Acute bacterial prostatitis

INTRODUCTION — 

The prostate is subject to various inflammatory disorders [1]. One of these syndromes is acute bacterial prostatitis, an acute infection of the prostate, usually caused by gram-negative organisms [2]. Acute bacterial prostatitis may be underdiagnosed in men presenting with acute urinary tract infection (UTI), particularly in men with febrile UTI [3]. Antimicrobial therapy remains the mainstay of treatment [4].

Acute bacterial prostatitis will be reviewed here. Chronic bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome are discussed in detail elsewhere. (See "Chronic bacterial prostatitis" and "Chronic prostatitis and chronic pelvic pain syndrome".)

Other causes of dysuria in men, including cystitis, acute complicated UTI, urethritis, and epididymitis, are also discussed elsewhere.

●(See "Acute simple cystitis in male adults".)

●(See "Acute complicated urinary tract infection (including pyelonephritis) in adults".)

●(See "Urethritis in adults and adolescents".)

●(See "Acute epididymitis in adolescents and adults".)

DEFINITIONS — 

In order to standardize definitions, improve diagnosis and treatment, and facilitate research, the United States National Institutes of Health (NIH) previously established an International Prostatitis Collaborative Network [5]. The 1999 classification scheme developed by this group remains the standard approach to prostatitis and defines the following syndromes (table 1):

●I. Acute bacterial prostatitis – Acute urogenital symptoms with evidence of bacterial infection of the prostate

●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

●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)

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

Evidence of inflammation or bacterial infection in the prostate 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.

However, acute bacterial prostatitis is often diagnosed without these formal urologic assessments, based on clinical presentation and physical examination in the context of known bacteriuria. (See 'Diagnostic evaluation' below.)

PATHOGENESIS — 

Entry of microorganisms into the prostate gland can occur through various routes:

●In most cases, bacteria migrate from the urethra or bladder through the prostatic ducts (contiguous spread), with intraprostatic reflux of urine (figure 1). As a result, there can be concomitant infection in the bladder or epididymis.

●Acute bacterial prostatitis can also occur from direct inoculation during transrectal prostate biopsy and transurethral manipulations (eg, catheterization and cystoscopy) [6,7]. (See "Prostate biopsy", section on 'Infection'.)

●Lymphatic and hematogenous spread are also potential, albeit less frequent, routes of bacterial invasion into the prostate [4].

EPIDEMIOLOGY

Prevalence — Overall, prostatitis syndromes are a very common presentation in the clinical setting and tend to occur in middle-aged and older men [8]. However, acute bacterial prostatitis likely accounts for only a minority of these cases.

An accurate estimate of the prevalence of acute bacterial prostatitis is not available, as the majority of studies were conducted prior to 2004 [8,9] and either summarized physician-diagnosed prostatitis (without a standardized definition) or relied on self-reported symptoms. Additionally, the clinical diagnosis of acute bacterial prostatitis is subject to many biases and might have varied over time.

Risk factors — Acute bacterial prostatitis can occur in the setting of cystitis, urethritis, or other urogenital tract infections. Thus, underlying conditions such as functional or anatomical anomalies (eg, urethral strictures, neurogenic bladder, obstruction from benign prostatic hypertrophy) that predispose to other urogenital infections can increase the risk of acute bacterial prostatitis.

Prostate infections following urogenital instrumentation, including chronic indwelling bladder catheterization, intermittent bladder catheterization, and prostate biopsy are well documented [10-12]. As an example, in a retrospective study of 1339 men who underwent transrectal ultrasound-guided prostate biopsy, 28 men (2.1 percent) developed acute bacterial prostatitis a mean of three days post-biopsy, despite receiving periprocedural fluoroquinolone prophylaxis [12]. Prostatitis following transrectal prostate biopsy infection or other prostate instrumentation is associated with a higher risk of drug-resistant bacteria compared with acute bacterial prostatitis that develops spontaneously [13-15]. Periprocedural antibiotic prophylaxis prior to prostate biopsy is generally recommended [16]. This is discussed in detail elsewhere. (See "Prostate biopsy", section on 'Prophylactic antibiotics'.)

MICROBIOLOGY — 

The pathogens associated with acute 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 bacteria are the most common, especially Enterobacterales (which include Escherichia coli, Proteus spp, and Klebsiella pneumoniae) and Pseudomonas species [6,14,17]. E. coli is the causative organism in over 50 percent of cases. Retrospective studies of men with acute bacterial prostatitis have repeatedly identified E. coli, Pseudomonas, and other Enterobacterales (Proteus, Klebsiella, Enterobacter, Citrobacter, and Serratia species) [6,7,14,15,17,18]. Pseudomonas seems to occur more commonly in men who have had instrumentation of the urinary tract, particularly transurethral urinary catheterization [14].

