Genetic Determinants Linked to MDR/XDR in Pseudomonas aeruginosa Strains from a Mexican Tertiary Hospital

TL;DR

This study identifies genetic factors linked to drug resistance in Pseudomonas aeruginosa strains from a Mexican hospital, highlighting the role of blaVIM and OprD mutations.

Contribution

The study identifies specific genetic determinants, including blaVIM and OprD mutations, contributing to MDR/XDR in Pseudomonas aeruginosa in a Mexican hospital setting.

Findings

blaVIM metallo-β-lactamase was detected in MDR/XDR Pseudomonas aeruginosa isolates.

Recurrent mutations in the oprD gene (S103T, T115K, L170F, G186P, T189V) were associated with imipenem resistance.

The findings emphasize the multifactorial nature of carbapenem resistance in Pseudomonas aeruginosa.

Abstract

Background: Pseudomonas aeruginosa is one of the leading agents causing healthcare-associated infections (HAIs) due to its intrinsic resistance, its capacity to acquire resistance mechanisms, and its persistence in hospital environments. In Mexico, it ranks among the most frequently reported pathogens in national surveillance systems. The aim of this study was to characterize antimicrobial resistance profiles and the genetic determinants associated with MDR/XDR phenotypes in P. aeruginosa strains from HAIs at Hospital Juárez de México (HJM). Methods: Sixty-three strains from patients with HAIs were analyzed. Identification was confirmed by 16S rRNA gene sequencing. Antimicrobial susceptibility testing followed CLSI guidelines. MDR/XDR phenotypes were classified according to the Latin American consensus for categorizing MDR, XDR, and PDR pathogens. Screening for resistance mechanisms was carried out by PCR for the main β-lactamases circulating at HJM. Finally, mutations in the oprD gene were detected in imipenem-resistant isolates through amino acid sequence alignment. Results: Resistant phenotypes allowed the identification of MDR and XDR profiles. Only the metallo-β-lactamase blaVIM was detected. Analysis of oprD porin sequences revealed recurrent mutations (S103T, T115K, L170F, G186P, and T189V) associated with imipenem resistance. Conclusions: In P. aeruginosa, the presence of blaVIM and structural alterations in OprD confirms the multifactorial nature of carbapenem resistance. These findings underscore the need to strengthen microbiological surveillance programs and antimicrobial stewardship strategies to mitigate the impact and spread of MDR/XDR isolates.

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