Quinolone-Resistant Salmonella enterica | CDC EID

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Volume 16, Number 11–November 2010
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Plasmid-mediated Quinolone Resistance among Non-Typhi Salmonella enterica Isolates, USA

Maria Sjölund-Karlsson, Comments to Author Rebecca Howie, Regan Rickert, Amy Krueger, Thu-Thuy Tran, Shaohua Zhao, Takiyah Ball, Jovita Haro, Gary Pecic, Kevin Joyce, Paula J. Fedorka-Cray, Jean M. Whichard, and Patrick F. McDermott
Author affiliations: Centers for Disease Control and Prevention, Atlanta, Georgia, USA (M. Sjölund-Karlsson, K. Joyce, J.M. Whichard); IHRC, Inc., Atlanta (R. Howie, G. Pecic); Atlanta Research and Education Foundation, Decatur, Georgia, USA (R. Rickert, A. Krueger); Food and Drug Administration, Laurel, Maryland, USA (T.-T. Tran, S. Zhao, P.F. McDermott); and US Department of Agriculture, Athens, Georgia (T. Ball, J. Haro, P.J. Fedorka-Cray)

Suggested citation for this article

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.

Severe Salmonella enterica infections are commonly treated with fluoroquinolones (e.g., ciprofloxacin) (1). In the United States, the antimicrobial drug susceptibility of Salmonella spp. isolated from humans, food animals, and retail meats is systematically monitored by the National Antimicrobial Resistance Monitoring System (NARMS). This program is a collaborative effort of the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration Center for Veterinary Medicine (FDA-CVM) and the US Department of Agriculture (USDA). Antimicrobial susceptibility to fluoroquinolones among Salmonella spp. has been monitored since the program's inception in 1996.

Although fluoroquinolone resistance in Enterobacteriaceae is predominantly due to topoisomerase mutations, 3 plasmid-mediated mechanisms have been described that confer decreased susceptibility to ciprofloxacin: quinolone resistance proteins (Qnr), Aac(6′)-Ib-cr, and QepA efflux (2). The Qnr proteins protect the DNA-gyrase from quinolones, Aac(6′)-Ib-cr modifies quinolones with a piperazinyl group, and QepA is involved in active efflux (2). Because patients have experienced treatment failure when infected with Salmonella isolates that displayed decreased susceptibility to fluoroquinolones, plasmid-mediated mechanisms are clinically relevant (3).

A survey of 12,253 NARMS non-Typhi Salmonella (NTS) isolates collected from humans from 1996 through 2003 identified 10 (0.08%) qnr-positive isolates (4). A second survey of NARMS NTS collected from humans during 2004–2006 showed an increase in the proportion of isolates harboring plasmid-mediated quinolone resistance mechanisms. Among 6,057 isolates, 17 qnr-positive isolates and 1 aac(6′)-Ib-cr-positive isolate were detected, representing 0.3% of the NTS collected during that time (5).

The increase in plasmid-mediated quinolone resistance among NTS isolated from humans in the United States prompted further studies to determine continued presence among NTS of human origin and possible reservoirs of these mechanisms. In this study, we investigated plasmid-mediated quinolone resistance mechanisms among NARMS NTS isolated from humans, food animals, and retail meat in the United States in 2007.

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Suggested Citation for this Article

Sjölund-Karlsson M, Howie R, Rickert R, Krueger A, Tran T-T, Zhao S, et al. Plasmid-mediated quinolone resistance among non-Typhi Salmonella enterica Isolates, USA. Emerg Infect Dis [serial on the Internet]. 2010 Nov [date cited]. http://www.cdc.gov/EID/content/16/11/1789.htm

DOI: 10.3201/eid1611.100464