Nontyphoidal Salmonella enterica (NTS) poses a major public health risk worldwide that is amplified by the existence of antimicrobial-resistant strains, especially those resistant to quinolones and extended-spectrum cephalosporins (ESC). Little is known on the dissemination of plasmids harboring the acquired genetic determinants that confer resistance to these antimicrobials across NTS serotypes from livestock in the United States. NTS isolates (n 183) from U.S. swine clinical cases retrieved during 2014 to 2016 were selected for sequencing based on their phenotypic resistance to enrofloxacin (quinolone) or ceftiofur (3rd-generation cephalosporin). De novo assemblies were used to identify chromosomal mutations and acquired antimicrobial resistance genes (AARGs). In addition, plasmids harboring AARGs were identified using short-read assemblies and characterized using a multistep approach that was validated by long-read sequencing. AARGs to quinolones [qnrB15, qnrB19, qnrB2, qnrD, qnrS1, qnrS2, and aac(6’)Ib-cr] and ESC (blaCMY-2, blaCTX-M-1, blaCTX-M-27, and blaSHV-12) were distributed across serotypes and were harbored by several plasmids. In addition, chromosomal mutations associated with resistance to quinolones were identified in the target enzyme and efflux pump regulation genes. The predominant plasmid harboring the prevalent qnrB19 gene was distributed across serotypes. It was identical to a plasmid previously reported in S. enterica serovar Anatum from swine in the United States (GenBank accession number KY991369.1) and similar to Escherichia coli plasmids from humans in South America (GenBank accession numbers GQ374157.1 and JN979787.1). Our findings suggest that plasmids harboring AARGs encoding mechanisms of resistance to critically important antimicrobials are present in multiple NTS serotypes circulating in swine in the United States and can contribute to resistance expansion through horizontal transmission.
|Original language||English (US)|
|Journal||Antimicrobial agents and chemotherapy|
|State||Published - Apr 2019|
Bibliographical noteFunding Information:
This work was supported by the Global Food Venture-MnDrive Initiative, the National Institute of Food and Agriculture (Animal Health Formula Fund project MIN-62-091) of the USDA, the Rapid Agricultural Response Fund (RARF), the Swine Disease Eradication Center (SDEC) at the University of Minnesota, and the GenomeTrakr project of the U.S. Food and Drug Administration (FDA). In addition, E.E. was supported by BARD, the United States-Israel Binational Agricultural Research and Development Fund, Vaadia-BARD Postdoctoral Fellowship award no. FI-565-17. We thank Colette Friedenson for her help reviewing the literature. The authors declare no conflict of interests.
Copyright © 2019 American Society for Microbiology. All Rights Reserved.
- Antimicrobial drug resistance