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Address correspondence to Dr. Seok Hoon Jeong, Department of Laboratory Medicine, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, 120-752 Seoul, Korea; tel 82-2-2228-2448; fax 82-2-313-0908; e-mail kscpjsh{at}yuhs.ac.
This study was performed to determine the mechanisms for acquiring carbapenem resistance in six clinical isolates of Acinetobacter baumannii. All isolates showed similar SmaI-macrorestriction patterns with less than 3 band differences by PFGE. The isolates showed a high level resistance (>32 mg/L) to both imipenem and meropenem by Etest. Phe-Arg-β-naphthylamide lowered the MICs of carbapenems. Real-time PCR experiments showed that expression levels of the adeB gene in the six A. baumannii isolates were 10- to 40-times higher than those of imipenem-susceptible strains. Direct sequencing of PCR products showed that all isolates carried the blaOXA-23 gene, which was preceded by ISAba1. The blaOXA-23 probe hybridized with approximately 500-kb I-CeuI chromosomal fragments, but not with a plasmid. These findings suggest that overexpression of the AdeABC efflux pump as well as chromosome-borne OXA-23 may play a role in acquiring carbapenem resistance in our A. baumannii isolates.
Keywords: carbapenem, meropenem, imipenem, Acinetobacter baumannii, antimicrobial resistance
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