Antibiotic resistance in Pseudomonas aeruginosa: mechanisms, diagnostic challenges, and omics-based diagnostic solutions

Abstract

Pseudomonas aeruginosa is considered a multidrug resistant opportunistic pathogen associated with severe infections in immunocompromised patients. Owing to its diverse intrinsic and adaptive resistance strategies, as well as its capacity for horizontal gene transfer, P. aeruginosa represents a major contributor to the global antimicrobial resistance burden. Its remarkable ability to evade antibiotics arises from a wide range of mechanisms, including efflux pumps overexpression, porin modification, enzymatic inactivation and target site modifications, alongside phenotypic adaptations such as biofilm and persister cell formation. These complex resistance strategies of the organism have fueled the global emergence of multidrug resistant, extensively drug resistant and even pan drug resistant strains. These strains significantly complicate the treatment strategies. Conventional culture-based diagnostics are still considered the gold standard, yet their delays and limitations in detecting heteroresistance and biofilm-associated tolerance hinder timely therapeutic intervention. Recent advances in omics-based approaches, including genomics, epigenomics, transcriptomics, proteomics, lipidomics, metabolomics, and phenomics, provide powerful alternatives for rapid and precise identification of resistant P. aeruginosa. In parallel, innovative diagnostic platforms such as microfluidic lab on chip systems and machine learning driven artificial intelligence further enhance diagnostic resolution. Therefore, multi omics integration, coupled with advanced platforms would be a revolutionary strategy to deliver comprehensive and rapid resistance profiling in precision diagnostics. To convert this potential into practice, proper planning, standardized protocols, clinical validation and cost-effective implementation are urgently needed. Together, these advancements pave the way toward outpacing resistance in P. aeruginosa and reducing the global burden of antimicrobial resistance.