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2002, Volume 5, Number 3, Pages 172-179
Table of contents    Previous  Article  Next   [PDF]
Management of prostatitis
H S Gurunadha Rao Tunuguntla and C P Evans

Department of Urology, University of California Davis School of Medicine and UC Davis Medical Center, Sacramento, California, USA

Correspondence to: C P Evans, Department of Urology, University of California, Davis School of Medicine, 4860 Y Street, Suite 3500, Sacramento, CA 95817, USA. E-mail:


Prostatitis is a common clinical entity with a prevalence rate of 5-9% and accounts for over 2 million hospital visits annually in the USA. It is traditionally classified into acute bacterial, chronic bacterial, abacterial prostatitis and prostatodynia. The recent consensus conference of the US National Institute of Diabetes and Digestive and Kidney Diseases in 2000 resulted in renewed interest in the prevalence, etiology, pathogenesis and treatment of the prostatitis syndromes. In this review, we present the contemporary knowledge and experience regarding the etiology, classification, evaluation and treatment of this condition including the role of transurethral microwave hyperthermia and transurethral needle ablation.

Prostate Cancer and Prostatic Diseases (2002) 5, 172-179. doi:10.1038/sj.pcan.4500604


prostatitis; expressed prostatic secretions; pelvic pain syndrome; midstream urine; microwave thermotherapy; prostatic massage; transurethral needle ablation


Prostatitis is a disease entity that is diagnosed by symptoms, microscopy of expressed prostatic secretions (EPS) and culture of EPS and segmented urine samples. It is a common medical condition. The estimated prevalence of prostatitis in the US is approximately 5-9%.1,2 Between 1990 and 1994 prostatitis accounted for over 2 million hospital visits per year of which approximately one-half are to urologists and one-half to primary care physicians. Prostatitis contributes to approximately 8% of urology office visits and 1% of primary care physician office visits.1 An average American urologist sees 100 patients with prostatitis per year. The disorder severely impairs the overall quality of life in the afflicted men.3

Currently, the etiology of prostatitis (more commonly referred to as 'prostatitis syndrome') is mostly unknown and the diagnostic criteria are weak.


Acute and chronic bacterial prostatitis syndromes are the best understood, but least common of the prostatitis syndromes. A causative pathogen is detected in only 5-10% of patients with prostatitis (Table 1).4 Most patients do not have bacteria in the urinary tract but do suffer from urinary symptoms, perineal/suprapubic or low back pain and fatigue. Acute bacterial prostatitis is a well recognized infectious disease of the lower urinary tract different from chronic prostatitis syndromes.5 Different forms of chronic prostatitis syndrome are poorly demarcated and are believed to be caused by both infectious/non-infectious inflammation of the prostate and non-inflammatory disease.6

Acute bacterial prostatitis results from acute infection of the prostate by recognized uropathogens (Table 1).7 The organisms ascend along the urethra/urethral catheters or reach the urinary tract by sexual transmission and rarely bacteremia or septicemia. Acute bacterial prostatitis is mainly due to aerobic Gram-negative rods, predominantly Escherichia coli and Pseudomonas spp. Obligate anaerobic bacteria rarely cause prostatitis. Fungi have recently been implicated in prostatitis in immunosuppressed patients.8 If left untreated, the infection may result in septicemia or prostatic abscess.

Chronic bacterial prostatitis is usually caused by Gram-negative bacteria such as Escherichia coli, Klebsiella and Proteus spp. and occasionally by Gram-positive bacteria such as Enterococcus fecalis, Staphylococcus and Streptococcus. Infections due to Gram-positive bacteria rarely result in recurrent urinary tract infection (UTI) (Table 1).

