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Accumulation of carbapenem resistance mechanisms in VIM-2-producing Pseudomonas aeruginosa under selective pressure

G Meletis1, N Vavatsi, M Exindari

  • 1Department of Clinical Microbiology, Hippokration General Hospital of Thessaloniki, Thessaloniki, Greece, meletisg@hotmail.com.

European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology
|September 25, 2013
PubMed

Insights

Pseudomonas aeruginosa is evolving carbapenem resistance through multiple mechanisms. This study observed an increase in resistance mechanisms and antibiotic MIC values between 2003-2005 and 2008-2010.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Pseudomonas aeruginosa exhibits resistance to carbapenems through various mechanisms, including carbapenemase genes, OprD porin downregulation, efflux pump overexpression, and cephalosporinase overproduction.
  • Understanding these resistance mechanisms is crucial for combating infections caused by this opportunistic pathogen.

Purpose of the Study:

  • To investigate the prevalence and accumulation of carbapenem resistance mechanisms in Pseudomonas aeruginosa isolates.
  • To compare resistance mechanisms and antibiotic susceptibility between two distinct time periods (2003-2005 and 2008-2010).

Main Methods:

  • Screening of 150 carbapenem-non-susceptible P. aeruginosa isolates (2008-2010) for carbapenemase production, OprD porin loss, efflux pump overexpression, and inducible AmpC beta-lactamase.
  • Assessment of the same resistance mechanisms in a historical collection of 30 P. aeruginosa isolates (2003-2005).
  • Determination of imipenem and meropenem Minimum Inhibitory Concentration (MIC) values.

Main Results:

  • The study identified an accumulation of various resistance mechanisms in VIM-2 producing P. aeruginosa isolates from 2008-2010.
  • A significant increase in imipenem MIC90 and the geometric mean MIC values for imipenem and meropenem was observed between the two study periods.
  • The findings indicate a rise in the complexity of carbapenem resistance mechanisms within P. aeruginosa populations over time.

Conclusions:

  • The accumulation of multiple carbapenem resistance mechanisms in Pseudomonas aeruginosa contributes to its evolutionary success under antibiotic pressure.
  • Continuous monitoring of resistance mechanisms and susceptibility patterns is essential for effective treatment strategies against P. aeruginosa infections.

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