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Antimicrob. Agents Chemother. doi:10.1128/AAC.01684-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Correlation of Antimicrobial Resistance with -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

^* To whom correspondence should be addressed. Email: jquale{at}downstate.edu.

	Abstract

Acinetobacter baumannii resistant to all -lactams, aminoglycosides, and fluoroquinolones has emerged in many medical centers. Potential mechanisms contributing to antimicrobial resistance were investigated in 40 clinical isolates endemic to New York City. The presence of various -lactamases, aminoglycoside modifying enzymes, and mutations in gyrA and parC was examined. Expression of the genes encoding the -lactamase AmpC, the efflux systems AdeABC and AbeM, and the OmpA-like porin was also examined by real time RT-PCR. No VIM, IMP, KPC, OXA-23-type, 24-type, or OXA-58 -lactamases were detected, although several isolates had acquired bla_SHV-5. Most cephalosporin-resistant isolates had increased 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 ISAba1upstream to the bla_OXA-51-like carbapenemase gene were resistant to meropenem, several remained susceptible to imipenem. Aminoglycoside modifying enzymes and gyrase mutations accounted for aminoglycoside and fluoroquinolone resistance, respectively. Increased expression of adeABC was not an important contributor for aminoglycoside or fluoroquinolone resistance but did correlate with reduced susceptibility to tigecycline. 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.