Genomic epidemiology and characterization of difficult-to-treat resistant Pseudomonas aeruginosa isolates co-harboring blaOXA-50 and crpP causing bronchiectasis

Difficult-to-treat resistant Pseudomonas aeruginosa (DTR-PA) is an MDR subset resistant to all first-line antipseudomonal agents. It is particularly concerning in respiratory infections like bronchiectasis, leading to poor outcomes, limited treatment options, and higher healthcare costs. This study aimed to investigate the antimicrobial resistance profiles and sequence types (STs) of Pseudomonas aeruginosa isolates, providing insight into their resistance patterns and the factors contributing to resistance. In 2021, 38 multidrug-resistant P. aeruginosa isolates were collected from bronchiectasis patients from a single medical center in Ningbo, China. The isolates were obtained from various clinical samples, including sputum, secretion, urine, and blood. Minimum inhibitory concentration testing revealed that 97.4% of the isolates were sensitive to amikacin and tobramycin, with none showing resistance to polymyxin B. Resistance rates to imipenem and meropenem were 84.2% and 57.9%, respectively, with 44.7% of isolates classified as DTR-PA. Multilocus sequence typing identified ST277 (18.4%), ST1076 (13.2%), and ST3012 (13.2%) as the predominant DTR-PA sequence types. The presence of bla_PAO, aph(3')-IIb, and catB7, in all isolates and bla_OXA-50 (16 isolates) and crpP genes (24 isolates) in coexisitance in 11 of 16 isolates, suggested a strong association with the DTR phenotype. Phylogenetic analysis grouped DTR-PA isolates into distinct evolutionary lineages (II and III), underscoring their genetic relatedness and potential for clonal spread. Our findings suggest that co-harboring bla_OXA-50 and crpP contributes to the development of DTR-PA, highlighting the need for continuous monitoring of these resistance determinants. While the study provides important insights into antimicrobial resistance in DTR-PA, further research is needed to explore resistance development across different infection sites and clinical settings.