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Streptomycin resistance in mycobacteria

N Honoré1, S T Cole

  • 1Unité de Génétique Moléculaire Bactérienne, Institut Pasteur, Paris, France.

Antimicrobial Agents and Chemotherapy
|February 1, 1994
PubMed
Summary

Streptomycin resistance in tuberculosis is linked to mutations in the rpsL gene or 16S rRNA. For naturally resistant bacteria, permeability barriers are likely the cause.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Streptomycin was the first antibiotic used for tuberculosis control.
  • It functions by inhibiting protein synthesis at the ribosomal level.

Purpose of the Study:

  • To investigate the molecular mechanisms of streptomycin resistance in clinical isolates of Mycobacterium tuberculosis.
  • To explore the role of ribosomal protein S12 and 16S rRNA in conferring resistance.

Main Methods:

  • Analysis of clinical isolates of Mycobacterium tuberculosis.
  • Sequencing of the rpsL gene and 16S rRNA.
  • Comparison of protein structure conservation across different mycobacteria.

Main Results:

  • Streptomycin resistance in some Mycobacterium tuberculosis isolates is associated with missense mutations in the rpsL gene (encoding ribosomal protein S12) or base substitutions at position 904 in the 16S rRNA.
  • The primary structure of ribosomal protein S12 is highly conserved among various mycobacteria, including naturally streptomycin-resistant species.
  • This conservation suggests that factors other than ribosomal protein structure contribute to natural resistance.

Conclusions:

  • Mutations in rpsL or 16S rRNA are key mechanisms for streptomycin resistance in Mycobacterium tuberculosis.
  • For naturally resistant mycobacteria, such as M. avium, M. gordonae, and M. szulgai, permeability barriers are likely the primary reason for their resistance to streptomycin.

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