Genetic basis of multidrug resistance in Acinetobacter baumannii clinical isolates at a tertiary medical center in Pennsylvania

Abstract

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 bla(OXA-23) and the 16S rRNA methylase gene armA predicted high-level resistance to imipenem and amikacin, respectively. bla(OXA-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 bla(OXA-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.

FIG. 1.

PFGE patterns of all pulsotypes identified in the study.

FIG. 2.

Schematic representation of the genetic environments of bla_OXA-23 from the United States, France, and Turkey. (A) Strain AB017 (investigated in the present study); (B) strain AB13 (7); (C) strain AcKOU1 (GenBank accession no. EF120622). The boundaries of Tn2006 and Tn2008 are indicated, along with the target site duplications (underlined). The 7-bp difference in the site of insertion of ISAba1 for strain AB13 is double underlined. Target site duplication was not identified within the available sequence for strain AcKOU1.