Molecular characterization of virulence and resistance determinants in clinical Pseudomonas aeruginosa isolates: a cross-sectional analysis of virulence-resistance associations

Naunyn Schmiedebergs Arch Pharmacol. 2026 Jul 12. doi: 10.1007/s00210-026-05706-x. Online ahead of print.

ABSTRACT

Pseudomonas aeruginosa is a clinically significant opportunistic pathogen characterized by intrinsic and acquired resistance mechanisms coupled with a diverse array of virulence determinants. This study investigated the distribution of P. aeruginosa in various clinical specimens (n = 382), its virulence genes, antimicrobial resistance patterns, and associations with total resistant P. aeruginosa (TRPA) phenotypes. The majority of isolates were recovered from sputum (24.3%) and endotracheal tube samples (22.5%). Virulence gene screening revealed moderate-to-high prevalence of lasB (55.0%), toxA (49.7%), pilA (53.7%), aprA (56.5%), phzS (45.0%), exoS (41.9%), and exoU (38.0%), indicating their widespread involvement in pathogenicity. Antimicrobial susceptibility profiling demonstrated the highest susceptibility to amikacin (56.3%) and gentamicin (52.4%), while resistance to carbapenems (imipenem 52.4%, meropenem 52.9%) and cephalosporins was alarmingly high. Based on resistance classification, 33.5% of isolates were MDR, and 9.7% XDR. Among ceftazidime-resistant isolates (n = 200), 83% harboured ESBL genes, with bla_CTX-M (38.0%) being most prevalent. Notably, 30.7% and 22.8% of isolates carried bla_NDM-1 and bla_OXA-48, respectively. Comparative analysis demonstrated statistically significant associations between TRPA phenotype and virulence genes: lasB (OR = 90.3), toxA (OR = 260.9), and pilA (OR = 32.6) (p < 0.0001). Resistance determinants such as bla_CTX-M (OR = 3.5), aac(6′)-Ib (OR = 2.9), qnrA (OR = 3.9), and co-carriage of NDM-1 + OXA-48 (OR = 4.9) were significantly enriched in TRPA isolates. These findings demonstrate a significant association between virulence and antimicrobial resistance traits, emphasizing the potential expansion of high-risk P. aeruginosa clones in clinical settings and highlighting the need for genomic surveillance and antimicrobial stewardship interventions.

PMID:42437416 | DOI:10.1007/s00210-026-05706-x