The exact etiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is not completely understood at present. Organs other than the prostate may be responsible for CP/CPPS symptoms. Multiple disorders that have been proposed to be causally associated include bladder neck obstruction, urethral stricture, detrusor sphincter dyssynergia and dysfunctional voiding.5,9 CPSS may be multifactorial and part of a more generalized pain disorder. Microbiologic, immunologic, neurologic, chemical, psychologic and anatomic factors are believed to be involved in its etiopathogenesis.10 High-pressure voiding, 'intra-prostatic reflux' of urine,11 autoimmune process,12,13 reflux of urine and metabolites (urate) into the prostatic ducts/acini14 and infection due to coagulase negative staphylococci, chlamydia, ureaplasma, anaerobes, or certain non-culturable organisms such as 'Biofilm' bacteria/viruses/cell-wall deficient bacteria15,16,17 have been suggested to result in chronic non-bacterial prostatitis/CPPS. The disorder has been found to be associated with increased blood flow to the prostatic capsule and diffuse flow throughout the prostatic parenchyma.18

Inflammation of the prostate as indicated by leukocytes in the EPS may be present in 50% of patients with CP/CPPS on random prostate biopsies.19 Interleukins (IL-1) and tumor necrosis factor (TNF-alpha) have been found in EPS from patients with CPPS.20 Nadler and associates found that IL-1beta and TNF-alpha levels in EPS are higher in men with category CPPS IIIA (inflammatory CPPS, with significant white cells in VB3/EPS/semen) than in those with IIIB.20

Chronic prostatitis has been reported with increased frequency in those with hypochondriasis, depression, hysteria, somatization and depression.21 About 43% of the patients with chronic prostatitis have elevated Minnesota Multiphasic Personality Inventory (MMPI) scores.

Similar to other chronic pain syndromes, patients with chronic nonbacterial prostatitis experience pain as the primary complaint, have a low relationship between symptoms and findings, and have a history of multiple unsuccessful treatments. It is often difficult to determine whether pain is the cause or the effect of other pathological processes. It is also difficult to attribute the pain to the prostate, since nonspecific musculoskeletal abnormalities can cause considerable discomfort in this region.


The clinical diagnosis of prostatitis depends on the history and physical examination, although there is no pathognomonic physical finding or laboratory test. The condition results in considerable morbidity and patients may experience symptoms for many years. Prostatitis is traditionally classified into four groups: acute bacterial, chronic bacterial, chronic nonbacterial and prostatodynia (Table 2). The National Institutes of Health (NIH) established an International Prostatitis Collaborative Network to improve diagnosis and treatment of prostatitis. This collaborative network has so far convened four consensus conferences (in 1995, 1998, 1999 and 2000) to define and classify the syndrome based on contemporary literature and clinical practice and thereby optimize the diagnosis and therapy.

The NIH consensus classification of prostatitis syndromes22 includes the following four categories:

  1. Acute bacterial prostatitis.
  2. Chronic bacterial prostatitis.
  3. Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS)
    1. Inflammatory
    2. Noninflammatory.
  4. Asymptomatic inflammatory prostatitis.

The new consensus classification recognizes pain as the primary component of the syndrome. The exclusion criteria include presence of active urethritis, urogenital cancer, urethral stricture, or neurovesical dysfunction. Patients with category III CPPS have discomfort or pain in the pelvic region for at least 3 months with variable voiding and sexual symptoms in the absence of demonstrable infection. Patients with the inflammatory subtype of CP/CPPS have leukocytes in their EPS/post-prostate massage urine or semen. In contrast, those with the non-inflammatory subtype have no evidence of inflammation.

Asymptomatic inflammatory prostatitis (evidence of inflammation in prostate biopsy/semen/EPS/voided bladder urine [VB3]; no symptoms) is diagnosed in those with no history of genitourinary tract pain and is often diagnosed during evaluation for other genitourinary pathology such as during prostatic biopsy to rule out prostate cancer in men with elevated serum prostate specific antigen (PSA) level or infertility evaluation (increased leukocyte count in seminal fluid).

