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Chronic bacterial prostatitis

Chronic bacterial prostatitis
Authors:
Alain Meyrier, MD
Prathit A Kulkarni, MD
Barbara W Trautner, MD, PhD
Section Editors:
Stephen B Calderwood, MD
Khalil G Ghanem, MD, PhD
Deputy Editor:
Allyson Bloom, MD
Literature review current through: Apr 2025. | This topic last updated: Apr 29, 2025.

INTRODUCTION — 

The prostate is subject to various inflammatory disorders [1]. One of these syndromes is chronic bacterial prostatitis, which is characterized by chronic or recurrent urogenital symptoms in the setting of documented or suspected bacterial infection of the prostate.

The clinical features, diagnosis, and management of chronic bacterial prostatitis will be reviewed here. Other prostatic syndromes, including acute bacterial prostatitis and chronic prostatitis/pelvic pain syndrome (ie, urogenital symptoms without bacterial infection), are discussed separately. (See "Acute bacterial prostatitis" and "Chronic prostatitis and chronic pelvic pain syndrome".)

DEFINITIONS — 

In order to standardize definitions of inflammatory prostatic conditions, improve diagnosis and treatment of these conditions, and facilitate research, the United States National Institutes of Health (NIH) previously established an International Prostatitis Collaborative Network [2]. The 1999 classification scheme developed by this group remains the standard approach to prostatitis and defines the following syndromes:

I. Acute bacterial prostatitis – Acute urogenital symptoms with evidence of bacterial infection of the prostate (see "Acute bacterial prostatitis")

II. Chronic bacterial prostatitis – Chronic or recurrent urogenital symptoms with evidence of bacterial infection of the prostate

IIIA. Chronic prostatitis/chronic pelvic pain syndrome, inflammatory – Chronic or recurrent urogenital symptoms with evidence of inflammation but not bacterial infection of the prostate (see "Chronic prostatitis and chronic pelvic pain syndrome")

IIIB. Chronic prostatitis/chronic pelvic pain syndrome, noninflammatory – Chronic or recurrent urogenital symptoms without evidence of inflammation or bacterial infection of the prostate (formerly designated prostatodynia) (see "Chronic prostatitis and chronic pelvic pain syndrome")

IV. Asymptomatic inflammatory prostatitis – Absence of urogenital symptoms but with incidental evidence of inflammation of the prostate (eg, found on a biopsy performed for a different purpose)

Evidence of inflammation or bacterial infection has historically been determined by the presence of inflammatory cells in, or bacterial growth from, expressed prostatic secretions, post-prostate massage urine, or seminal fluid [3].

Practically, most diagnostic testing for chronic bacterial prostatitis is done on urine and, if necessary, post-prostatic massage urine samples [4]. Prostatic massage maneuvers are typically performed by urologists but can be performed by anyone with expertise in the technique. (See 'Diagnosis' below.)

PATHOGENESIS — 

The pathogenesis of chronic bacterial prostatitis is thought to be the same as in acute infection. In most cases, bacteria migrate from the urethra or bladder through the prostatic ducts when urine refluxes into the prostate (figure 1). (See "Acute bacterial prostatitis", section on 'Pathogenesis'.)

Bacteria can also enter the prostate through hematogenous or lymphatic spread, although those routes are less common than contiguous spread through the genitourinary tract.

Chronic bacterial prostatitis can also be a complication of acute bacterial prostatitis that is inadequately treated [5]. (See 'Risk factors' below.)

EPIDEMIOLOGY

Prevalence — Overall, prostatitis syndromes are common and tend to occur in middle-aged and older males.

An accurate estimate of the prevalence of chronic bacterial prostatitis is not available, as the majority of studies evaluating this were conducted prior to 2004 and relied on either physician-diagnosed prostatitis (without a standardized definition) or self-reported symptoms, which make the results hard to generalize [6]. Additionally, the clinical diagnosis of chronic bacterial prostatitis is subject to many biases and might have varied over time.

Chronic bacterial prostatitis might also be underdiagnosed, as clinicians infrequently test for atypical organisms that could cause prostatitis. (See 'Microbiology' below.)

Risk factors — The risk factors for development of chronic bacterial prostatitis have not been clearly defined.

Chronic bacterial infection of the prostate can develop following an episode of acute prostatitis. In a retrospective review of 480 patients from Korea with acute bacterial prostatitis, the 49 patients (10 percent) who developed chronic infection were more likely to have a history of urinary tract manipulation, voiding symptoms, diabetes mellitus, and smoking [7]. However, this study did not analyze whether these factors were independently associated, and subsequent studies have not confirmed the findings [5].

Other suggested risk factors have included conditions that impair urinary flow (such as benign prostatic hyperplasia and urethral stricture) [8].

Prostatic stones might also contribute to the persistence of infection. In one study of males with chronic bacterial prostatitis, prostatic stones were associated with a higher likelihood of relapse following antimicrobial therapy [9].

MICROBIOLOGY — 

The pathogens associated with chronic bacterial prostatitis reflect the spectrum of organisms that cause urogenital tract infections in general, including cystitis, urethritis, and deeper genital tract infections (such as epididymitis):

Gram-negative enteric bacteria are classically the most common cause of chronic bacterial prostatitis. Specific pathogens include Escherichia coli, other Enterobacterales such as Klebsiella and Proteus species, and Pseudomonas [10].

Gram-positive pathogens, in particular Enterococcus faecalis, may be an increasingly frequent cause of chronic bacterial prostatitis. In some cohorts, E. faecalis is the most common isolate [11-14]. Staphylococcus aureus is a less-common gram-positive cause; this organism can reach the bladder and genitourinary tract through instrumentation, such as a urinary catheter, or bacteremia/disseminated infection [10,15-17].

