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.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Gulig PA,Doyle TJdoi
10.1128/IAI.61.2.504-511.1993subject
Has Abstractpub_date
1993-02-01 00:00:00pages
504-11issue
2eissn
0019-9567issn
1098-5522journal_volume
61pub_type
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.58.9.3116-3121.1990
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.38.3.871-876.1982
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journal_title:Infection and immunity
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pub_type: 杂志文章
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:1989-05-01 00:00:00
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更新日期:2002-07-01 00:00:00
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