Diagnostic evaluation

Acute bacterial prostatitis

This is a serious condition usually affecting men between 20 and 45 y of age and is associated with sudden onset of fever, chills and malaise. Patients often present with frequency, dysuria, poor stream, feeling of incomplete emptying and discomfort in the pelvis and abdomen. Sometimes there is also back pain.

Physical examination reveals a sick patient with tenderness in the area of the bladder. Rectal examination is very painful. A hot, enlarged, tender prostate is felt. Patients may sometimes have an abscess requiring drainage to control fever and infection.

The diagnosis is made on the basis of history, clinical examination and laboratory studies. Urinalysis may reveal bacteriuria and pyuria. Urine cultures are mandatory to define the cause and guide therapy. Cultures are always positive in patients with acute bacterial prostatitis. A CT scan is advised if the patient shows poor response to therapy or examination reveals a soft, tender prostate with a potential abscess.

Chronic bacterial prostatitis

This is a common cause of recurrent UTI in men. Patients with chronic prostatitis can be asymptomatic between episodes of recurrent UTI. Symptoms develop in presence of acute UTI due to E. coli, Klebsiella, Pseudomonas spp., Enterococci, Staphylococcus aureus or coagulase negative Staphylococcus.

Over 90% of symptomatic patients have chronic prostatitis/chronic pelvic pain syndrome. Patients have discomfort or pain in the pelvic region for at least 3 months, variable voiding and sexual symptoms in the absence of documented UTI.

Lower urinary tract localization studies

The lower urinary tract localization technique, Meares-Stamey four-glass test23 consists of collection of initial voided urine (VB1), mid stream or second voided urine (MSU/VB2) representing urethral and bladder specimens, respectively. Expressed prostatic secretions (EPS) are collected during prostatic massage. Voided bladder sample (VB3) is then collected after prostatic massage. All the specimens are cultured along with microscopic examination of the sediment in VB1, VB2 and VB3 and EPS is subjected to a wet mount microscopy. The test, however, is largely abandoned by urologists in North America since it is expensive, cumbersone, does not predict response to therapy and may lead to false-positive and false-negative results.24,25 Nickel suggested a more simple and less expensive screening technique (Pre- and post-massage test, PPMT).26 In this, urine specimens are collected before and after a vigorous prostatic massage. Increased number of uropathogenic bacteria and leukocytes in the post-massage specimen compared to the pre-massage sample indicate NIH category II prostatitis, whereas leukocytosis alone indicates NIH category IIIA. Category IIIB is suggested by an absence of bacteria or leukocytes in the post-massage specimen. While using this test, urethritis can be ruled out by a repeat VB1 collection. The positive predictive value and false-negative rate of PPMT are similar to the Meares-Stamey test.5

Shoskes and associates from the NIH Chronic Prostatitis Collaborative Network recently reported that by culturing EPS or semen for 5 days rather than the conventional 2 days, an additional 7.5% of CPPS patients would be found positive for bacteria localizing to the prostate gland.27

Chronic non-bacterial prostatitis/chronic pelvic pain syndrome

Symptoms of chronic non-bacterial prostatitis are different from those of chronic bacterial prostatitis and include pain in lower back, tip of the penis, suprapubic area, perineal discomfort, frequency, dysuria, weak stream, incomplete emptying and painful ejaculation.

Krieger and associates demonstrated that first urine and MSU have low sensitivity in CPPS, whereas the combination of EPS and post-massage urine are most useful for diagnosis.28 They also have shown that the leukocyte count in post-massage urine is more reliable compared with the analysis of EPS, which is sometimes difficult to recover. Such methods, although useful in some patients, have not been always reproducible.

By using 16S rRNA gene-based polymerase chain reaction (PCR), Hochreiter and associates recently found that bacteria are absent in histologically normal prostates and noted good correlation of inflammation with bacterial gene detection.29 They suggest that bacteria may have a role in inflammatory prostatitis.

