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Prostatitis is a common but poorly understood inflammatory process in male adults. A recent national survey estimates that almost 2 million visits are made annually in the United States for prostatitis. Eight percent of all urology visits and 1% of all primary care visits are for prostatitis. It is the most common urologic diagnosis in men over 50. The standard classification of prostatitis as acute bacterial and chronic bacterial is now clearly inadequate, as the majority of patients with prostatitis have a chronic condition for which no evidence of infection can be found. The NIH Consensus Conference on Prostatitis divides the disease into six categories. Categories I and II represent the traditional syndromes of acute and chronic bacterial prostatitis. Category III describes a chronic pelvic pain syndrome and is divided into subcategories A and B. Category III A is an inflammatory pelvic pain syndrome evidenced by WBCs in semen, expressed prostatic secretions, or postmassage urine. This category may also be described as a nonbacterial chronic prostatitis. Category III B is a noninflammatory pelvic pain syndrome most consistent with the term prostatodynia. Category IV is asymptomatic prostatitis in which inflammation is noted as part of a work-up for prostatic cancer or infertility.
The clinical diagnosis of acute bacterial prostatitis is usually straightforward. An acute illness develops with chills, fever, and local symptoms of back or perineal pain. Symptoms of frequency and dysuria are also present. Malaise, generalized myalgias, and prostration have been described. On rectal examination, the prostate is tender, swollen, and indurated. Urinary retention resulting from bladder outlet obstruction may be recognized by bladder percussion. Laboratory data will show an elevated peripheral WBC count. A midstream urine sample will usually have WBCs and more than 105 bacteria per milliliter on culture. Macrophages laden with fat droplets may also be seen. In the setting of acute bacterial prostatitis, prostatic massage may lead to bacteremia and is contraindicated.
As in other acute bacterial infections, identification of the etiologic agent is crucial to therapy. Most cases of acute bacterial prostatitis are caused by gram-negative enteric bacilli. Escherichia coli causes most community-acquired infections; more resistant gram-negative bacilli, such as Klebsiella and Pseudomonas, may cause hospital-acquired infection. Enterococcus faecalis is the only gram-positive coccus that frequently causes prostatitis. Staphylococci have been reported in some studies. In the antimicrobial era, Neisseria gonorrhoeae is only rarely isolated.
These organisms causing acute bacterial prostatitis are also implicated in urinary tract infection. Hypotheses on routes of infection explain this commonality. The several routes of infection in prostatitis are as follows: (a) reflux of infected urine into ejaculatory and prostatic ducts, (b) ascending urethral infection, (c) spread of colonic bacteria through the lymphatic system, and (d) hematogenous spread. Bacterial infections of the prostate are more common in patients with indwelling Foley catheters and condom catheters. Acute prostatitis has occurred in men after transurethral prostatic resection.
Recently, several investigators have described both a systemic and a local immune response in prostatitis. High levels of antigen-specific IgA become detectable immediately on diagnosis. A serum IgG response to specific antigen also occurs and declines slowly over months. Measurement of antigen-specific antibody may also be useful in determining response to therapy.
Patients with acute bacterial prostatitis should have blood cultures and urine Gram’s stain and culture before antimicrobial therapy. Gram-positive cocci seen in chains suggest enterococcal infection. Ampicillin plus an aminoglycoside is a regimen of choice. Most patients will have gram-negative bacilli on smear.
Trimethoprim-sulfamethoxazole is commonly used for community-acquired infection, as it provides broad coverage for most gram-negative bacilli. Although only lipid-soluble and basic antimicrobials penetrate the normal prostate gland, diffusion into an acutely inflamed prostate is less of a problem. The severe inflammation of acute prostatitis allows agents that normally diffuse poorly into prostatic secretions to attain therapeutic levels. Quinolones, particularly ciprofloxacin, the monobactam aztreonam, aminoglycosides, and third-generation cephalosporins have all been used successfully. Antimicrobial doses should attain therapeutic levels in the serum. Response is usually dramatic. Analgesia, hydration, bed rest, and stool softener are also recommended.
Complications of acute bacterial prostatitis include septicemia, prostatic abscess, and epididymitis. Chronic prostatitis may occur after infection in some patients. Prostatic abscess results from a mixed gram-negative and anaerobic infection. Treatment of prostatic abscess may require transurethral prostatectomy.
In most patients, chronic bacterial prostatitis presents as recurrent urinary tract infection or bacteriuria. Patients may have dysuria or other voiding symptoms. Chronic pain in the perineum, low back, penis, or scrotum is also described. Chills and fever are not common. Patients may give a prior history of acute bacterial prostatitis. On physical examination, the prostate may be tender, boggy, and indurated, or it may be normal.
