AI Article Synopsis
- The study investigated how six clinical isolates of Acinetobacter baumannii developed resistance to carbapenems, particularly focusing on genetic and expression factors.
- All isolates exhibited similar patterns of resistance with high levels to both imipenem and meropenem, and reduced susceptibility was noted when treated with Phe-Arg-beta-naphthylamide.
- Key findings included significantly higher expression of the adeB gene and the presence of the resistance gene bla(OXA-23), hinting that the overactivity of the AdeABC efflux pump and the chromosome-linked OXA-23 gene contribute to the resistance observed in these isolates.
Article Abstract
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-beta-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 bla(OXA-23) gene, which was preceded by ISAba1. The bla(OXA-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.
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