Genotypic and phenotypic landscape of carbapenem-resistant Pseudomonas aeruginosa isolated from respiratory and non-respiratory samples in a tertiary hospital.

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Gündoğdu H. B., Rakıcı E., Ejder N., Çopur Çiçek A., Özgümüş O. B.

BMC microbiology, 2026 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası:
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1186/s12866-026-04756-8
  • Dergi Adı: BMC microbiology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Directory of Open Access Journals
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • Recep Tayyip Erdoğan Üniversitesi Adresli: Evet

Özet

Background 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.

Methods 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).

Results 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.

Conclusions 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