The National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) provides a valid outcome measure for men with chronic prostatitis.1 The index is easily self-administered and is commonly used in clinical practice.

Identification of CPPS patients most likely to respond to antibiotics

Using a 16S recombinant RNA reverse transcriptase-polymerase chain reaction (RT-PCR) for the detection of bacterial genomic fragments, Shoskes and Shahed have shown that bacterial signals could predict the response to antibiotic therapy in men with NIH category III CPPS.13 These authors reported that patients with negative cultures and signals do not respond to antimicrobials and recommend that such patients should be managed by anti-inflammatory or neuromuscular therapies. This technique, however, has no practical significance as the test is currently unavailable to the average clinician.

Asymptomatic inflammatory prostatitis (AIP)

Men with AIP are asymptomatic and are detected by either prostatic biopsies performed for an elevated PSA or during an infertility work-up.31

Treatment (Figure 1a, 1b, 1c)

Acute bacterial prostatitis is almost always curable with appropriate antimicrobials and antibiotics such as fluoroquinolones and cephalosporins, respectively. Patients with chronic bacterial prostatitis, however, may have residual bacteria in the prostate following therapy.

NIH category I (acute bacterial prostatitis)

Oral fluoroquinolones are appropriate for patients who are able to tolerate fluids and can be managed on an outpatient basis. However, many patients with acute bacterial prostatitis need hospital admission due to the acute and severe pain, which requires intravenous (i.v.) fluids and i.v. antibiotics. Those on i.v. antibiotics are later switched to oral therapy as soon as possible based on the outcomes of cultures and susceptibility data.

The i.v. antibiotics commonly used include quinolones (ciprofloxacin or levofloxacin),5 gentamycin, cephalosporins, vancomycin, penicillin and trimethoprim-sulfamethoxazole (TMP-SMX) alone or in combination depending on the organism(s), whereas fluoroquinolones (ciprofloxacin/levofloxacin) or TMP-SMX5 may be used for outpatient therapy.32 The antibiotics should be continued for 4 weeks.5

Patients may benefit from alpha-blockers to relax the prostate and anti-inflammatory agents. Per-urethral catheterization is not advised as it may prolong the infection or result in epididymitis. Suprapubic cystostomy may occasionally be required for painful urinary retention. Patients also need bed rest, analgesics and stool softeners.

A poor response to antibiotic therapy may be due to the development of a prostatic abscess which, if documented by ultrasound or CT scan, can be drained by transurethral or transperineal approach.

NIH category II (chronic bacterial prostatitis)

Treatment of chronic bacterial prostatitis is of two types: curative and suppressive.

Curative therapy. This includes a 12-week course of TMP-SMX (30% cure rate) or fluoroquinolones (levofloxacin/norfloxacin/ciprofloxacin) (75% cure rate).5

Suppressive therapy. If the patient becomes asymptomatic but cultures remain positive after 4-6 weeks of antibiotics, a low-dose suppressive dose of antibiotic may need to be continued.5 This includes TMP-SMX, nitrofurantoin, tetracycline or cephalothin continued for 6-10 weeks.

If the patient continues to have symptoms after antibiotic therapy, repetitive prostatic massage is advised along with further course of antibiotics. Prophylactic low-dose antibiotics are indicated for those whose infection recurs.

The long-term results of antimicrobial therapy with regard to recurrence and symptom eradication, however, are unknown5 although eradication of the pathogen in EPS has been reported in 92% of patients 3 months after therapy and in 70-80% of those evaluated at 12-24 months.33 Results with TMP-SMX have remained poor (cure rates between 15 and 60%)34 compared to quinolones.35

Indications for surgery

Surgical therapy is only the last resort and is used for bladder neck obstruction, urethral strictures, and prostatic calculi in conjunction with persistent bacterial presence in the prostate. Radical transurethral resection of the prostate (TURP) or total prostatectomy is indicated only in those whose the prostatic fluid persistently grows the same bacterium, and only after the confirmation of the prostatic origin of the bacterium by prostatic biopsy.5 Radical TURP may result in incontinence and erectile dysfunction and may not always relieve symptoms.

