[Enzymatic resistance in Pseudomonas aeruginosa, clinical and laboratory aspects]

Area of Science:

• Microbiology
• Infectious Diseases
• Antimicrobial Resistance

Background:

• Pseudomonas aeruginosa is a significant cause of healthcare-associated infections.
• The pathogen exhibits remarkable adaptability, dissemination, and intrinsic antimicrobial resistance.
• Acquisition of resistance mechanisms via mobile genetic elements complicates treatment.

Purpose of the Study:

• To highlight the challenges in treating Pseudomonas aeruginosa infections.
• To detail the intrinsic and acquired resistance mechanisms of Pseudomonas aeruginosa.
• To underscore the clinical implications of multidrug, extensively drug, and pandrug resistance phenotypes.

Main Methods:

• Review of intrinsic resistance mechanisms, including reduced outer membrane permeability and efflux pumps.
• Analysis of acquired resistance through horizontal gene transfer (integrons, transposons, plasmids).
• Examination of enzymatic resistance, such as betalactamases (ESBLs, carbapenemases) and aminoglycoside-modifying enzymes.

Main Results:

• P. aeruginosa possesses intrinsic resistance via efflux pumps and AmpC cephalosporinase.
• Horizontal gene transfer facilitates the acquisition of diverse resistance determinants.
• The pathogen displays multidrug (MDR), extensively drug (XDR), and pandrug (PDR) resistance phenotypes.

Conclusions:

• Pseudomonas aeruginosa poses a significant therapeutic challenge due to its resistance profile.
• Understanding resistance mechanisms is crucial for effective treatment strategies.
• The emergence of MDR, XDR, and PDR phenotypes necessitates novel approaches to combat P. aeruginosa infections.