Affiliation:
1. Department of Immunology and Medical Microbiology, University of Florida College of Medicine, Gainesville 32610-0266.
Abstract
The virulence plasmids of Salmonella typhimurium and other invasive Salmonella serovars have long been associated with the ability of these bacteria to cause systemic infection beyond the intestines in orally inoculated animals. Genetic analysis of virulence genes on the high-molecular-weight plasmids has revealed that no more than five genes spanning a 6.2-kb region are sufficient to replace the entire plasmid for conferring virulence. However, the exact virulence function(s) encoded by these genes has not been elucidated. In this report, we measured the possible effect of the virulence plasmid on the growth rate of S. typhimurium in mice by two complementary procedures. The first procedure used segregation of a temperature-sensitive plasmid in vivo to provide a measure of bacterial divisions and the number of recovered marker plasmid-containing salmonellae as a measure of killing. In the second procedure, aroA deletions were transduced into virulence plasmid-containing and plasmid-cured S. typhimurium. Since AroA- salmonellae are inhibited for growth in vivo, if the virulence plasmid affected only growth rate, no difference in the recoveries of the paired AroA- strains would be seen. Virulence plasmid-containing S. typhimurium segregated the marker plasmid more rapidly than did the virulence plasmid-cured strain, and AroA- derivatives of both strains were recovered equally from mice. Therefore, the S. typhimurium virulence plasmid increased growth rate but had no detectable effect on killing or bacterial movement into deep tissues. To examine whether the plasmid accomplished this function by affecting the intracellular/extracellular location of bacteria, orally infected mice were injected with gentamicin to kill the extracellular bacteria. Wild-type and plasmid-cured S. typhimurium strains were equally resistant to gentamicin in vivo and hence most likely located intracellularly to equal degrees. When wild-type and plasmid-cured S. typhimurium strains were sequestered within peritoneal chambers in mice, the resulting extracellular growth was equal. Therefore, the virulence plasmid increases the growth rate of S. typhimurium in mice, probably within mouse cells.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Reference37 articles.
1. The primary effect of the Ity locus is on the rate of growth of Salmonella typhimurium that are relatively protected from killing;Benjamin W. H.;J. Immunol.,1990
2. The ability of Salmonella typhimurium to produce the siderophore enterobactin is not a virulence factor in mouse typhoid;Benjamin W. H.;Infect. Immun.,1985
3. Infections in cancer patients;Bodey G. P.;Cancer Treat.,1975
4. The Salmonella typhimurium virulence plasmid encodes a positive regulator of a plasmid-encoded virulence gene;Caldwell A. L.;J. Bacteriol.,1991
5. Revision of CDC surveillance case definition for acquired immunodeficiency syndrome;Centers for Disease Control.;Morbid. Mortal. Weekly Rep.,1987
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