NIH category IIIA (inflammatory chronic pelvic pain syndrome) and IIIB (non-inflammatory chronic pelvic pain syndrome)

In view of uncertainty about etiology, treatment of chronic nonbacterial prostatitis remains speculative. Most treatment is aimed at relieving symptoms and not at curing the disease. In addition, it is not clear whether therapy for IIIA and IIIB prostatitis syndromes should differ because the role of inflammation in these syndromes is incompletely understood.

Use of antibiotics in NIH category III is based on the uncertain etiology and the possibility that a potential pathogen or a cryptic nonculturable organism may be causative. A 6-week course has been suggested, which may be continued for a further 6 weeks if the symptoms improve.5 The same type of antibiotics that are used in category II are combined with agents for chlamydia and ureaplasma such as tetracyclines. Combination of analgesics, alpha-blockers (tamsulosin) antibiotics (TMP-SMX, fluoroquinolones or tetracycline), and muscle relaxants such as diazepam coupled with prostatic massage and supportive therapy (perineal support, pelvic floor physiotherapy, biofeedback and relaxation therapy) has been reported to yield higher cure rate and relief of pain and voiding symptoms compared to antibiotics alone and is the treatment option favored by most urologists.36 Alpha-1a blockers have been found to result in durable symptom relief and improved recurrence rates in both bacterial and non bacterial chronic prostatitis.37 Some patients with severe discomfort may require TURP.

Nickel advocated concurrent 'triple-therapy' for category IIIB prostatitis including high-dose alpha-blockade, a short-term narcotic analgesic and a muscle relaxant such as diazepam.5 The patient is advised to stay off work for the first 2 weeks, following which the narcotic analgesic is replaced by a nonsteroidal anti-inflammatory agent such as ibuprofen or acetaminophen with codeine and diazepam is tapered. The alpha-blocker is continued for 3 months or longer. Biofeedback, relaxation exercises, psychotherapy and lifestyle changes are advised if triple therapy fails.

Phytotherapies such as quercetin (a bioflavonoid),38 pentosan polysulfate,5 systemic medications (gabapentin, tricyclic antidepressants, and striated muscle relaxants), and stress reduction therapy have also been tried. Quercetin has been reported to result in symptom relief in 67% of patients in a preliminary double-blind placebo trial.38 Larger well-designed, randomized, placebo-controlled studies are, however, warranted.

Finasteride has been reported to provide symptom relief when used in patients with benign prostatic hyperplasia (BPH) and CPPS with improvement in the NIH-CPSI and BPH symptom scores,39 whereas pentosan polysulfate has been found to be effective in those with suprapubic pain and irritative voiding symptoms. Shahed and Shoskes have demonstrated induction of anti-oxidant enzyme gene expression in CPPS and suggested that CPPS may be targeted with anti-oxidant therapy.40

Heat therapies

Transurethral microwave hyperthermia41 and transurethral microwave thermotherapy (TUMT)42 have been used in the treatment of chronic nonbacterial prostatitis. These techniques increase temperature of the prostate resulting in symptom relief. TUMT has been reported to improve symptom scores by 74.9% with minimal morbidity.43 In a randomized, double-blind, sham-controlled study using validated prostatitis symptom severity index and symptom frequency questionnaires, Nickel and associates have demonstrated beneficial effect of TUMT compared to the sham group.42 Fifty per cent of patients in the sham group had a favorable response to a subsequent TUMT. Patients in the TUMT group continued to have symptomatic improvement over 21 months.

A few European studies have shown that transurethral needle ablation (TUNA) improves the symptoms and well being in patients with chronic nonbacterial prostatitis with small (<20 ml) prostates over a follow up period of 12 months.44,45 Those with severe symptoms (NIH score, 30-43) have been reported to have greater and earlier (at 3 months) improvement than those with mild to moderate symptom scores (score, <30) with 12% less requirement for analgesics, alpha-blockers and antibiotics compared with the non-TUNA group.

