Purpose Catheter associated urinary tract infections account for approximately 40% of all hospital acquired infections worldwide with more than 1 million cases diagnosed annually. Recent data from a catheter associated urinary tract infection animal model has shown that inflammation induced by catheterization releases host fibrinogen, which accumulates on the catheter. Further, Enterococcus faecalis catheter colonization was found to depend on EbpA (endocarditis and biofilm-associated pilus), a fibrinogen binding adhesin. We evaluated this mechanism in a human model. Materials and Methods Urinary catheters were collected from patients hospitalized for surgical or nonsurgical urological procedures. Catheters were subjected to immunofluorescence analyses by incubation with antifibrinogen antibody and then staining for fluorescence. Fluorescence intensity was compared to that of standard catheters. Catheters were incubated with strains of Enterococcus faecalis, Staphylococcus aureus or Candida to assess binding of those strains to fibrinogen laden catheters. Results After various surgical and urological procedures, 50 catheters were collected. In vivo dwell time ranged from 1 hour to 59 days. All catheters had fibrinogen deposition. Accumulation depended on dwell time but not on surgical procedure or catheter material. Catheters were probed ex vivo with E. faecalis, S. aureus and Candida albicans, which bound to catheters only in regions where fibrinogen was deposited. Conclusions Taken together, these data show that urinary catheters act as a binding surface for the accumulation of fibrinogen. Fibrinogen is released due to inflammation resulting from a urological procedure or catheter placement, creating a niche that can be exploited by uropathogens to cause catheter associated urinary tract infections.
|Number of pages||6|
|Journal||Journal of Urology|
|State||Published - Aug 1 2016|
- iatrogenic disease
- urinary tract infections