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Multiple antibiotic resistance in Staphylococcus aureus and Staphylococcus epidermidis: plasmids in strains

Pathology
|July 1, 1984
PubMed

Insights

Antibiotic resistance in hospital-acquired Staphylococcus strains was investigated. While some resistance genes were plasmid-borne in Staphylococcus aureus, they were chromosomal or plasmid-borne in Staphylococcus epidermidis, suggesting a shared gene pool.

Area of Science:

  • Clinical Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Nosocomial infections caused by antibiotic-resistant Staphylococcus aureus and Staphylococcus epidermidis pose significant healthcare challenges.
  • Understanding the genetic basis of antibiotic resistance in these pathogens is crucial for effective treatment and control strategies.
  • Previous studies have indicated the role of plasmids in mediating antibiotic resistance in staphylococci.

Purpose of the Study:

  • To compare plasmid DNA profiles of antibiotic-resistant Staphylococcus aureus and Staphylococcus epidermidis strains from a Melbourne hospital outbreak.
  • To identify the genetic elements responsible for resistance to specific antibiotics, including gentamicin, tobramycin, kanamycin, and tetracycline.
  • To investigate the potential for a common gene pool of resistance determinants between Staphylococcus aureus and Staphylococcus epidermidis.

Main Methods:

  • Plasmid DNA profiling was performed on antibiotic-resistant strains of Staphylococcus aureus and Staphylococcus epidermidis.
  • Restriction endonuclease analysis was used to characterize chloramphenicol resistance plasmids.
  • Antibiotic resistance genes were analyzed in relation to both plasmid and chromosomal DNA.

Main Results:

  • In Staphylococcus aureus, resistance to gentamicin, tobramycin, and kanamycin was encoded by plasmids ranging from 17 to 22 megadaltons (Md).
  • No similar plasmids were detected in Staphylococcus epidermidis strains; tetracycline resistance was chromosomal or plasmid-mediated (2.8 Md).
  • Restriction endonuclease analysis of 3 Md chloramphenicol resistance plasmids suggested a common gene pool between Staphylococcus aureus and Staphylococcus epidermidis isolates.

Conclusions:

  • The genetic basis of antibiotic resistance differs between Staphylococcus aureus and Staphylococcus epidermidis in this Melbourne hospital outbreak.
  • Despite differences in plasmid-borne resistance, evidence suggests a shared gene pool for resistance determinants, particularly for chloramphenicol resistance.
  • Further investigation into interspecies gene transfer mechanisms is warranted to understand the evolution of antibiotic resistance in staphylococci.

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