Assessment of the antimicrobial resistance mechanisms of Pseudomonas aeruginosa clinical strains

Assessment of the antimicrobial resistance mechanisms of Pseudomonas aeruginosa clinical strains

A.E. Alekseeva, N.F. Brusnigina, M.A. Makhova 

Academician I.N. Blokhina Nizhniy Novgorod Research Institute for Epidemiology and Microbiology, Nizhniy Novgorod

Background: Pseudomonas aeruginosa resistance to carbapenems is a major challenge in the field of human infectious diseases.

Aim: to assess the genetic mechanisms of antibacterial resistance of clinical strains of P. aeruginosa.

Materials and Methods: the study included whole-genome sequencing (MiSeq, Illumina) of six clinical strains of P. aeruginosa resistant to carbapenems. Bioinformatics analysis of sequencing results was performed using specialized web services and databases.

Results and Discussion: bioinformatics analysis has demonstrated that strains belong to epidemically significant, globally widespread sequence types 235 (n=3), 357 (n=2), and 654 (n=1). The genome structure of all studied P. aeruginosa strains contains serine β-lactamase PDC (molecular class C) and OXA-50-like (molecular class D) genes as well as aph(3’)-IIb, fosA, and catB7 genes. In addition, sequence-type 357 strains include extended-spectrum β-lactamase VEB genes. BlaVEB-14 has been described in sequence-type 357 for the first time. The VIM-2 metallo-β-lactamase determinant was identified only in sequence-type strain 654. In two sequence-type 235 strains, an In998-like integron carrying the extended-spectrum β-lactamase gene blaOXA-14 was identified. In all studied strains, mutations in the nalC gene were detected. These mutations increase the rate of elimination of antibacterial drugs due to the overexpression of the efflux proteins MexAB-OprM. Meanwhile, mutations in the porin protein gene OprD are associated with a decrease in carbapenem permeability. The combination of these two mechanisms may mediate carbapenem resistance of P. aeruginosa strains without carbapenemase activity.

Conclusion: our study describes the population structure of clinical carbapenem-resistant P. aeruginosa strains. The key mechanism of carbapenem resistance is mutational variability in chromosomal genes. These findings illustrate the need for the rational use of antibacterial drugs to prevent antibiotic-resistant pathogen spread.

Keywords: Pseudomonas aeruginosa, sequence type, mechanisms of resistance, mutations, blaVEB-14, blaOXA-14.

For citation: Alekseeva A.E., Brusnigina N.F., Makhova M.A. Assessment of the antimicrobial resistance mechanisms of Pseudomonas aeruginosa clinical strains. RMJ. 2023;10:48-51.