Outbreak of meropenem-resistant Serratia marcescens comediated by chromosomal AmpC β-lactamase overproduction and outer membrane protein loss

Borum Suh, Il Kwon Bae, Juwon Kim, Seok Hoon Jeong, Dongeun Yong, Kyungwon Lee

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

The aim of this study was to investigate the mechanisms involved in the meropenem resistance of Serratia marcescens clinical isolates. Meropenem-resistant (MIC range, 16 to 32 μg/ml) S. marcescens isolates were recovered from nine patients in a tertiary hospital in Seoul, South Korea, from June to November 2005. All the isolates shared identical or similar (>85% similarity) SpeI macrorestriction patterns, indicating clonal spread. PCR experiments did not detect any carbapenemase in those isolates. They carried the blaCTX-M-22 gene located on a 150-kbp plasmid of the incompatibility group L/M; however, the addition of clavulanic acid exhibited few effects on meropenem MICs. Although meropenem MICs were reduced 4- to 16-fold with the addition of boronic acid, no plasmid-borne AmpC β-lactamase gene was detected in PCR experiments. Real-time quantitative PCR experiments showed that expression levels of the chromosomal ampC gene in those isolates were 87.06 to 155.76 times higher than that of the reference strain ATCC 8100. SDS-PAGE showed a lack of the 42-kDa outer membrane protein (OmpF). In combination with the overproduction of the chromosomal AmpC enzyme, the loss of OmpF may have played a role in the acquisition of meropenem resistance in our isolates.

Original languageEnglish
Pages (from-to)5057-5061
Number of pages5
JournalAntimicrobial agents and chemotherapy
Volume54
Issue number12
DOIs
Publication statusPublished - 2010 Dec

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

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