Objective: The aims of this prospective clinical cohort study were to determine the prevalence of asymptomatic bacteriuria in dogs with cranial cruciate ligament disease and to determine which clinical parameters and clinicopathologic data are associated with asymptomatic bacteriuria. Another aim was to determine the incidence of surgical site infections in dogs with and without asymptomatic bacteriuria. Results: In 156 dogs with cruciate ligament disease, the prevalence of asymptomatic bacteriuria was 7.1%. Furthermore, the prevalence was 12.4% in female dogs and 0% in male dogs. The most common bacterial isolate was Escherichia coli. Patient sex, urine white blood cells/ high-powered field, and microscopic bacteriuria were significantly different between dogs with and without asymptomatic bacteriuria. Only 60% of dogs with microscopic bacteriuria had growth on urine aerobic culture. No significant difference was found in age, body weight, body condition score, duration of lameness, limb affected, or other urinalysis values between dogs with and without asymptomatic bacteriuria. Of the dogs that had 8-week repeat cultures, 2/3 dogs with asymptomatic bacteriuria had negative urine cultures and 3/43 without asymptomatic bacteriuria had positive urine cultures. Of 57 dogs that received surgery and had sufficient follow-up, 15 developed surgical site infection. All surgical site infections occurred in dogs without AB. The incidence of surgical site infection in this population was 26.3% (15/57). Conclusions: Prevalence of asymptomatic bacteriuria in dogs presenting with cranial cruciate ligament disease was similar to previously reported values in male and female dogs. This suggests that dogs with cranial cruciate ligament disease are not more prone to asymptomatic bacteriuria than dogs in previously studied populations. Preliminary data suggests that AB does not predispose dogs to SSI however further research and continued data collection is warranted. / Master of Science / Asymptomatic bacteriuria is defined as having bacteria in the urine without signs of lower urinary tract disease. The aim of this study was to determine the prevalence asymptomatic bacteriuria in dogs with cranial cruciate ligament disease. Additionally, another aim was to determine the incidence of surgical site infections after cranial cruciate ligament surgery in dogs with and without asymptomatic bacteriuria. Prevalence of asymptomatic bacteriuria in dogs presenting with cranial cruciate ligament disease was found to be similar to previously reported values in male and female dogs. This suggests that dogs with cranial cruciate ligament disease are not more prone to asymptomatic bacteriuria than dogs in previously studied populations. Preliminary data suggests that dogs with bacteria in the urine does not predispose dogs to SSI however further research and continued data collection is warranted.

Urinvägsinfektioner (UVI) är ett vanligt hälsoproblem som drabbar miljontals människor. Den allvarligaste formen, akut pyelonefrit (APN) kan ge svåra komplikationer. Urinvägspatogena Escherichia coli (UPEC) som orsakar APN uttrycker P fimbrier som specifikt binder till glykosphingolipider på ytan av uroepitelceller. Det sätter igång en toll-like receptor 4 (TLR4) beroende men LPS-oberoende immunreaktion. Den roll som interferon beta (IFN-β) spelar vid bakterieinfektioner är inte helt klarlagd men studier som gjorts på IFN-β knockoutmöss visade på en ökad infektionsbenägenhet och svåra njursymptom vid infektion med UPEC. IFN-β uttrycket i uroepitelceller som svar på bakterieinfektion undersöktes. För att ta reda på om uttrycket är P fimbrieberoende infekterades humana A498 njurcarcinomceller med den P fimbrieförsedda pyelonefritstammen CFT073 eller den icke-virulenta asymtomatisk bakterieuristammen E. coli 83972 och inkuberades i 1,5 respektive 4 timmar. Som kontroll användes celler som enbart behandlats med PBS. Uttrycket av IFN-β analyserades med immunofluorescens (IF) och konfokalmikroskopi, samt med Western blot. Resultaten från konfokalmikroskopi visade att celler som exponerats för CFT073 under 4 timmar uttryckte mest IFN-β medan cellerna som utsatts för E. coli 83972 visade på ett omvänt förhållande. Western blot visade på högst uttryck i de E. coli 83972-behandlade cellerna. IFN-β uttrycktes i alla celler, inklusive kontrollcellerna, i någon utsträckning. Det kan betyda att IFN-β även induceras på någon alternativ väg och/eller att det uttrycks konstitutivt av njurepitelceller. / Urinary tract infections (UTI) are a common health concern and affect millions of people. The most severe form of UTI, acute pyelonephritis (APN) is associated with serious complications. Uropathogenic Escherichia coli (UPEC) that cause APN express P fimbriae which specifically bind to glycosphingolipid molecules on the surface of urothelial cells. This triggers a toll-like receptor 4 (TLR4) mediated but LPS-independent innate immune response. The role of interferon beta (IFN-β) in bacterial infections is not well known but experiments with IFN-β knockout mice have shown an increased susceptibility and severe kidney pathology when infected with UPEC. IFN-β induction in urothelial cells in response to bacterial infection was investigated. To find out whether this response is P fimbriae dependent, A498 human kidney carcinoma epithelial cells were exposed to the P fimbriated CFT073 pyelonephritis strain or the non-virulent E. coli 83972 asymptomatic bacteriuria strain and incubated for 1.5 and 4 hours. For control, cells were treated with PBS alone. The IFN-β expression was analysed using immunofluorescence (IF) and confocal microscopy, and Western blot. Confocal microscopy results showed that the response to bacteria was both time- and dose-dependent. The highest IFN-β expression was detected in cells exposed to CFT073 for 4 hours, while cells exposed to E. coli 83972 showed an inverse relationship. Western blot analysis revealed that the highest expression was in the E. coli 83972 stimulated cells. IFN-β was expressed in all cells to some degree, including control cells. This could imply that IFN-β is induced by some other means and/or is constitutively expressed by kidney epithelial cells.