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Plasmid-mediated high-level resistance to aminoglycosides in Enterobacteriaceae due to 16S rRNA methylation

Marc Galimand1, Patrice Courvalin, Thierry Lambert

  • 1Unité des Agents Antibactériens, Institut Pasteur, 75724 Paris Cedex 15, France. galimand@pasteur.fr

Antimicrobial Agents and Chemotherapy
|July 25, 2003
PubMed

Insights

A novel gene, armA, found on a plasmid in Klebsiella pneumoniae, confers high-level resistance to multiple aminoglycoside antibiotics. This discovery highlights a new mechanism for antibiotic resistance in gram-negative pathogens.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • The emergence of antibiotic resistance in bacterial pathogens poses a significant global health threat.
  • Klebsiella pneumoniae is a common cause of hospital-acquired infections, often exhibiting multidrug resistance.

Purpose of the Study:

  • To identify and characterize the genetic basis of multidrug resistance in a clinical isolate of Klebsiella pneumoniae.
  • To investigate the function and origin of a novel aminoglycoside resistance gene.

Main Methods:

  • Plasmid isolation and characterization (pIP1204, ~80 kb).
  • Gene identification for resistance to beta-lactams, trimethoprim, sulfonamides, streptomycin-spectinomycin, and aminoglycosides.
  • Cloning of the novel gene 'armA' into Escherichia coli to assess its function.
  • Sequence analysis of the armA gene and comparison with known resistance genes.

Main Results:

  • The plasmid pIP1204 conferred resistance to multiple antibiotics, including beta-lactams, trimethoprim, sulfonamides, streptomycin-spectinomycin, and various aminoglycosides.
  • A newly identified gene, armA, was responsible for high-level resistance to specific aminoglycosides and fortimicin when expressed in E. coli.
  • Sequence analysis revealed ArmA shares similarity with 16S rRNA methyltransferases but its low GC content suggests a non-actinomycete origin.

Conclusions:

  • The novel armA gene confers significant, broad-range aminoglycoside resistance in gram-negative bacteria.
  • Posttranscriptional modification of 16S rRNA is a viable mechanism for high-level aminoglycoside resistance.
  • Understanding these resistance mechanisms is crucial for developing strategies against multidrug-resistant pathogens.

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