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Complex relationship between acquisition of beta-lactam resistance and loss of virulence in Streptococcus pneumoniae

V Rieux1, C Carbon, E Azoulay-Dupuis

  • 1Institut National de la Santé et de la Recherche Médicale, Hôpital Bichat-Claude Bernard, Paris, France.

The Journal of Infectious Diseases
|June 9, 2001
PubMed

Insights

This study found that acquired penicillin resistance in Streptococcus pneumoniae is linked to reduced virulence. Further research suggests specific genes like pbpX may impact growth and virulence.

Area of Science:

  • Microbiology
  • Genetics
  • Infectious Diseases

Background:

  • Previous studies indicated no highly virulent, penicillin-resistant Streptococcus pneumoniae strains.
  • Understanding the link between antibiotic resistance and bacterial virulence is crucial for public health.

Purpose of the Study:

  • To investigate the relationship between acquired penicillin resistance and virulence in Streptococcus pneumoniae.
  • To analyze isogenic mutants with specific genetic modifications conferring penicillin resistance.

Main Methods:

  • Generated single- and double-isogenic penicillin-resistant (Peni-R) mutants via transformation.
  • Used polymerase chain reaction (PCR) fragments of pbp2b and pbpX genes.
  • Performed sequence analysis of pbp2b and pbpX alleles.
  • Assessed bacterial virulence in a murine peritonitis model.

Main Results:

  • Acquired penicillin resistance was confirmed by sequence analysis of pbp2b and pbpX alleles.
  • Penicillin-resistant mutants exhibited significantly reduced virulence compared to the susceptible strain.
  • The pbpX mutant's phenotype remained stable after in vivo passage, suggesting its role in growth.
  • Virulent revertants showed no change in minimum inhibitory concentration (MIC), implying compensatory mutations.

Conclusions:

  • A clear relationship exists between acquired beta-lactam resistance and a loss of virulence in Streptococcus pneumoniae.
  • The pbpX gene appears to be involved in bacterial growth.
  • Compensatory mutations likely play a role in the restoration of virulence in resistant strains.

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