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Antimicrobial Agents and Chemotherapy, November 2008, p. 3837-3843, Vol. 52, No. 11
0066-4804/08/$08.00+0     doi:10.1128/AAC.00570-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Genetic Basis of Multidrug Resistance in Acinetobacter baumannii Clinical Isolates at a Tertiary Medical Center in Pennsylvania{triangledown}

Jennifer M. Adams-Haduch,1 David L. Paterson,1,2 Hanna E. Sidjabat,1 Anthony W. Pasculle,1,3 Brian A. Potoski,1,4 Carlene A. Muto,1,5 Lee H. Harrison,1,6 and Yohei Doi1*

Division of Infectious Diseases,1 Clinical Microbiology Laboratory,3 Antibiotic Management Program,4 Division of Hospital Epidemiology and Infection Control, University of Pittsburgh Medical Center,5 Infectious Diseases Epidemiology Research Unit, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania,6 University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, Brisbane, Australia2

Received 1 May 2008/ Returned for modification 14 July 2008/ Accepted 12 August 2008

A total of 49 unique clinical isolates of multidrug-resistant (MDR) Acinetobacter baumannii identified at a tertiary medical center in Pittsburgh, Pennsylvania, between August 2006 and September 2007 were studied for the genetic basis of their MDR phenotype. Approximately half of all A. baumannii clinical isolates identified during this period qualified as MDR, defined by nonsusceptibility to three or more of the antimicrobials routinely tested in the clinical microbiology laboratory. Among the MDR isolates, 18.4% were resistant to imipenem. The frequencies of resistance to amikacin and ciprofloxacin were high at 36.7% and 95.9%, respectively. None of the isolates was resistant to colistin or tigecycline. The presence of the carbapenemase gene blaOXA-23 and the 16S rRNA methylase gene armA predicted high-level resistance to imipenem and amikacin, respectively. blaOXA-23 was preceded by insertion sequence ISAba1, which likely provided a potent promoter activity for the expression of the carbapenemase gene. The structure of the transposon defined by ISAba1 differed from those reported in Europe, suggesting that ISAba1-mediated acquisition of blaOXA-23 may occur as an independent event. Typical substitutions in the quinolone resistance-determining regions of the gyrA and parC genes were observed in the ciprofloxacin-resistant isolates. Plasmid-mediated quinolone resistance genes, including the qnr genes, were not identified. Fifty-nine percent of the MDR isolates belonged to a single clonal group over the course of the study period, as demonstrated by pulsed-field gel electrophoresis.

* Corresponding author. Mailing address: Division of Infectious Diseases, University of Pittsburgh Medical Center, S829 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261. Phone: (412) 648-9445. Fax: (412) 648-8521. E-mail: doiy{at}dom.pitt.edu

{triangledown} Published ahead of print on 25 August 2008.

Antimicrobial Agents and Chemotherapy, November 2008, p. 3837-3843, Vol. 52, No. 11
0066-4804/08/$08.00+0     doi:10.1128/AAC.00570-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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