Sarah Kindiki, Sabella Kiprono, Oleg Reva, Peter Kuloba Nyongesa, Nyabera Nicholas Mogoi, Martin Welch, Anthony Sifuna
Pseudomonas aeruginosa is an important cause of surgical site infections (SSIs) and is characterized by extensive antimicrobial resistance and genomic plasticity. We analyzed 13 whole-genome sequences of clinical P. aeruginosa isolates recovered from SSIs at a Level 5 referral hospital in Western Kenya and integrated genomic analyses with antimicrobial susceptibility tests and phenotyping of quorum-sensing (QS). Multidrug resistance was common, with resistance observed primarily against ciprofloxacin, piperacillin, ceftazidime, and amikacin, whereas meropenem and piperacillin/tazobactam retained the greatest in vitro activity. Genomic analyses identified diverse sequence types, extensive variability in insertion sequences and genomic islands, and widespread conservation of intrinsic resistance determinants, whereas accessory antimicrobial resistance genes were infrequently detected and largely associated with genomic islands. Virulence-associated genes were predominantly chromosomal, although several showed strain-specific genomic island localizations. Functional QS analyses demonstrated that isolates with intact lasR and rhlR produced significantly higher levels of acyl-homoserine lactone signals than isolates carrying predicted loss-of-function mutations, whereas Pseudomonas quinolone signal production remained comparatively conserved. These findings provide a genomic baseline for P. aeruginosa causing SSIs in Western Kenya and highlight the importance of integrating whole-genome sequencing with phenotypic analyses to strengthen surveillance and inform antimicrobial stewardship and infection prevention strategies.