The role of subclinical infection in patients with urge incontinence has been largely ignored. The aim of this study was to test for the presence of intracellular bacteria in exfoliated urothelial cells obtained from the urine of patients with detrusor overactivity or mixed incontinence +/- a history of UTI, and compare this to a control group of patients with stress incontinence and no history of infection. Bacterial cystitis was assessed by routine microbiology and compared to microscopic analysis of urine by Wright staining. Subsequent analysis of urothelial cells by confocal microscopy was performed to determine the existence of intracellular bacteria. Bacterial cystitis was seen in 13% of patients based on routine microbiology. Wright staining of concentrated urothelial cells demonstrated the presence of bacteria in 72% of samples. Filamentous bacterial cells were observed in 51% of patients and were significantly more common in patients with detrusor overactivity. Intracellular Escherichia coli were observed by confocal microscopy. This study supports the possibility that a subset of patients with urge incontinence may have unrecognised chronic bacterial colonisation, maintained via an intracellular reservoir. In patients with negative routine microbiology, application of the techniques used in this study revealed evidence of infection, providing further insights into the aetiology of urge incontinence.

Introduction and hypothesisUrinary urge incontinence is a chronic, debilitating condition that is difficult to treat. Patients refractory to standard antimuscarinic therapy often experience recurrent urinary tract infections (rUTIs). The microbiota of these refractory patients with rUTI remains unexplored.MethodsA midstream urine (MSU) sample was collected from patients with refractory urge incontinence and coexistent rUTI during acute symptomatic episodes. Culture-based diagnosis was performed using routine microbiological methods. Culture-independent profiling was performed using bacterial 16S RNA profiling. E. coli strain typing was performed by amplicon pyrosequencing of the fimH gene.ResultsOver 2 years, 39 patients with refractory urge incontinence and coexistent rUTI were studied, yielding 9 severely affected cases. These 9 patients were carefully monitored for a further 2 years, resulting in the collection of 102 MSU samples, 70 of which were diagnosed as UTI (median of 8 UTIs/woman). Culture-independent analysis of 38 of these samples revealed the existence of a diverse urinary microbiota. Strain typing of E. coli identified instances of rUTI caused by the same persisting strain and by new infecting strains.ConclusionsPatients with refractory urge incontinence and coexistent rUTI possess a diverse urinary microbiota, suggesting that persistent bladder colonisation might augment the pathology of their chronic condition.

Bacteriuria, including "low-count" bacteriuria, is more prevalent in urinary incontinence when compared to continent female controls.

Objective To determine whether patients with detrusor instability (DI) were more likely to have bacterial cystitis or signi®cant bacteriuria on the urodynamictest day than were women with a stable bladder. Patients and methods A catheter specimen of urine was cultured (overnight in air) from 862 consecutive women at the time of urodynamic testing. The upper urinary tract was imaged, with cystoscopy when indicated, to exclude upper tract lesions or malignancy. The percentage of patients with pure idiopathic DI and those with mixed DI/genuine stress incontinence (GSI), in whom the urine culture was positive, was compared with the percentage who had a stable bladder (pure GSI or urodynamically normal) and a positive urine culture, both for the entire dataset and for women aged > or <65 years. Data were also analysed to detect the converse relationship; in those women found to have bacterial cystitis, the relative risk of being found urodynamically unstable or stable was determined. Results The likelihood of bacterial cystitis occurring in patients with idiopathic DI (5.6%) was signi®cantly greater than that in patients with GSI (1.1%; P = 0.009, Fisher's exact test). The proportion of patients with DI and signi®cant bacteriuria (15.4%) was signi®cantly greater than that in patients with GSI (7.9%; P = 0.02). In patients with combined pure and mixed DI, bacterial cystitis was signi®cantly more likely to occur (6.3%) than in GSI (P <0.001), but bacteriuria was no more likely (12.5%, P = 0.09). Conversely, of those women found to have bacterial cystitis, the relative risk of having an unstable bladder was increased (+1.56), but for those with bacteriuria the relative risk of detrusor instability was not increased. Conclusion There was a signi®cant association between idiopathic DI and bacterial cystitis, and we suggest that in some women with an unstable bladder, urinary infection may enhance detrusor contractility. Nevertheless, large-scale studies are needed of the temporal relationship between the onset of bacterial cystitis and the onset of DI.