Mechanisms of antibiotic resistance in Pseudomonas aeruginosa

Soboleva O.M., Parchutov A.I., Novitsky N.D.

Kemerovo State Medical University, Kemerovo, Russia

Pseudomonas aeruginosa occupies a leading position among nosocomial pathogens due to its mechanisms of antibiotic resistance. In the context of increasing resistance to antimicrobial drugs, this problem is becoming especially relevant for healthcare, requiring a detailed study of resistance mechanisms and the development of new treatment strategies.

The aim is to systematize modern data on the mechanisms of resistance of Pseudomonas aeruginosa, aimed at identifying key determinants affecting therapeutic efficacy.

To achieve the goal, a literature review of domestic and foreign publications was conducted. The analysis included the study of innate, acquired and adaptive mechanisms of resistance. Pseudomonas aeruginosa is characterized by a wide range of antibiotic resistance mechanisms. These include enzymatic inactivation of antibiotics by β-lactamases (AmpC, ESBL, MBL), reduction of membrane permeability due to mutations in porin proteins (e.g., OprD), and active excretion of antibiotics by efflux pumps, including the MexAB-OprM and MexXY-OprM systems. Horizontal transfer of resistance genes via integrons and plasmids plays a significant role. Additional mechanisms include biofilm formation to create a physical barrier preventing the penetration of antimicrobial agents and quorum sensing systems to regulate virulence and biofilm formation processes. The combination of these mechanisms determines the development of multiple and extremely pronounced resistance, which significantly complicates the therapy of infections caused by P. aeruginosa.

Conclusion. Pseudomonas aeruginosa demonstrates high plasticity in adaptation to antimicrobial drugs due to genetic diversity and the interaction of multiple resistance mechanisms. In order to combat this pathogen, new therapeutic approaches are needed to suppress resistance and prevent the spread of resistant strains.