The World Health Organization lists carbapenem-resistant Pseudomonas aeruginosa (CRPA) as a critical priority pathogen. However, the links between resistance phenotypes, virulence factors, and clonal spread remain incompletely understood. We aimed to characterize the genotypic and phenotypic landscape of clinical CRPA isolates and evaluate whether specimen source or type III secretion effectors (exoT/exoY) serve as predictors of antibiotic resistance. Fifty-eight consecutive CRPA isolates from respiratory and non-respiratory specimens were analyzed. Susceptibility to 10 antimicrobial agents was determined using an automated system. PCR was used to screen for seven carbapenemase genes, six virulence/quorum-sensing genes, and the efflux marker mexY. Macrorestriction patterns were typed by SpeI-PFGE. Statistical associations were assessed using two-tailed Fisher’s exact tests with Benjamini–Hochberg false-discovery-rate (FDR) correction (α = 0.05). Resistance rates were highest for piperacillin/tazobactam (91%), ceftazidime (81%), and cefepime (81%); notably, 34% of isolates exhibited a pan-drug-resistant (PDR) profile. Only three isolates (5%) carried blaVIM; no other carbapenemase genes were detected. Virulence markers were highly prevalent (exoY 66%, exoT 57%, algD 45%; lasR 91%, rhlR 95%). After FDR adjustment, neither virulence gene presence (exoT, exoY) nor specimen origin correlated significantly with resistance to β-lactams, aminoglycosides, or fluoroquinolones (lowest q = 0.093). Furthermore, gene prevalence did not differ significantly between respiratory and non-respiratory isolates. PFGE analysis revealed 41 distinct pulsotypes without a dominant clone, suggesting sporadic horizontal gene transfer rather than clonal expansion. This CRPA cohort is genetically diverse, multidrug-resistant, and lacks anatomical segregation by genotype. The presence of exoT/exoY does not appear to shape resistance phenotypes in this setting. Infection control strategies should prioritize the containment of mobile genetic elements and implement genome-based surveillance, rather than focusing solely on specific clones or infection sites.
GÜNDOĞDU et al. (Sat,) studied this question.