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Acute and chronic prostatitis discussion. Arnon Krongrad, MD, moderator.

Do we know which kind of prostatitis the patients had who were operated on by Dr. Krongrad?

Thanks.

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Pretty sure it's irrelevant. Most prostatitis cannot be diagnosed properly.
Interestingly, Guercini of Rome, Italy tested 56 guys who were classified as "Chronic non-bacterial" with ultrasound guided biobsy into infected areas, and found that about 80% were in fact bacterial.
Non bacterial just means the urologist cannot be bothered to look hard enough for bacteria beyond a standard culture (If your lucky enough to even be offered a culture).
Its easier for him to throw a ton of antibiotics at you regardless of their side effects. See link below for extract.

http://home.swipnet.se/isop/guercini.htm
I copied & pasted it below because the link is corrupted & hard to read:





Preview Introduction and Objectives: In the National Institute of Health Classification, prostatitis syndrome are categorized in clinical practice on the basis of bacteriuria and the number of inflammatory cells in prostatic secretion. According to these indications many patients are considered carriers of abacterial prostatitis and are treated as such. The presence of an agent inflecting the prostate cannot however be completely excluded. It could nest in acini or in fibrous-calcifications but still be active and capable of rendering the so called abacterial prostatitis chronic.

Methods: We recruited 56 of last 350 patients referred to our Centre because of prostatitis. The age-range was 18-46 years(average age 32 years). No patients was affected by bacteriuria. In the prostatic secretion all had at least 10 leucocytes per microscopic field according to Stamey's method (1966). Two-four weeks before prostatic secretion sampling, urethral swabs showed no patient was positive for Trichomonas vaginalis, Chlamydia Tracomatis, Micoplasma Hominis, Ureaplasma Urealyticum, HPV and Herpes Genitalis. Using the transperineal route, ultrasound guided needle aspirates were taken from sonographically dishomogenous areas in the prostate. Samples underwent histological analysis, routine cultures and DNA extraction to detect Chlamydia Tracomatis, Neisseria Gonorrhoeae and HPV using PCR amplification.

Results: Histological findings were indicative of inflammation in all 56 patients, with lymphocite aggregates being found rarely within the gland(19%)and mostly in the perigland area(46%)and stroma(35%). Cultures were positive for aerobic(56%) and anaerobic(23%)agents. Twenty-one patients(38%)presented with more than 2 species of microorganisms and 9(15%)with more than 3. DNA infected with Chlamydia Tracomatis was found in 19(34%)patients. The 9 samples(16%)with only anaerobic bacteria were associated with a high number of leucocytes in Stamey's test(>15).

Conclusions: The accuracy of needle sampling under ultrasound guidance using the transperineal route, excludes false positive results caused by contamination with pathogens in urethra. The high frequency of positivity for microorganisms detected, using these techniques, indicates studies on more patients should be performed, in order to revise the classification of prostatic syndromes and to define them more accurately.
We have known for many years that the prostate is a "dirty" organ. It is colonized with bacteria and viruses. So to find these by any approach is not surprising.

To make sense of the findings, one must step back and understand that many men with prostatic colonization with bacteria and/or visurses do not have prostatitis (here is one document in support; and here is another). In other words, there is no clear evidence that in most cases infectious agents are causally related to the symptoms of prostatitis. The question at the bedside and in the research laboratory then becomes how hard to try to look for agents that may not correlate with symptoms.

Let's look at the abstract presented. It demonstrates that there are infectious agents in the prostate -- we already knew this. It does not demonstrate any association of these agents or any agent with symptoms. I would suggest that before we reclassify clinical prostatitis, as is proposed, we show that symptoms are associated with these agents or any agent.

Better yet, we should not only show an association but a clinically meaninful application of these observations. What I mean is that a classification is really only useful if based upon it we cannot effect better treatment. If we can, for example, demonstrate that intra-prostatic Ureaplasma Urealyticum is associated with symptoms and that its treatment is both feasible and effective, then a "UU-prostatitits" classification is worth the effort. Otherwise, what's the point?

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