HOW DOES PROSTATITIS OCCUR?
There are several mechanisms in the etiology and pathogenesis of chronic prostatitis:
Dysfunctional high pressure voiding.
Many researchers hypothesize that the pain associated with prostatitis symptoms and subsequent irritative and obstructive voiding symptoms may be due to anatomical or physiological lower urinary tract obstruction. This defect may be as simple as a bladder neck problem, or may be a urethral stricture, detrusor sphincter incoordination, or a more subtle dysfunctional voiding pattern.
Intraprostatic Ductal Reflux
Many investigators have found intraprostatic ductal reflux in patients with prostatitis (especially the inflammatory category). The combination of high pressure voiding with an anatomical variation allows for intraprostatic ductal reflux.
Even in prostatitis due to known uropathogens such as E.coli, variable responses to microbial treatment suggest that bacteria may not be the primary etiological factor.
The Role of Common Organisms
E coli and other gram-negative bacteria can be localized in the prostatic fluid and are the causes of bacterial prostatitis as causes of recurrent urinary infections. In some of these patients, significant colonization of the ejaculate (bacteriospermia) may also be demonstrated. E.coli is responsible for both acute and chronic bacterial prostatitis. Other enteric bacteria such as klebsiella, serratia, enterobacter, proteus and pseudomonas are less common. Although enterococci and staphylococci can be localized in the prostate, their location in prostatitis is questionable and may be related to chronic pelvic pain syndrome. Staphyloccocus saphrophyticus has been isolated from prostatic secretions and these patients have responded to antibiotic therapy.
The Role of Rarely Encountered Organisms
Although most patients with chronic prostatitis have clear clinical findings, there is no evidence of bacterial colonization or infection in the prostate. Antibiotherapy administered to these patients often provides temporary benefits. These patients state that the complaints started with sexual activity and they often had an episode of urethritis. M.genitalium, U.urealyticum, C trachomatis, corynebacteriums, anaerobic bacteria are possible factors in these patients.
Many investigators have investigated the immunological process in nonbacterial prostatitis, which does not seem to be due to microorganisms. Chronic prostatitis may be secondary to immunologically mediated inflammation due to some unknown antigens or may be due to an autoimmune process.
Researchers suggest that simple reflux of urine and its metabolites (urate) into prostatic ducts may lead to inflammation in acini.
Many researchers suggest a neuromuscular etiology in inflammatory and non-inflammatory prostatitis. The chronic pain associated with these syndromes is strictly neuropathic in character. One hypothesis is that noninflammatory prostatitis syndrome may occur as a type of reflex sympathetic dystrophy. This view can be evaluated if the perineum/pelvic wall is considered as a distal extremity. The symptoms of all patients with noninflammatory prostatitis are very similar to those of patients with reflex sympathetic dystrophy with one arm affected.