Co-Morbidities of Interstitial Cystitis

Introduction: This study aimed to estimate the proportion of patients with Interstitial Cystitis/Painful Bladder Syndrome (IC/BPS) with systemic dysfunction associated co-morbidities such as irritable bowel syndrome (IBS) and fibromyalgia (FM). Material and Methods: Two groups of subjects with IC/BPS were included: 1) Physician diagnosed patients with IC/BPS and 2) Subjects meeting NIDDK IC/PBS criteria based on a questionnaire (ODYSA). These groups were compared to healthy controls matched for age and socio-economic status. NIDDK criteria required: pain with bladder filling that improves with emptying, urinary urgency due to discomfort or pain, polyuria > 11 times/24 hrs, and nocturia > 2 times/night. The ODYSA instrument evaluates symptoms pertaining to a range of disorders including chronic fatigue, orthostatic intolerance, syncope, IBS, dyspepsia, cyclic vomiting syndrome, headaches and migraines, sleep, Raynaud’s syndrome and chronic aches and pains. Results: IC/BPS was diagnosed in 26 subjects (mean age 47 +/- 16 yrs, 92% females), 58 had symptoms of IC/BPS by NIDDK criteria, (mean age 40 +/- 17 yrs, 79% females) and 48 were healthy controls (mean age 31+/- 14 yrs, mean age 77%). Co-morbid complaints in the IC/BPS groups included gastrointestinal symptoms suggestive of IBS and dyspepsia, sleep abnormalities with delayed onset of sleep, feeling poorly refreshed in the morning, waking up before needed, snoring, severe chronic fatigue and chronic generalized pain, migraines and syncope. Discussion: Patients with IC/BPS had co-morbid central and autonomic nervous system disorders. Our findings mirror those of others in regard to IBS, symptoms suggestive of FM, chronic pain and migraine. High rates of syncope and functional dyspepsia found in the IC/BPS groups merit further study to determine if IC/BPS is part of a diffuse disorder of central, autonomic and sensory processing affecting multiple organs outside the bladder

Fluoroquinolone Resistance in Ureaplasma parvum in the United States

We report the first case of naturally occurring fluoroquinolone resistance in Ureaplasma spp. from the United States. Resistance in this case probably developed as a result of mutations in the gyrA and parC genes of the DNA gyrase/topoisomerase IV complex that occurred in the presence of antimicrobial selective pressure

Rate and risk factors for sacral nerve stimulator lead breakage at the time of lead revision or explantation

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Biofilms on Indwelling Artificial Urinary Sphincter Devices Harbor Complex Microbe–Metabolite Interaction Networks and Reconstitute Differentially In Vitro by Material Type

The artificial urinary sphincter (AUS) is an effective treatment option for incontinence due to intrinsic sphincteric deficiency in the context of neurogenic lower urinary tract dysfunction, or stress urinary incontinence following radical prostatectomy. A subset of AUS devices develops infection and requires explant. We sought to characterize biofilm composition of the AUS device to inform prevention and treatment strategies. Indwelling AUS devices were swabbed for biofilm at surgical removal or revision. Samples and controls were subjected to next-generation sequencing and metabolomics. Biofilm formation of microbial strains isolated from AUS devices was reconstituted in a bioreactor mimicking subcutaneous tissue with a medical device present. Mean patient age was 73 (SD 10.2). All eighteen artificial urinary sphincter devices harbored microbial biofilms. Central genera in the overall microbe–metabolite interaction network were Staphylococcus (2620 metabolites), Escherichia/Shigella (2101), and Methylobacterium-Methylorubrum (674). An rpoB mutation associated with rifampin resistance was detected in 8 of 15 (53%) biofilms. Staphylococcus warneri formed greater biofilm on polyurethane than on any other material type (p < 0.01). The results of this investigation, wherein we comprehensively characterized the composition of AUS device biofilms, provide the framework for future identification and rational development of inhibitors and preventive strategies against device-associated infection