MP8-16 THE ROLE OF TYPE I PILI IN ADHERENCE AND INVASION INTO NEUROGENIC BLADDER EPITHELIUM IN A SPINAL CORD INJURY RAT MODEL

Abstract

You have accessJournal of UrologyInfections/Inflammation of the Genitourinary Tract: Kidney & Bladder1 Apr 2014MP8-16 THE ROLE OF TYPE I PILI IN ADHERENCE AND INVASION INTO NEUROGENIC BLADDER EPITHELIUM IN A SPINAL CORD INJURY RAT MODEL Tara Ortiz, Ramiro Madden-Fuentes, Rajeev Chaudhry, Zarine Balsara, Yuping Tang, John Wiener, Sherry Ross, and Patrick Seed Tara OrtizTara Ortiz More articles by this author , Ramiro Madden-FuentesRamiro Madden-Fuentes More articles by this author , Rajeev ChaudhryRajeev Chaudhry More articles by this author , Zarine BalsaraZarine Balsara More articles by this author , Yuping TangYuping Tang More articles by this author , John WienerJohn Wiener More articles by this author , Sherry RossSherry Ross More articles by this author , and Patrick SeedPatrick Seed More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.359AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES E. coli is the most common etiology of urinary tract infections (UTI). Type I pili mediate E. coli urothelium adherence and cellular invasion in the functionally intact urinary tract. The neurogenic bladder (NB) is associated with recurrent urinary tract infections, but the underlying mechanisms remain poorly understood. We hypothesized that the neurogenic bladder microenvironment is permissive to bacterial persistence such that type I pili are unnecessary for establishing infection in the NB. METHODS Six week old, female Sprague-Dawley rats underwent T10 spinal cord transection to produce a NB phenotype followed by a 14 day recovery period. Prophylactic antibiotics were administered during the recovery period and stopped 72 hours prior to infection. Spinal cord injured (SCI) and intact control rats were inoculated by transurethral catheterization with 103 and 106 colony forming units (CFU), respectively, in a competitive infection using a 1:1 ratio of the prototypic wild type human cystitis E. coli strain UTI89 and an isogenic type 1 pili repressed strain. PB and NPB were enumerated at 24 hr post infection in bladders and kidneys using differential antibiotic resistance of the two strains. Wilcoxon rank-sum test was performed to compare groups. RESULTS Bacteria without type I pili established infection in the bladders of SCI animals, but not in the sham controls (3 x 10ˆ4 vs. 0 CFU/organ, p<0.001). In the SCI bladders, PB and NPB CFU were statistically equivalent at 24 hr post infection. Both bacterial strains infected the kidneys of SCI animals, but not controls (NPB 3 x 10ˆ2 vs. 0 CFU/organ, p=0.03; PB 8 x 10ˆ2 vs. 0 CFU/organ, p<0.001). CONCLUSIONS Type I pili are necessary to establish bladder infection in neurologically intact animals, but not in the NB phenotype. These data suggest that there are alternative bacterial mechanisms for persistence in the NB bladder. Additionally, SCI animals are susceptible to upper tract infection with both PB and NPB, whereas the sham controls are not. Reflux associated with elevated bladder pressures and physiologic changes in the urothelium are postulated to account for these differences. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e80 Peer Review Report Advertisement Copyright & Permissions© 2014MetricsAuthor Information Tara Ortiz More articles by this author Ramiro Madden-Fuentes More articles by this author Rajeev Chaudhry More articles by this author Zarine Balsara More articles by this author Yuping Tang More articles by this author John Wiener More articles by this author Sherry Ross More articles by this author Patrick Seed More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...