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Replication of the Ordered, Nonredundant Library of Pseudomonas aeruginosa strain PA14 Transposon Insertion Mutants
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Emergence of carbapenem resistance due to the novel insertion sequence ISPa8 in Pseudomonas aeruginosa

Randal C Fowler1, Nancy D Hanson1

  • 1Creighton University School of Medicine, Department of Medical Microbiology and Immunology, Center for Research in Anti-Infectives and Biotechnology, Omaha, Nebraska, United States of America.

Plos One
|March 12, 2014
PubMed

Insights

Pseudomonas aeruginosa in cystic fibrosis patients develops carbapenem resistance through insertion sequence ISPa8. This novel mechanism highlights how genetic elements influence antibiotic susceptibility in chronic infections.

Area of Science:

  • Microbiology
  • Genetics
  • Infectious Diseases

Background:

  • Chronic Pseudomonas aeruginosa infections in cystic fibrosis patients often lead to antibiotic resistance.
  • Carbapenem resistance is a significant challenge in treating these persistent infections.

Purpose of the Study:

  • To investigate the mechanisms of carbapenem resistance emergence in Pseudomonas aeruginosa from cystic fibrosis patients.
  • To identify genetic alterations responsible for meropenem resistance.

Main Methods:

  • Selection of carbapenem-resistant mutants using subinhibitory meropenem concentrations.
  • Characterization of resistance mechanisms, including insertion sequence analysis and Southern blotting.

Main Results:

  • Nine carbapenem-resistant mutants were generated from a clinical P. aeruginosa isolate.
  • Novel insertion sequence ISPa8 was identified within or near the oprD gene in all mutants.
  • ISPa8 insertions occurred at different positions, and multiple copies were found in mutant genomes.

Conclusions:

  • Transposition of insertion sequence ISPa8 is a key mechanism driving carbapenem resistance in Pseudomonas aeruginosa.
  • Understanding these genetic mechanisms is crucial for effective antimicrobial chemotherapy in cystic fibrosis patients.

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