Dissecting the genotypic features of a fluoroquinolone-resistant Pseudomonas aeruginosa ST316 sublineage causing ear infections in Shanghai, China.

Abstract

Limited information is available regarding the genomic characteristics of P. aeruginosa causing ear infections. Our aim is to characterize the genotypic features of an emerging ST316 sublineage causing aural infections in Shanghai. A total of 199 ear swab isolates were subjected to whole genome sequencing (WGS). Complete genomes for two isolates were resolved. We showed this recently emerged sublineage exhibited high-level resistance to fluoroquinolones (FQs) primarily by accumulation of known mutations in quinolone resistance determining regions (QRDRs). Loss-of-function mutations in mexR and mexCD were frequently detected. Mutations in fusA1 (P166S) and parE (S492F) were resident in this sublinage about 2 years after its emergence. Recombination events might be a key driver of genomic diversity in this sublineage. Convergent evolution events on Multidrug-resistant (MDR) determinants were also observed. We generated predictive machine models and identified biomarkers of resistance to gentamicin, fosfomycin, and cefoperazone-sulbactam in this sublineage. This sublineage tended to be less virulent by loss of a series virulence genes represented by ppkA, rhlI, and iron uptake- and antimicrobial activity-related genes. Specific mutations were detected in pilU and lpxB genes that related to surface structures. Moreover, this sublineage differed from non-ST316 isolates in several ways, including virulence genes related to cell surface structure. Our analysis suggested acquisition of a roughly 390 kbp MDR plasmid carrying qnrVC1 might play an important role in the success of this sublinage. Clonal expansion of this sublineage exhibiting enhanced adaptation to cause ear infections is concerning, which requires urgent control measures to be implemented.