Article

Plasmid-mediated quinolone resistance among non-Typhi Salmonella enterica isolates, USA.

Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Emerging Infectious Diseases (Impact Factor: 7.33). 11/2010; 16(11):1789-91. DOI: 10.3201/eid1611.100464
Source: PubMed

ABSTRACT We determined the prevalence of plasmid-mediated quinolone resistance mechanisms among non-Typhi Salmonella spp. isolated from humans, food animals, and retail meat in the United States in 2007. Six isolates collected from humans harbored aac(6')Ib-cr or a qnr gene. Most prevalent was qnrS1. No animal or retail meat isolates harbored a plasmid-mediated mechanism.

0 Bookmarks
 · 
131 Views
  • Source
    01/2011; 4(3):99-101.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Three mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6')-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this study, 130 non-Typhi Salmonella enterica isolates from chickens were analysed for the prevalence of plasmid-mediated quinolone resistance (PMQR) determinants as well as the co-existence of oqxAB and extended-spectrum β-lactamase (ESBL) genes. The genes oqxAB, aac(6′)-Ib-cr, blaCTX-M-9G and blaTEM were present alone or in combination in 40 (30.8%), 40 (30.8%), 55 (42.3%) and 2 (1.5%) isolates, respectively. Most of the oqxAB–blaCTX-M-9G-positive isolates (17/28) carried transferable ST2-IncHI2 plasmids containing an oqxAB cassette and blaCTX-M-14 flanked by insertion sequences IS10 or ISEcp1 upstream and IS903 downstream. The oqxAB–blaCTX-M-9G-positive isolates from a local area showed similar pulsed-field gel electrophoresis (PFGE) patterns, whilst the isolates from different areas were genetically divergent, suggesting that both clonal expansion in local areas and horizontal transmission contributed to the spread of ST2-IncHI2 plasmids containing oqxAB and blaCTX-M-14 This is the first report on the prevalence of ST2-IncHI2 plasmids concomitantly carrying oqxAB and blaCTX-M-14. in Salmonella and also the first description of the genetic environment of oqxAB–blaCTX-M. The genetic linkage of oqxAB–blaCTX-M-9G in non-Typhi Salmonella likely facilitates the spread of antibiotic-resistant Salmonella and poses a threat for clinical treatment of salmonellosis.
    International Journal of Antimicrobial Agents 09/2014; 44(3). DOI:10.1016/j.ijantimicag.2014.05.014 · 4.26 Impact Factor

Full-text (3 Sources)

Download
31 Downloads
Available from
May 22, 2014