The Role of the IncF Plasmid and Its Resident Entry Exclusion Gene on Plasmid Exclusion

cause significant illnesses worldwide. There has been a marked increase in resistance to fluoroquinolones and β-lactams/cephalosporins, antibiotics commonly used to treat salmonellosis. However, serovars vary in their resistance to these and other antibiotics. The systemic virulence of some serovars is due to a low copy number, IncF plasmid (65-100 kb) that contains the ADP-ribosylating toxin, SpvB. This virulence plasmid is present in only nine serovars. It is possible that the -virulence plasmid excludes other plasmids and may explain why antibiotic resistance is slow to develop in certain serovars such as . Enteritidis. The distribution of plasmid entry exclusion genes / and / are variable in IncF and IncI plasmids, respectively and may account for differences in emergent antimicrobial resistance for some serovars. The goal of this study is to determine the contribution of the -virulence plasmid in F-plasmid exclusion. From conjugation experiments, . Typhimurium exhibited lower conjugation frequency with incFI and incFII plasmids when the -virulence plasmid is present. Furthermore, introduction of cloned incFI into a "plasmidless" . Typhimurium LT2 strain and DH5α excluded incFI plasmid. However, deletion of the virulence plasmid did not affect plasmid exclusion significantly compared to a control deletion. In addition, differences in F plasmid conjugation in natural isolates did not correlate with IncF or SpvB-virulence plasmid genotype. There appear to be other plasmid or chromosomal genes at play in plasmid exclusion that may be responsible for the slow development of antibiotic resistance in certain serovars.