Abstract

Catheter-associated urinary tract infections (UTI c) remain the most common nosocomial infection. Although usually benign, UTI c cause bacteremia in 2–4% of patients and have been associated with a case fatality rate three times as high as nonbacteriuric patients. Risk factors for UTI c identified in multivariate analyses include increasing duration of use, female sex, absence of systemic antibiotics, and disconnection of the catheter-collecting tube junction. Recent studies suggest that most episodes of low colony count bacteriuria (10 2-10 4 cfu/ml) rapidly progress to high (≥10 5/ml) colony counts within 24–48 hours. In persons with long-term catheterization, bacteriuria inevitably develops and the infecting strains change frequently. In this setting, Proteus and Morganella species produce catheter encrustations and persistent bacteriuria. Routes of bacterial entry have been well defined and differ by gender, with the periurethral route predominating in women and the intraluminal route in men. Growth of bacteria in biofilms on the inner surface of catheters promotes encrustation and may protect bacteria from antimicrobial agents. Bacterial virulence factors have not been well characterized in UTI c, but fimbrial adhesins have been associated with bacterial persistence in the catheterized urinary tract, and urease production has been associated with stone formation and catheter encrustation. Recent efforts to prevent UTI c have focused mainly on preventing bacterial entry to the urinary tract or eradicating bacteriuria after its onset and have been largely unsuccessful. Systemic antimicrobials, sealed tubing and catheter junctions, silver ion-coated catheters, and antiseptics in the collecting bag have all been efficacious in one or more controlled trials. Failure to stratify patients by major risk factors, especially gender, antimicrobial exposure, and catheter duration, makes interpretation of many trials difficult. Further research in the areas of innovative catheter system design, bacterial-host epithelial cell interaction, and targeted antimicrobial prophylaxis seem the most likely approaches to controlling UTI c in the future.

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