This Article Full Text Full Text (PDF) Other Versions of this Article: AAC.01684-07v1 52/9/2999    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Google Scholar Articles by Bratu, S. Articles by Quale, J. PubMed PubMed Citation Articles by Bratu, S. Articles by Quale, J.

Next Article 

Antimicrobial Agents and Chemotherapy, September 2008, p. 2999-3005, Vol. 52, No. 9
0066-4804/08/$08.00+0     doi:10.1128/AAC.01684-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Correlation of Antimicrobial Resistance with β-Lactamases, the OmpA-Like Porin, and Efflux Pumps in Clinical Isolates of Acinetobacter baumannii Endemic to New York City

Division of Infectious Diseases, SUNY Downstate Medical Center, Brooklyn, New York

Received 31 December 2007/ Returned for modification 3 March 2008/ Accepted 20 June 2008

Acinetobacter baumannii strains resistant to all β-lactams, aminoglycosides, and fluoroquinolones have emerged in many medical centers. Potential mechanisms contributing to antimicrobial resistance were investigated in 40 clinical isolates endemic to New York City. The isolates were examined for the presence of various β-lactamases, aminoglycoside-modifying enzymes, and mutations in gyrA and parC. Expression of the genes encoding the β-lactamase AmpC, the efflux systems AdeABC and AbeM, and the OmpA-like porin was also examined by real-time reverse transcription-PCR. No VIM, IMP, KPC, OXA-23-type, OXA-24-type, or OXA-58 β-lactamases were detected, although several isolates had acquired bla_SHV-5. Most cephalosporin-resistant isolates had increased levels of expression of ampC and/or had acquired bla_SHV-5; however, isolates without these features still had reduced susceptibility to cefepime that was mediated by the AdeABC efflux system. Although most isolates with ISAba1 upstream of the bla_OXA-51-like carbapenemase gene were resistant to meropenem, several remained susceptible to imipenem. The presence of aminoglycoside-modifying enzymes and gyrase mutations accounted for aminoglycoside and fluoroquinolone resistance, respectively. The increased expression of adeABC was not an important contributor to aminoglycoside or fluoroquinolone resistance but did correlate with reduced susceptibility to tigecycline. The expression of abeM and ompA and phenotypic changes in OmpA did not correlate with antimicrobial resistance. A. baumannii has become a well-equipped nosocomial pathogen; defining the relative contribution of these and other mechanisms of antimicrobial resistance will require further investigation.

Published ahead of print on 30 June 2008.

This article has been cited by other articles:

• Adams, M. D., Goglin, K., Molyneaux, N., Hujer, K. M., Lavender, H., Jamison, J. J., MacDonald, I. J., Martin, K. M., Russo, T., Campagnari, A. A., Hujer, A. M., Bonomo, R. A., Gill, S. R. (2008). Comparative Genome Sequence Analysis of Multidrug-Resistant Acinetobacter baumannii. J. Bacteriol. 190: 8053-8064 [Abstract] [Full Text]