The etiologic agents responsible for chronic prostatitis are generally those that cause urinary tract infection. E. coli is the most important community-acquired pathogen; more resistant gram-negative bacilli such as Pseudomonas aeruginosa are more likely to be hospital-acquired. E. faecalis also is responsible for chronic prostatitis, but usually as part of a mixed infection with gram-negative bacilli. Series of patients with Staphylococcus epidermidis have been reported. Mycoplasma hominis and Ureaplasma urealyticum were cultured in 82 of 597 patients in one series. Higher concentrations of these organisms were found in expressed prostatic secretions than in first-voided specimens. Chlamydia species have not been as well established as etiologic agents. Granulomatous prostatitis is usually caused by tuberculosis or fungal infection but may occur without a clear-cut etiology.
There is a consensus that the diagnosis of chronic prostatitis is best made by quantitative cultures of concomitantly obtained specimens from urethra, midstream bladder urine, and prostatic secretions. Quantitative cultures of four carefully collected specimens are compared, including first-voided 10 mL (VB1), midstream urine (VB2), prostatic secretions obtained after prostatic massage (expressed prostatic secretions), and first-voided 10 mL after prostatic massage (VB3). In bacterial prostatitis, bacteria in the prostatic specimens (expressed prostatic secretions and VB3) are tenfold higher than in the first two specimens. The test may be simplified by comparing bacterial growth before and after prostatic massage.
The pharmacokinetics of antimicrobials in the prostate is complex. Many antimicrobials with activity against gram-negative bacilli diffuse poorly into prostatic tissue. Trimethoprim-sulfamethoxazole appears to achieve the best prostatic fluid levels. The quinolones also achieve good levels (although many data come from a dog model). In general, antimicrobial bases achieve better levels than acids. To diffuse through the prostate, the antimicrobial must be lipid-soluble and not bound to plasma proteins. Trimethoprim-sulfamethoxazole has been the best-studied antimicrobial for chronic prostatitis. With full-dose therapy for 4 weeks or more, a relapse rate of at least 40% is reported. Some clinicians recommend a more extensive period of therapy, as long as 6 months. Direct injection of antimicrobials into the prostate has been reported to be successful in Belgium, but it is controversial and rarely used in the United States. Extensive studies using quinolones have been undertaken, but criteria for diagnosis and successful therapy vary widely.
When antimicrobial therapy and suppressive therapy fail, transurethral prostatectomy, which has been highly successful in limited studies, may be considered.
It is now commonly accepted that nonbacterial prostatitis, a prostatic inflammatory syndrome in which bacteria are not present, is much more common than chronic bacterial prostatitis. The causes of nonbacterial prostatitis remain elusive. Organisms such as Mycoplasma, Chlamydia, and Trichomonas may be responsible in some cases, but other, noninfectious etiologies are probably more important. One theory maintains that abnormal voiding results in urinary reflux causing chemical or immunologically mediated reflux. It has also been hypothesized that alcohol, caffeine, and certain foods may induce an inflammatory prostatitis. Recently, the use of alpha blockers for the treatment of chronic prostatitis has been shown to be beneficial for both bacterial and nonbacterial prostatitis. Antibiotics for nonbacterial prostatitis are usually not effective. Transurethral microwave thermal therapy has shown benefit in nonbacterial prostatitis in comparison with sham. Transurethral needle ablation, which heats the prostate, is also being studied.
Prostatodynia or category III B prostatitis causes prostatic symptoms without inflammation or urinary tract infection. Irritative voiding symptoms and prostatic tenderness are common, but prostatic secretions are noninflammatory and not infected. It has been postulated that this syndrome is caused by spasticity of the bladder neck and prostatic urethra. Psychologic factors and stress may also play a role. (S.L.B.)
Barbalias GA, et al. Alpha-blockers for the treatment of chronic prostatitis in combination with antibiotics. J Urol 1998;159:883.
Alpha blockers were found to be beneficial in bacterial prostatitis, nonbacterial prostatitis, and prostatodynia. Patients with nonbacterial prostatitis did better on alpha blockers than on a combination of antibiotics and alpha blockers.
Becopoulos T, et al. Acute prostatitis: which antibiotic to use first. J Chemother 1990;2:244.
Describes serum and prostatic tissue concentrations of six antimicrobials administered to 48 patients just before prostatectomy.