Fastidious atypical organisms, such as Chlamydia trachomatis and Ureaplasma urealyticum, have also been associated with chronic prostatitis, although whether they have a causative role is uncertain. C. trachomatis has been isolated from the prostate and appears to reside in prostatic tissue (rather than represent a contaminant from the urethra) [18,19]; in some studies, it has been associated with an increased risk of inflammatory prostatitis [20]. U. urealyticum is also often frequently identified in urine and prostatic fluid, but the clinical significance of this is unclear. In one study of 409 patients with prostatitis syndromes, U. urealyticum was recovered from 18 percent of prostatic fluid specimens [21]; however, it is frequently isolated from asymptomatic males as well [22]. The study also preceded National Institutes of Health (NIH) consensus definitions of prostatitis, so it is uncertain how many of the 409 patients had inflammatory prostatitis.

Other possible atypical etiologic agents include Trichomonas vaginalis and Mycoplasma genitalium [10,23,24]. As an example, in one study from China that included 235 patients with chronic prostatitis, M. genitalium was detected by polymerase chain reaction (PCR) of post-massage urine and prostatic secretions in 10 percent compared with only 3 percent of healthy control patients, suggesting that M. genitalium could contribute to prostatic infection [23]

Rarely, fungi (such as Cryptococcus or Blastomyces) or Mycobacterium tuberculosis can cause chronic prostatitis [25,26]. These unusual pathogens may be more likely to occur in patients with underlying immunosuppression.

CLINICAL MANIFESTATIONS — 

The clinical presentation of chronic bacterial prostatitis can be quite subtle.

Presenting features – Classically, males with chronic bacterial prostatitis present with recurrent urinary tract infection symptoms (including urinary frequency, dysuria, urgency, and perineal discomfort) and repeated isolation of the same organism from the urine. However, only the minority of patients present with this classic pattern, and most have only one or some of these features [10]. Other symptoms and signs can include pain (in the perineum, lower abdomen, testicles, and penis, or with ejaculation), bladder irritation, bladder outlet obstruction, and sometimes blood in the semen [27-29]. Chronic bacterial prostatitis is not clearly associated with a higher incidence of sexual dysfunction. These primary features of chronic prostatitis have been incorporated into the National Institutes of Health chronic prostatitis symptom index (NIH-CPSI) and span the three domains of pain, urinary function, and quality of life [30].

Regardless of the specific constellation of symptoms, by definition, they occur over a prolonged period of at least three months [17].

Lack of severe/systemic illness – In chronic bacterial prostatitis, unlike in acute bacterial prostatitis, systemic symptoms of infection, such as fever, are usually absent.

Nonspecific examination and laboratory findings – Physical examination of patients with chronic bacterial prostatitis can often be normal. Digital rectal examination could demonstrate a normal prostate or, in some instances, nodularity, tenderness, or bogginess.

Peripheral leukocytosis is often absent. Prostate-specific antigen (PSA) levels are also variable. In one study of individuals who had chronic bacterial prostatitis documented as part of a treatment trial, only 25 percent had an elevated PSA (>4 ng/mL) [31]. PSA elevation is less likely in chronic than in acute bacterial prostatitis [17].

DIAGNOSIS

Clinical suspicion — The possibility of chronic bacterial prostatitis should be considered in male patients who present with chronic or recurrent urogenital symptoms over the course of at least three months. Repeated episodes of cystitis that recur soon after discontinuation of antibiotic therapy are particularly suspicious. Chronic bacterial prostatitis should also be suspected in individuals with previous acute bacterial prostatitis and persistent or recurrent symptoms following treatment. (See 'Clinical manifestations' above.)

Such individuals will usually have had urine cultures performed. If an organism associated with chronic bacterial prostatitis is repeatedly isolated from multiple urine cultures over time in a patient with consistent symptoms (eg, pelvic pain, dysuria), this constellation of findings may suggest chronic bacterial prostatitis. In such patients, comparing cultures before and after prostatic massage (the two-glass test, discussed below) can add more diagnostic certainty. If cultures demonstrate only organisms that are not associated with prostatitis, such as coagulase-negative staphylococci or Corynebacterium, we do not attribute chronic bacterial prostatitis to those isolates and pursue additional evaluation in such cases.

Furthermore, urine culture is not highly sensitive for chronic bacterial prostatitis, and additional testing, as discussed below, is frequently necessary to establish the diagnosis.

Pyuria does not distinguish bacterial prostatitis as it can be seen in noninfectious inflammatory prostatitis as well, but lack of pyuria reduces concerns for inflammation (infectious or not) in the prostate. In such cases, noninfectious prostatitis/chronic pelvic pain syndrome is more likely. (See "Chronic prostatitis and chronic pelvic pain syndrome", section on 'Diagnosis'.)

Establishing the diagnosis — When chronic bacterial prostatitis is suspected, we refer patients to a urologist for testing of prostatic secretions/post-prostatic massage urine. Primary care doctors and internal medicine subspecialists can also obtain expressed prostatic secretions, although sensitivity of prostatic fluid testing appears higher when obtained by experts in prostate care [32].

Prostatic massage involves applying gentle stroking pressure from the peripheral aspects of the prostate to the midline and from the base to the apex, over both lobes, for approximately one minute. During the massage, prostatic secretions are collected from the urethral meatus. Urine is also collected before and after the massage. All specimens are sent for microscopy and culture.

In a patient with consistent symptoms, the diagnosis of chronic bacterial prostatitis can be established when the level of uropathogenic bacterial growth is at least 10-fold greater in post-prostatic massage specimens compared with urine collected prior to massage [33]. Results are difficult to interpret if pre-massage urine has high levels of bacteriuria, but it is reasonable to make the presumptive diagnosis of chronic bacterial prostatitis in a symptomatic individual with growth of the same uropathogen on repeated urine specimens and post-prostatic massage specimens. Microscopy showing >12 white blood cells (WBC) per high-powered field in post-prostatic massage specimens (when there is no pyuria in pre-prostatic massage specimens) suggests prostatic inflammation and thus also supports the diagnosis of chronic bacterial prostatitis in an individual with positive cultures.

