Salmonella are less likely to develop plasmid mediated drug resistance due to its resident F-like plasmid and specifically the entry exclusion gene, traS

Abstract

Salmonella enterica are gram-negative intracellular pathogens responsible for foodborne gastroenteritis worldwide. Like other members of the Enterobacteriaecea, there has been a marked increase in Salmonellas resistance to third generation -lactams/cephalosporins, antibiotics commonly used to treat salmonellosis in children. However, resistance to this and other antibiotic is not uniformly distributed among S. enterica serovars. The virulence of Salmonella is due to a low copy number, FII plasmid (65kb - 100 kb) that contains the ADP-ribosylating toxin, SpvB. This virulence plasmid is present in only a few Salmonella serovars (S. Choleraesuis, S. Dublin, S. Enteritidis, and S. Typhimurium). We believe that the spvB-virulence plasmid excludes other large molecular weight plasmids and may explain why antibiotic resistance is slow to develop in certain Salmonella serovars (ex. S. Enteritidis vs. S. Kentucky). The goal of this study is to determine the contribution of the Salmonella spvB-virulence plasmid to plasmid exclusion. From conjugation experiments, S. Typhimurium exhibits lower conjugation frequency with F plasmids when the spvB-virulence plasmid is present. Furthermore, introduction of cloned FI traS into “plasmidless” S. Typhimurium LT2 strain and Escherichia coli DH5 excluded FI plasmid. However deletion of the virulence plasmid traS did not affect plasmid exclusion significantly compared to control, spvB deletion. In addition, differences in F plasmid conjugation in natural Salmonella isolates did not correlate with F and virulence plasmid genotype. The slow development of antibiotic resistance in certain Salmonella serovars may be attributed to entry exclusion mediated by different mechanisms encoded by either plasmid or chromosomal genes.