Urethral Catheters, Condom Catheters, and Nosocomial Urinary Tract Infections

There is an emerging body of data indicating that a symptomatic urinary tract infection (UTI) results not just from bacteria being in urine but from bacteria in some way perturbing urinary epithelium. Fortunately, the normal urinary tract has a number of defense mechanisms that prevent or minimize those bacteria-epithelial cell interactions that are disadvantageous to the hose Although most organisms causing UTI have colonized the periurethral area previously, the urethra itself is an effective obstacle to bladder inoculation. If organisms traverse the urethra and enter the bladder, the next urination will clear 99.9% of these bacteria, a process enhanced by TammHorsfall protein and oligosaccharides that are suspended in urine and that bind bacteria. Even after the most effective micturition, however, a film of urine remains adjacent to the bladder mucosa. Fortunately, glycosaminoglycan overlays bladder epithelium and inhibits bacterial adherence to epithelial cells. Moreover, there appears to be a poorly understood bacteriocidal mechanism closely associated with bladder mucosa; this is effective even in the absence of polymorphonuclear leukocytes or antibodies. An acute inflammatory response is initiated, at least in part, by cytokines released from infected epithelial cells. The last protective effort of an epithelial cell is a sacrificial one: exfoliation of the cell allows attached organisms to be voided from the host. Polymorphonuclear leukocytes arrive within hours and ingest infecting bacteria and either may kill them or carry them into the urine, where the phagocytes are voided with their captured prey. Antibodies and cell-mediated immunity are part of a slower response, but perhaps useful in the later stages of the acute infection. The use of a urethral catheter can thwart some of these defense mechanisms. Insertion of the cathe er may push or drag urethral organisms into the bladder, and the catheter's lumen and external surfaces continue to act as bacterial conduits through the urethra. The catheter enhances uropathogen colonization of the urethra, particularly in women. The inner and outer surfaces of the catheter become nich s for adherent bacteria, which form a biofilm that covers and secures them against urine flow and polymorphonuclear leukocytes. As a foreign body, the catheter may blunt adequate antibacterial polymorphonuclear leukocyte function. Catheter drainage often is imperfect, and larger volumes of urine remain in the bladder. Finally, the presence of the catheter may mechanically damage the adjacent glycosaminoglycan layer and epithelium. Nevertheless, each year millions of urethral athet rs ar placed in patients in acute-care hospitals, in long-term-care units, and for home healthcare use. The incidence of bacteriuria is 3% to 10% per day of indwelling urethral catheterization. Consequently, the duration of catheterization is the most important risk factor for the development of bacteriuria. The majority of catheterized patients are bacteriuric by the end of 30 days, a convenient dividing line between short-term (generally hospital) and long-term (generally nursing home or home) catheterization. Although usually asymptomatic, catheter-associated b cteriuria may be complicated acutely by fever, acute pyelonephritis, bacteremia, and death; and, over prolonged catheterization, by urinary tract stones, local peri-urinary infections, chronic pyelonephritis and interstitial nephritis, renal failure, and (over years) bladder cancer.