Virulence of Escherichia coli strains with R-plasmid mediated penicillin resistance in mice infections

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Y Obana1, T Nishino

  • 1Department of Microbiology, Kyoto Pharmaceutical University.

Insights

Conjugative R-plasmids in Escherichia coli were studied for their effect on virulence. Penicillinase II-producing R-plasmids reduced bacterial virulence in mice, suggesting cell envelope alterations, not the plasmid itself, caused the change.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Pathogenesis

Background:

  • Escherichia coli strains can harbor conjugative R-plasmids conferring antibiotic resistance.
  • Virulence factors in bacterial pathogens are crucial for disease development.
  • The impact of R-plasmid carriage on bacterial virulence is not fully understood.

Purpose of the Study:

  • To investigate the influence of conjugative R-plasmids encoding penicillinase on the virulence of Escherichia coli host strains.
  • To determine if R-plasmid transfer affects the pathogenicity of highly virulent E. coli strains in a murine model.

Main Methods:

  • Transfer of R-plasmids encoding penicillinase I, II, and III into specific virulent Escherichia coli strains (177, KC-14, 444).
  • Assessment of transconjugant virulence in mice through infection studies.
  • Analysis of virulence in revertant strains where R-plasmids were eliminated.

Main Results:

  • Escherichia coli strains receiving penicillinase I or III-producing R-plasmids maintained parental virulence levels.
  • Transconjugants with penicillinase II-producing R-plasmids exhibited significantly reduced virulence in mice.
  • Revertant strains, lacking the R-plasmid, regained virulence equivalent to the original host strain.

Conclusions:

  • The reduced virulence observed in some transconjugants is unlikely to be directly caused by the transferred R-plasmid itself.
  • Alterations in bacterial cell envelope components, such as lipopolysaccharides, may be responsible for the observed decrease in virulence.
  • Further research is needed to elucidate the specific mechanisms underlying R-plasmid-mediated changes in bacterial pathogenicity.

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