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Journal Article
Research Support, N.I.H., Extramural
Chronic prostatitis: Charlottesville to Seattle.
Journal of Urology 2004 December
PURPOSE: Since few men with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) have culturable bacteria by traditional approaches, we used sensitive molecular methods to determine presence of fastidious microorganisms.
MATERIALS AND METHODS: We evaluated 135 men with CP/CPPS by standardized clinical evaluation, and by lower tract localization cultures and chamber counts of expressed prostatic secretions of leukocytes. We excluded from study patients with bacteriuria, bacterial prostatitis, urethritis or positive urethral cultures. Prostate biopsy was obtained using a double-needle technique to limit contamination. We chose molecular approaches because previous studies had used culture antigen detection in urine, urethral swabs and expressed prostatic secretions. However, interpretation of such studies is complicated because urogenital samples often acquire bacteria while passing through the urethra. We used specific and broad-spectrum polymerase chain reaction (PCR) assays.
RESULTS: Only 10 (8%) of the 135 subjects had positive specific PCR assays, including Mycoplasmia genitalium, Chlamydia trachomatis and Trichomonas vaginalis. Our findings suggested that C. trachomatis, T. vaginalis and M. genitalium may be identified in some patients with CP/CPPS, even among men with no evidence of urethritis and with negative urethral cultures and other assays. The broad-spectrum PCR assays provided the most provocative findings. DNA encoding tetracycline resistance was identified in 25% of subjects, and 77% of subjects had evidence of 16S rDNAs. The white blood cell concentration in the prostatic secretions correlated with identification of 16S rDNAs in prostate tissue (p <0.01).
CONCLUSIONS: Delineating the precise role of these organisms in the etiology of CP/CPPS may help define better diagnostic and treatment algorithms.
MATERIALS AND METHODS: We evaluated 135 men with CP/CPPS by standardized clinical evaluation, and by lower tract localization cultures and chamber counts of expressed prostatic secretions of leukocytes. We excluded from study patients with bacteriuria, bacterial prostatitis, urethritis or positive urethral cultures. Prostate biopsy was obtained using a double-needle technique to limit contamination. We chose molecular approaches because previous studies had used culture antigen detection in urine, urethral swabs and expressed prostatic secretions. However, interpretation of such studies is complicated because urogenital samples often acquire bacteria while passing through the urethra. We used specific and broad-spectrum polymerase chain reaction (PCR) assays.
RESULTS: Only 10 (8%) of the 135 subjects had positive specific PCR assays, including Mycoplasmia genitalium, Chlamydia trachomatis and Trichomonas vaginalis. Our findings suggested that C. trachomatis, T. vaginalis and M. genitalium may be identified in some patients with CP/CPPS, even among men with no evidence of urethritis and with negative urethral cultures and other assays. The broad-spectrum PCR assays provided the most provocative findings. DNA encoding tetracycline resistance was identified in 25% of subjects, and 77% of subjects had evidence of 16S rDNAs. The white blood cell concentration in the prostatic secretions correlated with identification of 16S rDNAs in prostate tissue (p <0.01).
CONCLUSIONS: Delineating the precise role of these organisms in the etiology of CP/CPPS may help define better diagnostic and treatment algorithms.
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