Comparing pre- and post-prostatic massage specimens is sometimes referred to as the “two-glass test.” It is a modification of the classic method for evaluating for chronic bacterial prostatitis, the Meares-Stamey four-glass test [15]. Although the four-glass test is described extensively in the literature, it is cumbersome and infrequently used in practice, even among specialists. In one survey of urologists, 80 percent reported they never or rarely performed the four-glass test [4]. Furthermore, the two-glass test appears highly specific compared with the four-glass test (although it is less sensitive) [33]. Nevertheless, it may be helpful to understand how the four-glass test is performed and interpreted, since many studies categorize patients based on its results. The test involves collecting four specimens in sequence: the first 5 to 10 mL of voided urine after cleaning the periurethral area (VB1, urethral sample), a midstream urine sample (VB2, bladder sample), prostatic secretions expressed following digital prostate massage (EPS, prostatic sample), and the first 5 to 10 mL of voided urine following the massage (VB3, prostatic sample). All specimens are submitted for microscopy and cultures. The finding of pathogens on culture of prostatic samples (EPS and VB3) exclusively or at a level 10 times higher than in urethral and bladder samples (VB1 and VB2) is diagnostic of chronic bacterial prostatitis [27]. For the test to be interpretable, the colony count in VB2 must be less than 103/mL, since the presence of bacteria in the bladder sample can prevent identification of a small number of organisms in the prostate. Chronic bacterial prostatitis is suspected when VB3 has more than 12 WBCs per high-power field; >20 WBCs per high-power field is generally diagnostic unless WBCs were also present in VB2.

Additional evaluation for diagnostic uncertainty — If repeated urine cultures are negative and cultures of post-prostatic massage specimens are unrevealing (or unavailable), additional testing can help to identify a potential pathogen, which could then support the diagnosis of chronic bacterial prostatitis. Specifically, we test for sexually transmitted infections or other atypical organisms and also submit semen for culture, although the accuracy of results from semen testing is uncertain. If these tests do not identify a pathogen, nonbacterial chronic prostatitis/chronic pelvic pain syndrome is more likely. (See "Chronic prostatitis and chronic pelvic pain syndrome", section on 'Diagnosis'.)

Testing specimens for atypical organisms – In males who are sexually active, we also send urine or urethral swabs for nucleic acid amplification testing for C. trachomatis, M. genitalium, and T. vaginalis. Although it remains uncertain whether all these organisms play a causative role in chronic bacterial prostatitis, it is reasonable to attribute symptoms to them if no other potential pathogen grows on other cultures [10,18,19,22,23]. (See 'Microbiology' above.)

In the rare cases when fungal or mycobacterial pathogens are suspected, cultures for these can be performed on expressed prostatic secretions or prostate biopsy specimens [34].

Uncertain role of semen culture – Semen specimens collected by the patient may be more practical than post-prostatic massage specimens, but the reliability of semen cultures in the diagnosis of chronic bacterial prostatitis has not been established. We submit semen specimens for culture if post-prostatic massage specimens are unrevealing or unavailable; however, we interpret the results critically because of the possibility of false-positive results, particularly with gram-positive organisms [17]. If organisms that are not typical urinary tract pathogens (such as gram-positive organisms other than Enterococcus species) grow on semen culture, we suggest repeating cultures to ensure continued growth before attributing symptoms to that organism.

Some studies have suggested that semen culture has higher sensitivity than post-prostatic massage specimens [35,36]. In one of those studies, patients who had a urinary tract pathogen grow on semen culture but not from post-prostatic massage specimens still experienced improvement in prostatitis symptoms with directed antibiotic symptoms, suggesting that the organism identified on semen culture could have been the microbial cause of chronic bacterial prostatitis [36]. However, many of the gram-positive organisms that are identified on semen culture but not post-prostatic massage specimens are coagulase-negative staphylococci and other skin commensals, which have an uncertain role in chronic bacterial prostatitis and may just reflect contamination of the specimen [35].

Caveats about response to presumptive treatment – Because of the challenges in obtaining informative cultures to confirm the diagnosis of chronic bacterial prostatitis, patients with persistent symptoms of prostatitis but no clear evidence of bacterial infection are sometimes treated presumptively. Lack of response to antibiotics makes the diagnosis of chronic bacterial prostatitis improbable. However, an apparent antibiotic response does not necessarily confirm the diagnosis; in trials evaluating fluoroquinolones for chronic prostatitis/chronic prostatic pain syndrome (CP/CPPS; ie, without evidence of bacterial infection), both antibiotic and placebo groups experienced symptom improvement with no statistically significant differences between them [37,38]. (See 'Definitions' above.)

DIFFERENTIAL DIAGNOSIS — 

The primary differential diagnosis of chronic bacterial prostatitis is chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), in which symptoms are similar, but there is no clear evidence of a bacterial infection (see 'Definitions' above). Because obtaining useful prostatic specimens to confirm a diagnosis of chronic bacterial prostatitis can be challenging and urine culture has lower sensitivity, the distinction is not always readily established. Thus, some clinicians will trial antibiotic therapy in patients with prostatitis symptoms despite no evidence of infection; in such cases, no or minimal response to antibiotics suggests CP/CPPS. (See 'Additional evaluation for diagnostic uncertainty' above and "Chronic prostatitis and chronic pelvic pain syndrome".)

Noninflammatory disorders of the prostate, bladder, and urinary tract can also lead to the persistent irritative (urgency, frequency, nocturia) and obstructive (slow stream, hesitancy, dribbling) urinary symptoms that are observed with chronic bacterial prostatitis. Prostatic and urine cultures would be negative in such cases and there would be no evidence of inflammation. The evaluation of men with lower urinary tract symptoms is discussed in detail elsewhere. (See "Lower urinary tract symptoms in males".)

Individuals who have repeatedly positive urine cultures but no lower urinary tract symptoms likely have asymptomatic bacteriuria. (See "Asymptomatic bacteriuria in adults", section on 'Definition of asymptomatic bacteriuria'.)