Heat therapies in prostatitis are currently only experimental with potential for minimal benefit. They may be offered as a last resort in patients willing to accept the potential morbidity and likelihood of failure of symptom relief.5

NIH category IV (asymptomatic inflammatory prostatitis, AIP)

No specific treatment is warranted in these patients except in those with elevation of PSA or infertility.

Role of prostatic massage in prostatitis

Prostatic massage has recently been re-popularized,46 partly due to the failure of medical therapy to improve symptoms and partly due to the belief that chronic bacterial infection exists in the blocked prostatic ducts or microabscesses. Antibiotic coverage is recommended along with prostatic massage as the latter can disseminate the intraprostatic cryptic bacteria.5

In a recent study, 46% of evaluable patients had more than 60% improvement in the symptom severity, whereas 27% had improvement in the frequency of symptoms.47 Thirty-three per cent of patients experienced a marked subjective improvement. The combination of prostatic massage and antibiotics for refractory prostatitis albeit promising, needs further confirmation.48


Prostatitis is diagnosed by symptoms or microscopy/culture of segmented urine samples and expressed prostatic secretions. The condition is poorly understood and difficult to treat. From a diagnostic and therapeutic standpoint, bacterial prostatitis should be distinguished from chronic pelvic pain syndrome. Further research is warranted to better understand the etiology and pathogenesis of prostatitis syndrome and thereby improve the diagnosis and therapy of this common condition. Agents that modulate the inflammatory response and the intercellular and neurobiological signaling may, in future, play an important role in the treatment of chronic pelvic pain syndrome. Future randomized studies should focus on determination of the true efficacy of various treatment modalities. Studies aimed at more effective delivery of antimicrobial/immunological agents may improve the outcome of therapy.


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3 McNaughton-Collins M et al. Quality of life is impaired in men with chronic prostatitis: results from the NIH Cohort Study [Abstract 98]. J Urol 2000; 163: ((Suppl)) 23.

4 Weidner W et al. Chronic prostatitis: a thorough search for etiologically involved microorganisms in 1461 patients. Infection 1991; 19: ((Suppl 3)) 119-125.

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7 Nickel JC, Bruce AW, Reid G. Pathogenesis, diagnosis and treatment of the prostatitis syndromes. In: Krane, RJ, Siroky MB (eds) Clinical Urology Lippincott: Philadelphia, 1994, p 925.

8 Elert A et al. Isolated candial prostatitis. J Urol 2000; 163: 244. MEDLINE

9 Kaplan SA et al. Pseudodyssynergia (contraction of the external sphincter during voiding) misdiagnosed as chronic nonbacterial prostatitis and the role of biofeedback as a therapeutic option. J Urol 1997; 157: 2234. MEDLINE

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12 Nickel JC et al. Pathogenesis of chronic bacterial prostatitis in an animal model. Br J Urol 1990; 66: 47. MEDLINE

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31 Dimitrakov J et al. Recent developments in diagnosis and therapy of the prostatitis syndromes. Curr Opinion Urol 2001; 11: 87-91.

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39 Leskinen M, Lukkarinen O, Marttila T. Effects of finasteride in patients with inflammatory chronic pelvic pain syndrome: a double-blind, placebo-controlled, pilot study. Urology 1999; 53: 502-505. MEDLINE

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Figure 1a Management algorithm for prostatitis syndromes.

Figure 1b Figure 1 Continued.

Figure 1c Figure 1 Continued.


Table 1 Bacteriology of acute/chronic prostatitis

Table 2 Traditional classification of prostatitis

Received 7 March 2002; revised 24 April 2002; accepted 6 May 2002
2002, Volume 5, Number 3, Pages 172-179
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