Figure 1.
Figure 2.
Figure 3.
Figure 4.
Figure 5.
Global trends in antimicrobial susceptibility and resistance of Proteus mirabilis in selected regions of the world [7–8, 19, 25, 27,28,29,30,31,32]_
| World region | Dominant epidemiological problems | Most frequently observed resistance | Key clinical trends |
|---|---|---|---|
| Asia | High percentage of MDR and ESBL strains and infections associated with urolithiasis | Fluoroquinolones, third-generation cephalosporins, trimethoprim/sulfamethoxazole | Increase in CAUTI-related infections and ESBL-producing strains |
| Middle East | Rapid spread of MDR and AmpC strains in nosocomial infections | β-lactams, fluoroquinolones, aminoglycosides | Increase in infections among hospitalized and long-term catheterized patients |
| Europe | Increasing frequency of infections associated with medical biomaterials and biofilm | Fluoroquinolones, cephalosporins, trimethoprim/sulfamethoxazole | Growing significance of AmpC strains and chronic CAUTI |
| South America | Regional differences in antimicrobial susceptibility, increase in nosocomial infections | Third-generation cephalosporins, fluoroquinolones | Maintaining high efficacy of carbapenems and amikacin |
| North America | Increase in infections associated with long-term care and biomateriale | Fluoroquinolones, trimethoprim/sulfamethoxazole | Greater importance of antimicrobial stewardship and targeted therapy |
| Poland | Increase in nosocomial infections caused by ESBL and AmpC strains | Fluoroquinolones, β-lactams, aminoglycosides | Rising frequency of MDR strains in catheter-associated infections |
Key virulence determinants of Proteus mirabilis and their clinical significance [4,5,6, 9–10, 14]
| Virulence mechanism | Biological significance | Clinical significance |
|---|---|---|
| Urease | Urea hydrolysis and urine alkalization | Struvite urolithiasis, catheter encrustation and obstruction |
| Swarming motility | Active bacterial migration across solid surfaces | Spread of infection within the urinary tract |
| MR/P, PMF, UCA/NAF fimbriae | Adhesion to uroepithelium and biomaterials | Catheter colonization and CAUTI development |
| Biofilm formation | Protection of bacteria against antibiotics and immune response | Chronic and recurrent infections |
| Crystalline biofilm | Precipitation of mineral crystals within the biofilm | Catheter obstruction and chronic colonization |
| Hemolysins | Host cell damage | Increased inflammation and tissue damage |
| ZapA metalloprotease | Degradation of immunoglobulins and modulation of the immune response | Maintenance of chronic infection |
| Quorum sensing | Regulation of virulence and biofilm gene expression | Bacterial adaptation to chronic infection |