ANTIBIOTIC THERAPY — 

Given the indolent nature of chronic bacterial prostatitis, patients are typically treated for chronic bacterial prostatitis in the outpatient setting rather than in the hospital. Furthermore, antibiotic therapy can usually be deferred until a causative pathogen has been identified on culture and susceptibilities confirmed. Thus, antibiotic selection is typically based on the susceptibility profile of the isolate; our approach to selection is outlined below. (See 'Initial approach for most patients' below.)

Although trials and observational studies have evaluated individual antibiotic agents for chronic bacterial prostatitis, prospective randomized controlled trials comparing agents from different classes are limited, so comparative efficacy is unknown [39]. Furthermore, studies of antimicrobial treatment of chronic prostatitis often include males with inflammatory chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) in which an infectious etiology is not clearly established, so the results may not reflect outcomes with documented infection.

Given the lack of comparative clinical data, antibiotic penetration into the prostate is an important consideration for agent selection. The barrier between the microcirculation and the prostate gland stroma limits drug entry to passive diffusion, which permits only nonprotein-bound, lipophilic antimicrobial agents to reach therapeutic levels within the gland. In addition, the low pH of prostatic fluid allows antibiotics with alkaline pKas (such as fluoroquinolones and sulfonamides) to achieve high concentrations in prostatic tissue more readily than antibiotics with acidic pKas. Although antibiotics penetrate more readily in the setting of inflammation [40], agents that have optimal prostatic penetration in the absence of inflammation are ideal choices for chronic bacterial prostatitis, which is characterized by minimal inflammation.

Initial approach for most patients

Fluoroquinolones or TMP-SMX — Antibiotic therapy can usually be deferred until a causative pathogen has been identified on culture and susceptibilities confirmed. For patients with an initial episode of chronic bacterial prostatitis caused by a susceptible organism, either fluoroquinolones (ciprofloxacin or levofloxacin) or trimethoprim-sulfamethoxazole (TMP-SMX) are appropriate first-line choices, taking into consideration the potential for adverse events in the specific patient. These options are also reasonable for empiric therapy in a patient with suspected chronic bacterial prostatitis and no informative cultures, depending on local resistance rates in uropathogens. Some of the contributors of this topic prefer fluoroquinolones, since supporting data are more extensive than for TMP-SMX; one author favors TMP-SMX given the potential severity of the side effects associated with fluoroquinolones. All patients should be counseled on and monitored for potential side effects with prolonged antibiotics. For directed treatment of Enterococcus or sexually transmitted pathogens, other antibiotics are preferred. (See 'Considerations for specific pathogens' below.)

TMP-SMX – For chronic bacterial prostatitis, the dose of TMP-SMX is one double-strength tablet (160 mg trimethoprim and 800 mg sulfamethoxazole) orally twice daily for six weeks.

Like fluoroquinolones, TMP-SMX achieves high levels in the prostate. However, TMP-SMX has not been as extensively studied as the fluoroquinolones and has historically been given for longer than six weeks [10,15]. In a review of small studies of males with documented chronic bacterial prostatitis, initial clinical cure rates with TMP-SMX for three months were 68 to 100 percent (weighted average 85 percent), although the relapse rate over several years of follow up was approximately 64 percent [41]. In the absence of robust evidence regarding duration of therapy, treatment for six weeks is likely reasonable for an initial course of antibiotics.

TMP-SMX has been associated with a higher rate of allergic reactions that prompt emergency care compared with other antibiotics [42]. Severe adverse effects with TMP-SMX are uncommon but include neutropenia, severe hypokalemia, and severe dermatologic reactions. Adverse effects of TMP-SMX are discussed in detail elsewhere. (See "Trimethoprim-sulfamethoxazole: An overview", section on 'Adverse effects and precautions'.)

Fluoroquinolones – Appropriate fluoroquinolone agents include ciprofloxacin 500 to 750 mg orally twice daily or levofloxacin 500 to 750 mg orally daily, each given for four weeks; it is reasonable to extend the duration to six weeks for slow response. For ciprofloxacin or levofloxacin, we usually use the 500 mg rather than 750 mg daily dose pending data that suggest differential efficacy. The 500 mg dose of levofloxacin has been used successfully for bacterial prostatitis and has been associated with fewer side effects resulting in discontinuation [43]. However, it is reasonable to use the 750 mg dose, particularly in cases where the minimum inhibitory concentration (MIC) of the organism is elevated within the susceptible range.

Fluoroquinolones are the drug class best studied for documented chronic bacterial prostatitis. In open-label trials and trials comparing different fluoroquinolone regimens, fluoroquinolones have six-month clinical cure rates of about 60 to 70 percent when given for four weeks or longer [14,39,44-47]. Although one trial suggested higher clinical improvement rates with levofloxacin compared with ciprofloxacin [47], other trials have not found clinically meaningful efficacy differences between fluoroquinolone agents [14,39]. However, shorter courses (less than four weeks) of higher doses of fluoroquinolones have been associated with an increased likelihood of relapse [43]. Fluoroquinolones are also preferred options for chronic bacterial prostatitis because they achieve high levels in the prostate.

However, prolonged use of fluoroquinolones has been associated with several serious side effects, and patients should be counselled about and monitored for these effects. As examples, tendinitis and tendon rupture have been reported in patients receiving prolonged fluoroquinolone therapy, especially in those >60 years of age receiving glucocorticoids [48]. Other potential serious effects include aortic aneurysm/dissections and neuropsychiatric toxicity. Adverse effects of fluoroquinolones are discussed in detail elsewhere. (See "Fluoroquinolones", section on 'Adverse effects'.)

Other potential alternatives — There are limited data on the best approach to treatment for patients who have chronic bacterial prostatitis due to a typical uropathogen (eg, gram-negative bacillus) but cannot use a fluoroquinolone or TMP-SMX. Potential options include fosfomycin, doxycycline, or minocycline, depending on susceptibility testing. We reserve oral beta-lactam antibiotics for cases in which other options are not active against the isolate or cannot be used for other reasons. These alternative agents are generally given for six weeks.