Brunner H, Weidner W, Schiefer H. Studies on the role of Ureaplasma urealyticum and Mycoplasma hominis in prostatitis. J Infect Dis 1983;147:807.
Provides evidence based on quantitative cultures of expressed prostatic secretions that both Ureaplasma and M. hominis can cause chronic prostatitis.
Chodak GW. Prostatitis, epididymitis and balanoposthitis. In: Kass EH, Platt R, eds. Current therapy in infectious disease, 3rd ed. Toronto: BC Decker, 1990.
Outlines a comprehensive treatment approach to acute prostatitis.
Collins MM, et al. How common is prostatitis? A national survey of physician visits. J Urol 1998;159:1224.
There are more than 2 million office visits annually for prostatitis in the United States. About 1% of all primary care visits are for some syndrome of prostatitis. Fewer than 10% of these cases can be proved to be bacterial.
Kot T, Pettit-Young N. Acute and chronic bacterial prostatitis: a review of treatment approaches. Compr Ther 1990;16:54–59.
Reviews diagnostic methods and treatment for prostatitis.
Krieger JN, Egan KJ. Comprehensive evaluation and treatment of 75 men referred to chronic prostatitis clinic. Urology 1991;38:11.
The authors describe their clinical experience with a chronic prostatitis clinic. A comprehensive approach to diagnosis led to specific treatment in 49% of patients.
Krieger JN, et al. Diagnosing prostatitis: a clinical dilemma. Patient Care 1998;2 (Summer Suppl).
Includes the NIH classification of prostatitis. Summarizes features of the prostatitis syndromes. Describes modification of the four-glass test for diagnosis.
Lipsky BA. Urinary tract infections in men. Epidemiology, pathophysiology, diagnosis, and treatment. Ann Intern Med 1989;110:138.
Gram-negative bacilli are responsible for 75% of cases of acute bacterial prostatitis.
Meares EM Jr. Prostatic abscess. J Urol 1986;136:1281.
Editorial summarizes important issues of diagnosis. Transrectal ultrasound and computed tomography are adjunctive diagnostic tools. There is some controversy as to the role of percutaneous aspiration versus transurethral incision.
Meares EM Jr. Prostatitis. Med Clin North Am 1991;75:405.
Detailed review of types of prostatitis and their diagnosis and treatment. Includes discussion of immune response in bacterial prostatitis. Recommends 30 days of therapy for acute prostatitis.
Naber KG. Use of quinolones in urinary tract infections and prostatitis. Rev Infect Dis 1989;11(Suppl 1321):37.
Quinolones are shown to achieve good concentrations in prostatic tissue and seminal fluid.
Naber KG. The role of quinolones in the treatment of chronic bacterial prostatitis. Infection 1991;19(Suppl 3):S170.
A review of 23 studies of the efficacy of quinolones in bacterial prostatitis. Most were not randomized, and many did not include adequate follow-up.
Neal DE Jr, et al. Experimental prostatitis in nonhuman primates. II. Ascending acute prostatitis. Prostate 1990;17:233.
Summarizes findings on a prostatitis model in primates. Ascending route of infection is documented by serial cultures and histopathology.
Nickel JC, Costerton JW. Coagulase-negative Staphylococcus in chronic prostatitis. J Urol 1992;147:398.
Coagulase-negative staphylococci were cultured from prostatic biopsy specimens and seen on histologic exam.
Pewitt EB, et al. Urinary tract infections in urology, including acute and chronic prostatitis. Infect Dis Clin North Am 1997;11:623.
Gives brief update of each prostatic syndrome.
Roberts RO, et al. Prevalence of a physician-assigned diagnosis of prostatitis: the Olmsted County study of urinary symptoms and health status among men. Urology 1998;51:578.
Community-based prevalence of physician-assigned diagnosis of prostatitis is high, similar to that of ischemic heart disease. Men who have a single episode of a prostatitis syndrome had a 20% to 50% chance of a second episode.
Shortliffe LM, Wehner N. The characterization of bacterial and nonbacterial prostatitis by prostatic immunoglobulins. Medicine (Baltimore) 1986;65:399.
A detailed review of the local and systemic immune response in prostatitis.
Weidner W, et al. Semen parameters in men with and without proven chronic prostatitis. Arch Androl 1991;26:173.
Compares semen analysis of patients with chronic prostatitis versus controls. An increase in bacteriospermia and an increase in number of leukocytes were present in the chronic group.
Wolfson JS, Hooper DC. Fluoroquinolone antimicrobial agents. Clin Microbiol Rev 1989;2:378.
Reviews the efficacy of quinolones in prostatitis.

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