Plasmid-Mediated Quinolone Resistance Genes, <i>aac</i>(<i>6</i>′)-<i>Ib-cr</i>, <i>qnrS</i>, <i>qnrB</i>, and <i>qnrA</i>, in Urinary Isolates of <i>Escherichia coli</i> and <i>Klebsiella pneumoniae</i> at a Teaching Hospital, Thailand

Abstract

A total of 121 Escherichia coli (47 extended-spectrum β-lactamase [ESBL] and 74 non-ESBL producers) and 75 Klebsiella pneumoniae isolates (49 ESBL and 26 non-ESBL producers) were collected from urine samples between October 2010 and April 2011 at a university hospital and assessed for the presence of plasmid-mediated quinolone resistance (PMQR) genes. Twenty-seven E. coli (22.3%) and 49 K. pneumoniae (65.3%) isolates harbored PMQR genes, which mostly consisted of aac(6')-Ib-cr and qnrS, followed by qnrB and qnrA. Among the 76 PMQR-positive isolates, 15 (19.7%) and 2 (2.6%) carried 2 and 3 different PMQR genes, respectively. However, qnrC, qnrD, and qepA were not found in any isolate. The PMQR genes were more prevalent in ESBL producers than in non-ESBL producers (42.6% versus 9.5% in E. coli and 81.6% versus 34.6% in K. pneumoniae). Approximately 35%-60% of the PMQR-positive isolates were susceptible or intermediately susceptible to fluoroquinolones. The enterobacterial repetitive intergenic consensus-PCR method revealed that most PMQR-positive isolates belonged to different strains, indicating the spread of these resistance determinants. PMQR gene transfer by conjugation was successful in 10%-25% of the test donors. This study showed a high prevalence of PMQR genes among both organisms. Clinical use of fluoroquinolones for the treatment of infections caused by fluoroquinolone-susceptible strains harboring PMQR genes may lead to decreased therapeutic efficacy.