Correlation between virulence genotype and fluoroquinolone resistance in carbapenem-resistant Pseudomonas aeruginosa

Hye Hyun Cho1, Kye Chul Kwon2, Semi Kim2

  • 1Department of Biomedical Laboratory Science, Jeonju Kijeon College, Jeonju, Korea.

Abstract

Insights

Carbapenem-resistant Pseudomonas aeruginosa strains with the exoU gene showed higher fluoroquinolone resistance and more mutations than those with the exoS gene. This highlights a link between specific virulence factors and antibiotic resistance.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Genetics

Background:

  • Pseudomonas aeruginosa is a significant opportunistic pathogen causing hospital-acquired infections.
  • The type III secretion system (TTSS) is crucial for P. aeruginosa virulence, with ExoU being a key effector impacting disease severity.
  • Carbapenem resistance in P. aeruginosa is a growing clinical concern.

Purpose of the Study:

  • To investigate the relationship between TTSS effector genotype (exoS vs. exoU) and fluoroquinolone resistance in carbapenem-resistant P. aeruginosa.
  • To analyze the correlation between TTSS genotype, fluoroquinolone resistance, and target site mutations.

Main Methods:

  • Sixty-six carbapenem-resistant P. aeruginosa strains were analyzed.
  • Fluoroquinolone (ciprofloxacin, levofloxacin) minimum inhibitory concentrations (MICs) were determined.
  • PCR and sequencing were used to identify TTSS effector genotypes and mutations in quinolone resistance-determining regions (gyrA, gyrB, parC, parE).

Main Results:

  • Strains with the exoU genotype exhibited significantly higher fluoroquinolone resistance (93.2%) compared to exoS strains (45.0%).
  • exoU+ strains were more likely to possess multiple resistance mutations (97.6%) than exoS+ strains (70%).
  • Increasing numbers of resistance mutations correlated with higher MIC values.

Conclusions:

  • Fluoroquinolone overuse contributes to increased resistance and virulence in carbapenem-resistant P. aeruginosa.
  • A distinct association exists between the exoU genotype, heightened fluoroquinolone resistance, and the presence of specific resistance mutations.

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