FosfomycinFosfomycin is a reasonable alternative when fluoroquinolones and TMP-SMX cannot be used, although susceptibility testing often has to be requested specifically. The optimal dose is uncertain; we generally suggest 3 g orally every 48 to 72 hours for six weeks. Some studies have reported good outcomes with fosfomycin, in some cases at unconventionally high doses, for treatment of prostatitis with organisms resistant to other agents [49-53]. As an example, in a prospective study of 44 patients with chronic bacterial prostatitis (59 percent due to multidrug-resistant organisms), three- and six-month cure rates were 80 and 73 percent with fosfomycin dosed at 3 g once daily for one week then 3 g every 48 hours for a total of 6 to 12 weeks [52]. However, about 20 percent of patients experienced diarrhea on this regimen. Other case series and reports generally describe favorable outcomes with little evidence of toxicity in patients with chronic bacterial prostatitis [49,51-53].

Fosfomycin also appears to achieve reasonable intraprostatic concentrations in uninflamed prostatic tissue.

TetracyclinesDoxycycline (100 mg orally twice daily) and minocycline (100 mg orally twice daily) have good prostatic penetration [54] and are a reasonable alternative option for susceptible organisms. However, clinical data supporting their use for chronic bacterial prostatitis are limited, and they might have less inherent antimicrobial activity against typical genitourinary pathogens.

Beta-lactams – Oral beta-lactams are a possible alternative, although we only use them if other options are not feasible and monitor closely for effect. If oral beta-lactams are used, we favor higher doses (eg, cefuroxime 500 mg to 1 g three times daily, cefpodoxime 200 to 400 mg twice daily) and ideally consult with a pharmacist to ensure adequate oral bioavailability. Penetration of beta-lactams (including cephalosporins) into the prostate is variable [54], and it is uncertain whether higher doses can achieve sufficient tissue levels. Therefore, they have not historically been used to treat chronic bacterial prostatitis and informative clinical data are limited. Nevertheless, a trial of an oral beta-lactam is an appropriate approach for organisms that are resistant to all other oral options rather than using an intravenous regimen.

In some cases, the resistance pattern of the causative organism might render intravenous agents the only effective options. In cases of complicated drug resistance or intolerance to oral therapy, we advise consultation with an expert in the treatment of chronic bacterial prostatitis.

Nitrofurantoin, although useful for cystitis, should not be used for chronic bacterial prostatitis because of poor prostatic penetration.

Duration of therapy — As discussed elsewhere, we give fluoroquinolones for four weeks and non-fluoroquinolone antibiotics for six weeks. However, in individuals who have a definite but slow response to therapy, a longer duration (eg, up to 12 weeks) may be reasonable if the regimen is well tolerated. In contrast, stopping antibiotics after a shorter duration (eg, two to four weeks) is appropriate for patients who had no positive microbiology, are being presumptively treating for chronic bacterial prostatitis, and have minimal or no response to treatment; CP/CPPS is a more likely diagnosis in such cases. (See "Chronic prostatitis and chronic pelvic pain syndrome".)

Data informing the duration of therapy are limited to mainly noncomparative open-label trials or observational studies, which have evaluated fluroquinolones for four or more weeks and non-fluoroquinolone agents for more than six weeks. One trial comparing two, three, and four weeks of a fluoroquinolone reported higher relapse rates with the shorter durations [43]. (See 'Initial approach for most patients' above.)

Considerations for specific pathogens

Enterococcus — For directed therapy of chronic enterococcal prostatitis, data are limited, and the optimal approach is uncertain. We favor initial treatment with oral amoxicillin (1 g three times daily). Amoxicillin is highly active against susceptible enterococci; however, we use a high dose since beta-lactams have suboptimal penetration into the prostate. If amoxicillin is not appropriate because of resistance or allergies, other options include linezolid and fluoroquinolones, but each has drawbacks. Adverse effects (eg, thrombocytopenia) may preclude use of linezolid for the duration of treatment for prostatitis, and resistance to fluroquinolones can emerge rapidly in enterococci. Some experts, including other UpToDate authors, suggest using a combination of amoxicillin and a fluoroquinolone, but we reserve that for patients who do not respond to initial monotherapy. (See "Treatment of enterococcal infections".)

The duration is discussed elsewhere. (See 'Duration of therapy' above.)

Chlamydia or other sexually transmitted infection

Chlamydia trachomatisAzithromycin (1 g weekly for four weeks) or doxycycline (100 mg twice daily for four weeks) can be used to treat prostatic infections associated with C. trachomatis [55-57]. In a small randomized trial of 125 adult men with chronic bacterial prostatitis and documented C. trachomatis infection, those doses of azithromycin and doxycycline resulted in equivalent rates of microbial eradication (approximately 80 percent) and clinical cure (approximately 70 percent) [57]. In another trial, men randomly assigned to azithromycin (500 mg daily for three days each week for three weeks) had higher rates of bacterial eradication (80 versus 39 percent) and clinical cure (69 versus 34 percent) compared with those who received ciprofloxacin (500 mg twice daily for 20 days) [58]. Although doxycycline is preferred over azithromycin for C. trachomatis genitourinary infections, because of superior microbiologic outcomes with seven days of doxycycline versus single-dose azithromycin [59], the data do not suggest a difference for prostatitis when using longer courses.

Mycoplasma – Our approach to treatment of M. genitalium prostatitis is the same as for other genitourinary infections, although a longer duration may be warranted for prostatitis. These regimens are discussed in detail elsewhere. (See "Mycoplasma genitalium infection", section on 'Regimen selection for M. genitalium'.)

For patients with sexually transmitted infections, management of sex partners is important to prevent reinfection. (See "Treatment of Chlamydia trachomatis infection in adults and adolescents", section on 'Management of sex partners' and "Mycoplasma genitalium infection", section on 'Partner management'.)

