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Ribosomal resistance of clinical enterococcal to streptomycin isolates
Antimicrobial Agents and Chemotherapy
|March 1, 1984
Abstract:
The mechanism of high-level resistance to streptomycin was studied in 12 clinical isolates of Streptococcus faecalis. Six strains produced streptomycin-modifying enzymes. Each of three enzyme-negative strains tested demonstrated ribosomal resistance to streptomycin. Lack of ribosomal susceptibility is a significant cause of high-level streptomycin resistance among clinical enterococcal isolates.
Insights
High-level streptomycin resistance in Streptococcus faecalis is often caused by modifying enzymes. However, some strains show resistance due to ribosomal changes, indicating a significant mechanism for enterococcal antibiotic resistance.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Streptococcus faecalis (now Enterococcus faecalis) is a common cause of nosocomial infections.
- High-level streptomycin resistance (HLSR) is a growing clinical concern, limiting treatment options.
- Understanding resistance mechanisms is crucial for effective antimicrobial stewardship.
Purpose of the Study:
- To investigate the mechanisms underlying high-level streptomycin resistance in clinical isolates of Streptococcus faecalis.
- To differentiate between enzymatic modification and ribosomal alterations as causes of HLSR.
Main Methods:
- Analysis of 12 clinical isolates of Streptococcus faecalis.
- Determination of streptomycin-modifying enzyme production in resistant strains.
- Assessment of ribosomal susceptibility to streptomycin in enzyme-negative strains.
Main Results:
- Six of the 12 isolates produced streptomycin-modifying enzymes.
- Three enzyme-negative isolates exhibited resistance attributed to ribosomal alterations.
- Ribosomal insusceptibility was identified as a key factor in HLSR.
Conclusions:
- Both streptomycin-modifying enzymes and ribosomal resistance contribute to HLSR in Streptococcus faecalis.
- Ribosomal insusceptibility is a significant mechanism driving HLSR in clinical enterococcal isolates.
- These findings highlight the diverse strategies employed by bacteria to resist antibiotics.