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Ciprofloxacin and trimethoprim cause phage induction and virulence modulation in Staphylococcus aureus

Christiane Goerke1, Johanna Köller, Christiane Wolz

  • 1Institut für Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Tübingen, Elfriede-Aulhorn-Str. 6, 72076 Tübingen, Germany. christiane.goerke@med.uni-tuebingen.de

Antimicrobial Agents and Chemotherapy
|December 27, 2005
PubMed

Insights

Antibiotics like ciprofloxacin and trimethoprim can trigger the induction of bacteriophages (viruses that infect bacteria) in Staphylococcus aureus. This phage induction leads to increased expression of bacterial virulence factors, potentially impacting infections.

Area of Science:

  • Microbiology
  • Bacteriology
  • Molecular Biology

Background:

  • Bacteriophages integrating into the beta-hemolysin (hlb) gene are common in human Staphylococcus aureus.
  • These phages often carry accessory virulence factors like staphylokinase (sak) and enterotoxins.

Purpose of the Study:

  • To investigate the effects of ciprofloxacin and trimethoprim on phage induction and virulence factor expression in Staphylococcus aureus.
  • To analyze phage mobilization and virulence modulation in clinical isolates and laboratory strains.

Main Methods:

  • Treatment of Staphylococcus aureus lysogens with subinhibitory concentrations of ciprofloxacin and trimethoprim.
  • Monitoring of phage induction, delysogenization, and phage replication.
  • Analysis of recA transcription to assess SOS response involvement.
  • Quantification of phage-encoded virulence gene (sak) expression.

Main Results:

  • Subinhibitory antibiotic concentrations induced delysogenization and dose-dependent phage replication.
  • Ciprofloxacin treatment enhanced recA transcription, indicating SOS response activation.
  • Phage induction correlated with increased expression of the sak gene, driven by latent phage promoters.

Conclusions:

  • Ciprofloxacin and trimethoprim can induce hlb-converting phages in Staphylococcus aureus.
  • Antibiotic-induced phage activation modulates bacterial virulence, potentially affecting infection dynamics.

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