Management of recurrences — Recurrence of chronic bacterial prostatitis is common. Some studies have reported relapse rates up to 25 to 50 percent after initial treatment [14,60]. Management of recurrence involves evaluation of underlying reasons for recurrence and repeat antibiotic therapy.

Evaluate underlying cause of recurrence – All patients with recurrent symptoms of chronic bacterial prostatitis should have repeat cultures to confirm the presence of infection and identify the pathogen. If the original pathogen is isolated again and has developed resistance, the new susceptibility pattern should inform antibiotic selection. However, recurrence following initial antibiotic therapy is not necessarily due to bacterial resistance. Other potential causes could be related to underlying prostate disease (eg, leading to impaired urinary flow), incomplete adherence to therapy, and drug interactions that reduce antibiotic availability. These potential contributors should be addressed before retreatment. Additionally, the possibility of an incorrect diagnosis of chronic bacterial prostatitis should be considered, particularly if all cultures are negative. (See 'Diagnosis' above and "Chronic prostatitis and chronic pelvic pain syndrome", section on 'Diagnostic approach'.)

Repeat antibiotic therapy – Our approach to retreatment of chronic bacterial prostatitis is the same as that to initial therapy and depends on the susceptibility of the pathogen isolated following recurrence. Fluoroquinolones generally remain the treatment of choice, even if this class of drug was used for the initial treatment course, unless a resistant organism is detected. TMP-SMX remains the primary alternative. If using the same drug to treat recurrent chronic bacterial prostatitis, we suggest extending the duration (eg, from four to six weeks for fluoroquinolones and from 6 to 6 to 12 weeks for other agents). (See 'Initial approach for most patients' above.)

ADDRESSING URINARY OBSTRUCTION — 

Difficulty with urine initiation, a sensation of incomplete emptying, or post-void dribbling should prompt evaluation for urinary obstruction, referral to a specialist in urology, and correction of any functional or anatomic predisposition to chronic bacterial prostatitis. These issues are discussed in detail elsewhere. (See "Lower urinary tract symptoms in males", section on 'Diagnostic testing for persistent or complicated symptoms' and "Lower urinary tract symptoms in males", section on 'Further management by etiology'.)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Bacterial prostatitis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Microbiology and risk factors – Gram-negative rods, in particular Escherichia coli, are the most common causes of chronic bacterial prostatitis. Other organisms, including enterococci and Chlamydia trachomatis are also potential causes. Risk factors are not well defined but include prior acute bacterial prostatitis, impaired urinary flow, and prostatic stones. (See 'Epidemiology' above and 'Microbiology' above.)

Clinical features – The classic presentation is a syndrome of recurrent symptoms of urinary tract infection (urinary frequency, dysuria, urgency, and perineal discomfort) and repeated bacteriuria with the same organism; most patients present with only a subset of those features. Other common symptoms include abdominal, testicular, and penile pain and other symptoms of storage or voiding dysfunction. (See 'Clinical manifestations' above.)

Diagnosis – The possibility of chronic bacterial prostatitis should be considered in male patients who present with chronic or recurrent urogenital symptoms over the course of at least three months, who have repeated episodes of cystitis soon after discontinuing antibiotics, or who have persistent or recurrent symptoms after an episode of acute bacterial prostatitis. Isolating the same organism from multiple urine cultures over time in such patients is highly suggestive of chronic bacterial prostatitis. The diagnosis can be established when the level of uropathogenic bacteria is at least 10-fold greater in post-prostatic massage specimens compared with urine collected prior to massage. We perform additional testing to identify a pathogen (testing for sexually transmitted infections, semen culture) for patients with persistent symptoms but negative urine and prostatic cultures. (See 'Diagnosis' above.)

Differential diagnosis – The main differential diagnosis is chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), which is characterized by prostatitis symptoms without evidence of infection. If antibiotics are presumptively given in such cases, minimal or no response suggests CP/CPPS rather than chronic bacterial prostatitis. (See 'Differential diagnosis' above and "Chronic prostatitis and chronic pelvic pain syndrome".)

Initial antibiotic therapy – Antibiotic therapy can usually be deferred until a causative pathogen has been identified on culture and susceptibilities confirmed. For most susceptible isolates, we suggest a fluoroquinolone (eg, ciprofloxacin 500 mg twice daily or levofloxacin 500 to 750 mg once daily) for four weeks or trimethoprim-sulfamethoxazole (one double-strength tablet orally twice daily) for six weeks (Grade 2C). Both have excellent prostate penetration, and limited data suggest associated clinical cure rates of over 60 percent at three to six months. All patients should be counseled on and monitored for potential side effects with prolonged antibiotics. (See 'Fluoroquinolones or TMP-SMX' above.)

If neither fluoroquinolones nor TMP-SMX can be used, potential alternatives that are less studied include fosfomycin, doxycycline, and minocycline; we reserve oral beta-lactams for patients who have no other options. We generally give non-fluoroquinolone options for six weeks. (See 'Other potential alternatives' above.)

Treatment of certain pathogens (eg, Enterococcus or C. trachomatis) warrants a distinct approach. (See 'Considerations for specific pathogens' above.)

Recurrent prostatitis – Chronic bacterial prostatitis recurs following initial therapy in approximately 30 percent of cases. Prior to retreatment, we assess potential causes of recurrence, including emergent resistance to the initial antibiotic, incomplete adherence, drug interactions, or incorrect diagnosis. Antibiotic selection follows the same approach as for initial therapy. If there is no resistance, the antibiotic used initially can be used again, although we use a longer duration than previously. (See 'Management of recurrences' above.)

Addressing urinary obstruction – Any functional or anatomic urological issues that impede urinary flow and predispose to chronic bacterial prostatitis should be corrected, if possible. (See "Lower urinary tract symptoms in males", section on 'Further management by etiology'.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges Thomas Fekete, MD, who contributed to earlier versions of this topic review.

