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Extended laboratory diagnostics of chronic prostatitis

  • Gavrusev A.,
  • Strotsky V.,
  • Rubanik L.,
  • Poleshchuk N.

PII: S1569-9056(16)15076-6

DOI: 10.1016/S1569-9056(16)15076-6

Introduction & Objectives: Recurrences after the treatment of chronic prostatitis (category III) are developed in 30-70% of cases. In 85-90% of cases of chronic prostatitis bacterial pathogen can not be identified by the routine bacteriological tests. The probable cause of chronic abacterial prostatitis are noncultivated microorganisms. The aim of our study was to determine the rate of detection of nonbacterial uropathogens in urethral swabs and expressed prostatic secretions of patients affected by chronic recurrent prostatitis by extended laboratory research.

Material & Methods: The study involved 283 patients affected by chronic recurrent prostatitis. The subjects ranged in age from 20 to 59 (median – 31). All included patients had history of recurrent prostatitis symptoms with repeated courses of antibacterial therapies. Time between recurrences was from 1 to 6 months (median – 2.7). Baseline symptoms were evaluated with a NIH-CPSI questionnaire. All patients underwent extended laboratory examination of urethral swabs and expressed prostatic secretions (EPS) including light microscopy (Giemsa stain), McCoy cell culture and liquid medium for the cultivation of Trichomonas vaginalis (TV), PCR, ELISA for detection of Chlamydia trachomatis (CT), Herpes simplex virus-1,2 (HSV-1,2) and electron microscopy. When latent inflammation and a small amount of microorganisms in tested materials, we used the method of preliminary accumulation of uropathogens in cell culture and subsequent identification their by PCR. EPS was collected after urination to prevent of the urethral contamination. Diagnosis was based on positive results of at least two methods.

Results: By extended laboratory diagnostics we detected uropathogens in 261 (92.2%) of 283 patients. CT was identified in 239 (84.4%), TV – in 209 (73.8%) and HSV-1, 2 – 95 (33.5%) patients. In 81.6% of cases the infection was mixed: chlamydial-trichomonas – 115 (40.6%), chlamydial-trichomonas and viral – 94 (33.2%). Chlamydial monoinfection was identified in 18.4%. Pathogenic organisms were not identified only in 22 (7.8%) patients. The highest diagnostic sensitivity was the method of preliminary accumulation of uropathogens (93.5%). In 75 (26.5%) patients bacteria were detected in the prostate secretions: Gram-positive (Staphylococcus, Streptococcus) in 73.8% and Gram-negative (Enterobacteriaceae) in 26.2%. Electron microscopy confirmed the existence of the previously described various morphological variants of TV: amastigot, rounded and amoeboid cells. In all cases, the pathogens were found in the EPS. In 18.1% of cases TV was detected only in the EPS and was absent in the urethra. This supports a causal role in the pathogen of prostatitis development.

Conclusions: The use of extended laboratory diagnostics identifies the mixed non-bacterial uropathogens in most patients affected by chronic recurrent prostatitis that should determine the further etiological treatment of the disease.