Self-transmissible plasmids in staphylococci that encode resistance to aminoglycosides

Area of Science:

• Microbiology
• Molecular Biology
• Infectious Diseases

Background:

• Nosocomial infections caused by antibiotic-resistant staphylococci are a growing concern.
• Gentamicin resistance in staphylococci poses a significant challenge in clinical settings.
• Understanding the mechanisms of antibiotic resistance transfer is crucial for infection control.

Purpose of the Study:

• To investigate the transfer of high-level gentamicin, tobramycin, and kanamycin resistance between staphylococci.
• To characterize the plasmids mediating aminoglycoside resistance and their transfer mechanisms.
• To assess the prevalence of conjugative plasmids in clinical staphylococcal isolates.

Main Methods:

• Filter mating experiments were performed to transfer antibiotic resistance between staphylococcal strains.
• Plasmid DNA was analyzed to determine size and associated resistance genes.
• Conjugation-like transfer mechanisms were investigated through DNase resistance and cell-to-cell contact assays.

Main Results:

• High-level resistance to gentamicin, tobramycin, and kanamycin was transferable via plasmids (38–54 kb).
• These plasmids conferred intermediate resistance to amikacin and netilmicin, and resistance to ethidium bromide; some also produced beta-lactamase.
• Conjugative plasmids were prevalent in gentamicin-resistant Staphylococcus aureus and Staphylococcus epidermidis from outbreaks and bacteremic adults, but less so in other clinical isolates.

Conclusions:

• Self-transmissible plasmids are key mediators of aminoglycoside resistance spread in staphylococci.
• The evolution and dissemination of these conjugative plasmids likely contribute to the increasing incidence of gentamicin-resistant staphylococcal nosocomial infections.
• Targeting plasmid transfer mechanisms could be a strategy for combating resistant staphylococcal infections.