  1. Pontari MA, Joyce GF, Wise M, et al. Prostatitis. J Urol 2007; 177:2050.
  2. Krieger JN, Nyberg L Jr, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA 1999; 282:236.
  3. Krieger JN, Jacobs RR, Ross SO. Does the chronic prostatitis/pelvic pain syndrome differ from nonbacterial prostatitis and prostatodynia? J Urol 2000; 164:1554.
  4. McNaughton Collins M, Fowler FJ Jr, Elliott DB, et al. Diagnosing and treating chronic prostatitis: do urologists use the four-glass test? Urology 2000; 55:403.
  5. Marquez-Algaba E, Pigrau C, Bosch-Nicolau P, et al. Risk Factors for Relapse in Acute Bacterial Prostatitis: the Impact of Antibiotic Regimens. Microbiol Spectr 2021; 9:e0053421.
  6. Roberts RO, Lieber MM, Rhodes T, 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.
  7. Yoon BI, Kim S, Han DS, et al. Acute bacterial prostatitis: how to prevent and manage chronic infection? J Infect Chemother 2012; 18:444.
  8. Sharp VJ, Takacs EB, Powell CR. Prostatitis: diagnosis and treatment. Am Fam Physician 2010; 82:397.
  9. Zhao WP, Li YT, Chen J, et al. Prostatic calculi influence the antimicrobial efficacy in men with chronic bacterial prostatitis. Asian J Androl 2012; 14:715.
  10. Lipsky BA, Byren I, Hoey CT. Treatment of bacterial prostatitis. Clin Infect Dis 2010; 50:1641.
  11. Cai T, Mazzoli S, Meacci F, et al. Epidemiological features and resistance pattern in uropathogens isolated from chronic bacterial prostatitis. J Microbiol 2011; 49:448.
  12. Magri V, Marras E, Perletti G. Chronic bacterial prostatitis: enterococcal disease? Clin Infect Dis 2011; 53:1306.
  13. Cornia PB, Takahashi TA, Lipsky BA. The microbiology of bacteriuria in men: a 5-year study at a Veterans' Affairs hospital. Diagn Microbiol Infect Dis 2006; 56:25.
  14. Bundrick W, Heron SP, Ray P, et al. Levofloxacin versus ciprofloxacin in the treatment of chronic bacterial prostatitis: a randomized double-blind multicenter study. Urology 2003; 62:537.
  15. Schaeffer AJ. Clinical practice. Chronic prostatitis and the chronic pelvic pain syndrome. N Engl J Med 2006; 355:1690.
  16. Naber KG, Busch W, Focht J. Ciprofloxacin in the treatment of chronic bacterial prostatitis: a prospective, non-comparative multicentre clinical trial with long-term follow-up. The German Prostatitis Study Group. Int J Antimicrob Agents 2000; 14:143.
  17. Brehm TJ, Trautner BW, Kulkarni PA. Acute and Chronic Infectious Prostatitis in Older Adults. Infect Dis Clin North Am 2023; 37:175.
  18. Bruce AW, Reid G. Prostatitis associated with Chlamydia trachomatis in 6 patients. J Urol 1989; 142:1006.
  19. Poletti F, Medici MC, Alinovi A, et al. Isolation of Chlamydia trachomatis from the prostatic cells in patients affected by nonacute abacterial prostatitis. J Urol 1985; 134:691.
  20. Park H, Sim SM, Lee G. The presence of Chlamydia is associated with increased leukocyte counts and pain severity in men with chronic pelvic pain syndrome. Urology 2015; 85:574.
  21. de la Rosette JJ, Hubregtse MR, Meuleman EJ, et al. Diagnosis and treatment of 409 patients with prostatitis syndromes. Urology 1993; 41:301.
  22. Krieger JN, Lee SW, Jeon J, et al. Epidemiology of prostatitis. Int J Antimicrob Agents 2008; 31 Suppl 1:S85.
  23. Mo X, Zhu C, Gan J, et al. Prevalence and correlates of Mycoplasma genitalium infection among prostatitis patients in Shanghai, China. Sex Health 2016.
  24. Krieger JN, Riley DE. Chronic prostatitis: Charlottesville to Seattle. J Urol 2004; 172:2557.
  25. Meares EM Jr. Prostatitis: A review. Urol Clin North Am 1975; 2:3.
  26. Chuang AY, Tsou MH, Chang SJ, et al. Mycobacterium abscessus granulomatous prostatitis. Am J Surg Pathol 2012; 36:418.
  27. Orland SM, Hanno PM, Wein AJ. Prostatitis, prostatosis, and prostatodynia. Urology 1985; 25:439.
  28. Müller A, Mulhall JP. Sexual dysfunction in the patient with prostatitis. Curr Opin Urol 2005; 15:404.
  29. Krieger JN, Egan KJ, Ross SO, et al. Chronic pelvic pains represent the most prominent urogenital symptoms of "chronic prostatitis". Urology 1996; 48:715.
  30. Litwin MS, McNaughton-Collins M, Fowler FJ Jr, et al. The National Institutes of Health chronic prostatitis symptom index: development and validation of a new outcome measure. Chronic Prostatitis Collaborative Research Network. J Urol 1999; 162:369.
  31. Schaeffer AJ, Wu SC, Tennenberg AM, Kahn JB. Treatment of chronic bacterial prostatitis with levofloxacin and ciprofloxacin lowers serum prostate specific antigen. J Urol 2005; 174:161.
  32. Cai T, Tamanini I, Odorizzi K, et al. The diagnostic yield of the Meares & Stamey test can be significantly improved by symptom-based patient selection and the experience of the test performer. Prostate Cancer Prostatic Dis 2024; 27:300.
  33. Nickel JC, Shoskes D, Wang Y, et al. How does the pre-massage and post-massage 2-glass test compare to the Meares-Stamey 4-glass test in men with chronic prostatitis/chronic pelvic pain syndrome? J Urol 2006; 176:119.
