Background. According to the literature, bacterial count of uropathogens isolated from expressed prostate secretion and urine which is sufficient for a diagnosis of bacterial prostatitis I and II categories, remains contradictory. Undoubtedly, the identification of microorganisms from affected organ in high titers indicates the presence of a relevant infectious-inflammatory process. In turn, there is no consensus on the development of bacterial prostatitis at lower titers of uropathogens. Thus, the aim of our study was to identify and compare the potential features of the development and occurrence of an infectious inflammatory process in the prostate during the reproduction of bacterial prostatitis in an animal model using a low titer of causative uropathogens.
Materials and methods. A total of 16 «New Zealand» mature male rabbits aged 24±2 weeks old with weight of 3.5±0.3 kg were examined. Inoculation was performed via transurethral route, according to the developed experimental technique. E. coli was used as bacterial agent with a count of 1 x 103 CFU/ml, 1 x 105 CFU/ml and 1 x 107 CFU/ml. All animals were randomized into 4 groups of 4 individuals depending on the titer of the inoculated microorganisms (groups 1–3, respectively), group 4 – control (with inoculation by Sol. NaCl 0.9%). Sacrification and vivisection were performed on days 1, 3, 7 and 14 of the control days. Biopsy specimens from the lower urinary tract and internal genital organs of laboratory animals (bladder, urethra, prostatic complex - 6 biopsies #1A-1D, 2A, 2B) were evaluated morphologically and bacteriologically. Analytical evaluation of the experimental data was presented using descriptive statistical methods.
Results. In experimental groups (Groups 1–3), bacteriological examination of prostatic complex biopsies showed growth of microflora in all samples in titers of 101-107 CFU / ml. In group 1, the maximum concentration of uropathogen was observed on day 7, compared to day 1 in both groups 2 and 3. In all observed cases, the highest degree of bacterial contamination was noted in the biopsy specimens from paraprostatic tissues and distal part of the prostate, which was 4.0±1.7 lg CFU/ml and 3.5±1.9 lg CFU/ml, respectively, and the smallest in proximal prostatic loci (1C) and bladder neck (2B) – 3.0±1.2 lg COE / ml and 3.0±1.7 lg COE / ml, respectively. According to the morphological study, a relevant progression of the suppurative and destructive inflammation (with foci of colliquation necrosis) was identified in group 1 in the biopsies from the prostate with a maximum degree of changes on day 7 with subsequent formation of loose connective tissue proliferation areas by 14 days. This indicates the conversion of the inflammatory process to the chronic stage. These changes corresponded with the results of histopathological studies in groups 2 and 3 where higher titers of bacterial agent were used. In group 4 (control) the commensal flora was bacteriologically determined in the biopsies, but there were no signs of inflammation, according to the results of the morphological study.
Conclusion. In experimental model, we found that E. coli 103 CFU / ml induces the development of a phasic inflammatory process in the structures of the prostatic complex. These processes resulted in the formation of irreversible proliferative changes. As a consequence, it shold be recommended to consider these signs of contamination when evaluating the results of bacteriological examination of expressed prostate secretion/urine samples during planning treatment strategy.

Keywords: low counts, causative uropathogens, bacterial prostatitis, experimental models