Draft Genome Sequences of Four Salmonella enterica Strains Isolated from Turkey-Associated Sources

We report the draft genomes of four Salmonella enterica isolates evaluated for the contribution of plasmids to virulence. Strains SE163A, SE696A, and SE710A carry plasmids demonstrated to facilitate plasmid-associated virulence, while SE819 is less virulent and has been used as a recipient for conjugation experiments to assess plasmid-encoded virulence mechanisms.

outbreaks associated with meat and poultry products over the last few years in the United States and other countries (1). In the United States alone, it is estimated that more than 1 million Salmonella infections occur annually, resulting in nearly 20,000 hospitalizations and 400 deaths (2). Some S. enterica serovars cause more invasive infections than others; for example, a previous study demonstrated that the Heidelberg and Typhimurium strains were more invasive, responsible for 13% and 6% of infections, respectively, compared to the other serovars (3). Many Salmonella strains carry plasmids that harbor genes that contribute to increased virulence and antimicrobial resistance (4,5). Previous studies in our laboratory characterized the impact of plasmids in S. enterica on antimicrobial resistance and virulence (4,5).
We sequenced four S. enterica strains designated SE163A, SE696A, SE710A, and SE819, isolated from turkey-associated sources. SE163A and SE696A are virulent strains that possess plasmids including incompatibility group (Inc) FIB, IncA/C, and IncX4 (VirB/D4 type 4 secretion system-encoding plasmid) that carry virulence and/or antimicrobial resistance-associated genetic factors (5,6). SE819 is a less virulent strain that lacks these virulence and antimicrobial resistance plasmids and has served as a recipient strain for studies evaluating the contribution of plasmids to antimicrobial resistance and virulence (4,6,7). Studies have demonstrated that genetic factors encoded by these transmissible SE163A-and SE696A-associated plasmids contribute to antibiotic resistance and the virulence in Salmonella species (6)(7)(8). SE710A also contains IncFIB, IncA/C, and IncX4 plasmids; however, con-tribution of these plasmids in virulence has not been examined for this isolate. Genome analysis of these particular S. enterica strains will be beneficial to our future understanding of the role of plasmid-encoded factors that contribute to virulence and antibiotic resistance.
Genomic DNA was extracted using a DNeasy blood and tissue kit (Qiagen, Valencia, CA, USA) and sequenced by the DNA Sequencing Core Facility at the University of Arkansas for Medical Sciences (UAMS; Little Rock, AR, USA). The DNA library was constructed with a Nextera XT DNA sample prep kit according to the manufacturer's protocol (Illumina, San Diego, CA, USA), and sequencing was performed using the Illumina MiSeq with 2 ϫ 250 paired-end reads. CLC Genomics Workbench version 8.5.1 (Qiagen, Germantown, MD, USA) was used for the trimming and de-novo assembly of the paired-end reads.
Draft genomes of these four S. enterica strains were annotated using the Rapid Annotation using Subsystem Technology (RAST) server (9), the Pathosystems Resource Integration Center (PATRIC) (10), and the NCBI Prokaryotic Genome Annotation Pipeline (PGAP) ( Table 1). The GϩC content for these strains is identical, with an estimate of 52.1%. Annotation using PATRIC (10) revealed that strain SE163A contains 5,448 coding sequences, in which 4,637 encode functional proteins, while 811 encode hypothetical proteins. Strain SE696A contains 5,296 coding sequences, in which 4,584 encode functional proteins and 712 encode hypothetical proteins. Strain SE710A possesses 5,337 coding sequences, in which 4,626 proteins have functional assignments and 711 encode as hypothetical. Strain SE819 contains 5,103 cod- ing regions, in which 4,450 encode functional proteins and 653 are assigned as hypothetical proteins. Accession number(s). The genome sequences of SE163A, SE696A, SE710A, and SE819 were deposited in GenBank under the accession numbers shown in Table 1.

ACKNOWLEDGMENTS
The research project and B.K.K. are supported by the FDA Commissioner's Fellowship Program. The Sequencing Facility is supported in part by grants from NIH to UAMS's Translational Research Institute (UL1TR000039) and the Center for Microbial Pathogenesis and Host Inflammatory Responses (P20GM103625). The opinions expressed in this manuscript are solely the responsibility of the authors and do not necessarily represent the official views and policy of the U.S. Food and Drug Administration or National Institutes of Health. Reference to any commercial materials, equipment, or process does not in any way constitute approval, endorsement, or recommendation by the Food and Drug Administration.