  34. Miller JM, Binnicker MJ, Campbell S, et al. A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology. Clin Infect Dis 2018; 67:e1.
  35. Budía A, Luis Palmero J, Broseta E, et al. Value of semen culture in the diagnosis of chronic bacterial prostatitis: a simplified method. Scand J Urol Nephrol 2006; 40:326.
  36. Magri V, Wagenlehner FM, Montanari E, et al. Semen analysis in chronic bacterial prostatitis: diagnostic and therapeutic implications. Asian J Androl 2009; 11:461.
  37. Nickel JC, Downey J, Clark J, et al. Levofloxacin for chronic prostatitis/chronic pelvic pain syndrome in men: a randomized placebo-controlled multicenter trial. Urology 2003; 62:614.
  38. Alexander RB, Propert KJ, Schaeffer AJ, et al. Ciprofloxacin or tamsulosin in men with chronic prostatitis/chronic pelvic pain syndrome: a randomized, double-blind trial. Ann Intern Med 2004; 141:581.
  39. Perletti G, Marras E, Wagenlehner FM, Magri V. Antimicrobial therapy for chronic bacterial prostatitis. Cochrane Database Syst Rev 2013; :CD009071.
  40. Aagaard J, Madsen PO. Bacterial prostatitis: new methods of treatment. Urology 1991; 37:4.
  41. Kurzer E, Kaplan S. Cost effectiveness model comparing trimethoprim sulfamethoxazole and ciprofloxacin for the treatment of chronic bacterial prostatitis. Eur Urol 2002; 42:163.
  42. Shehab N, Patel PR, Srinivasan A, Budnitz DS. Emergency department visits for antibiotic-associated adverse events. Clin Infect Dis 2008; 47:735.
  43. Paglia M, Peterson J, Fisher AC, et al. Safety and efficacy of levofloxacin 750 mg for 2 weeks or 3 weeks compared with levofloxacin 500 mg for 4 weeks in treating chronic bacterial prostatitis. Curr Med Res Opin 2010; 26:1433.
  44. Giannarini G, Mogorovich A, Valent F, et al. Prulifloxacin versus levofloxacin in the treatment of chronic bacterial prostatitis: a prospective, randomized, double-blind trial. J Chemother 2007; 19:304.
  45. Naber KG, Roscher K, Botto H, Schaefer V. Oral levofloxacin 500 mg once daily in the treatment of chronic bacterial prostatitis. Int J Antimicrob Agents 2008; 32:145.
  46. Naber KG, European Lomefloxacin Prostatitis Study Group. Lomefloxacin versus ciprofloxacin in the treatment of chronic bacterial prostatitis. Int J Antimicrob Agents 2002; 20:18.
  47. Zhang ZC, Jin FS, Liu DM, et al. Safety and efficacy of levofloxacin versus ciprofloxacin for the treatment of chronic bacterial prostatitis in Chinese patients. Asian J Androl 2012; 14:870.
  48. van der Linden PD, Sturkenboom MC, Herings RM, et al. Fluoroquinolones and risk of Achilles tendon disorders: case-control study. BMJ 2002; 324:1306.
  49. Marino A, Stracquadanio S, Bellanca CM, et al. Oral Fosfomycin Formulation in Bacterial Prostatitis: New Role for an Old Molecule-Brief Literature Review and Clinical Considerations. Infect Dis Rep 2022; 14:621.
  50. Cunha BA, Gran A, Raza M. Persistent extended-spectrum β-lactamase-positive Escherichia coli chronic prostatitis successfully treated with a combination of fosfomycin and doxycycline. Int J Antimicrob Agents 2015; 45:427.
  51. Grayson ML, Macesic N, Trevillyan J, et al. Fosfomycin for Treatment of Prostatitis: New Tricks for Old Dogs. Clin Infect Dis 2015; 61:1141.
  52. Karaiskos I, Galani L, Sakka V, et al. Oral fosfomycin for the treatment of chronic bacterial prostatitis. J Antimicrob Chemother 2019; 74:1430.
  53. Los-Arcos I, Pigrau C, Rodríguez-Pardo D, et al. Long-Term Fosfomycin-Tromethamine Oral Therapy for Difficult-To-Treat Chronic Bacterial Prostatitis. Antimicrob Agents Chemother 2015; 60:1854.
  54. Charalabopoulos K, Karachalios G, Baltogiannis D, et al. Penetration of antimicrobial agents into the prostate. Chemotherapy 2003; 49:269.
  55. Martin DH, Mroczkowski TF, Dalu ZA, et al. A controlled trial of a single dose of azithromycin for the treatment of chlamydial urethritis and cervicitis. The Azithromycin for Chlamydial Infections Study Group. N Engl J Med 1992; 327:921.
  56. Chiarini F, Mansi A, Tomao P, et al. Chlamydia trachomatis genitourinary infections: laboratory diagnosis and therapeutic aspects. Evaluation of in vitro and in vivo effectiveness of azithromycin. J Chemother 1994; 6:238.
  57. Skerk V, Krhen I, Lisić M, et al. Comparative randomized pilot study of azithromycin and doxycycline efficacy in the treatment of prostate infection caused by Chlamydia trachomatis. Int J Antimicrob Agents 2004; 24:188.
  58. Skerk V, Schönwald S, Krhen I, et al. Comparative analysis of azithromycin and ciprofloxacin in the treatment of chronic prostatitis caused by Chlamydia trachomatis. Int J Antimicrob Agents 2003; 21:457.
  59. Centers for Disease Control and Prevention (CDC) 2021 Sexually Transmitted Infection Treatment Guidelines, section on Chlamydial Infections. Available at: https://www.cdc.gov/std/treatment-guidelines/chlamydia.htm (Accessed on January 09, 2025).
  60. Weidner W, Ludwig M, Brähler E, Schiefer HG. Outcome of antibiotic therapy with ciprofloxacin in chronic bacterial prostatitis. Drugs 1999; 58 Suppl 2:103.
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