutations in the oprD gene and a related decrease in gene expression were found in 21 and 5 isolates, respectively. However, all imipenemresistant P. aeruginosa isolates showed no significant expression of OprD in the outer membrane as compared with that of carbapenem-susceptible PAO1 strain. Overexpression of genes associated with efflux pumps, including mexB, mexD, mexF, and mexY, was not found in any imipenem-resistant isolate. One imipenem-resistant P. aeruginosa isolate overexpressed the ampC gene. Our results show that the low permeability of drugs due to the mutational inactivation of OprD is primarily responsible for carbapenem resistance in bloodstream isolates of P. aeruginosa from Korean hospitals. |