Instrumentation of the prostate, particularly prostate biopsy, has been associated with subsequent acute bacterial prostatitis due to organisms with broad resistance to antibiotics, including fluoroquinolone-resistant E. coli and Pseudomonas aeruginosa [11,14]. This is likely related to the use of periprocedural prophylactic fluoroquinolones.

●Less commonly, gram-positive cocci (including Staphylococcus aureus, streptococci, and enterococci) can cause acute bacterial prostatitis [14,15,19]. Acute staphylococcal prostatitis can result from hematogenous seeding due to bacteremia associated with a remote S. aureus infection. Thus, isolation of S. aureus from prostatic secretions or from the urine in a male who has not had any instrumentation of the urinary tract should prompt evaluation for a remote or endovascular staphylococcal infection.

●In certain populations, other organisms should be considered:

•Sexually active males can have sexually transmitted urogenital infections, such as urethritis and epididymitis, which also acutely involve the prostate. In such cases, Neisseria gonorrhoeae and Chlamydia trachomatis are important pathogens. Such infections tend to occur more often in younger males but can occur at any age. (See "Urethritis in adults and adolescents", section on 'Epidemiology and microbiology' and "Acute epididymitis in adolescents and adults", section on 'Etiology and risk factors'.)

•In patients or travelers from regions where Burkholderia pseudomallei is endemic (eg, southern and southeast Asia or northern Australia) this uncommon organism has also been described as a cause of acute prostatitis and prostatic abscess [20-22]. (See "Melioidosis: Epidemiology, clinical manifestations, and diagnosis".)

Other less-common causes of prostatitis include fungal organisms, such as Candida, Coccidioides, and Histoplasmosis [23], and mycobacteria (Mycobacterium tuberculosis, Mycobacterium abscessus, and Bacillus Calmette-Guérin) [24-27]. (See "Candida infections of the bladder and kidneys", section on 'Prostate abscess' and "Manifestations and treatment of nonmeningeal extrathoracic coccidioidomycosis", section on 'Prostatic infection' and "Infectious complications of intravesical BCG immunotherapy", section on 'Localized disease'.)

Recurrent infection after completion of therapy (usually within four weeks) is usually caused by the same organism that was found in the original infection [28].

CLINICAL MANIFESTATIONS

Presenting features — The clinical presentation of acute prostatitis is generally not subtle.

●Symptoms and signs – Patients are typically acutely ill, with fever, chills, malaise, and myalgias. They are often more ill than patients with acute simple cystitis, among whom fever and systemic signs of infection are absent. Dysuria, irritative urinary symptoms (frequency, urgency, urge incontinence), and pelvic or perineal pain are common symptoms. Patients may also complain of pain at the tip of the penis, perineum, scrotum, and inner part of the leg. Swelling of the acutely inflamed prostate can cause voiding symptoms, ranging from dribbling and hesitancy to acute urinary retention. On exam, the prostate is often firm, edematous, and tender.

As an example, in a retrospective study of 371 males who were diagnosed with acute bacterial prostatitis clinically, fever was present in 80 percent, urinary symptoms in 73 percent, and pelvic pain in 43 percent [15]. An abnormal digital rectal exam was noted in 83 percent. In another retrospective review of 614 cases of men who presented to an emergency department in Spain and were diagnosed with acute bacterial prostatitis, irritative symptoms were observed most commonly (93 percent), with obstructive symptoms (poor stream, hesitancy) reported in 25 percent; on digital rectal examination, the prostate was painful in 90 percent, and prostate size was judged as grade 1 or 2 (on a scale of 1 to 4, with 1 indicating no enlargement) in 75 percent [14]. In this series, only 34 percent of patients were febrile. Variability in presentation across studies may be related to care setting or differences in how acute bacterial prostatitis was diagnosed.

Patients who have impaired sensation (eg, neurogenic bladder) or impaired communication (eg, because of cognitive deficits) may have more subtle clinical presentations.

●Laboratory findings – Common laboratory findings include an elevated white blood cell count, pyuria, bacteriuria, and, occasionally, positive blood cultures. Inflammatory markers (erythrocyte sedimentation rate, C-reactive protein) are elevated in most cases. Inflammation of the prostate can also lead to an elevated serum prostate specific antigen (PSA) level [29]. (See "Measurement of prostate-specific antigen", section on 'Prostatic inflammation and infection'.)

Complications (including prostatic abscess) — Complications of acute bacterial prostatitis include bacteremia, epididymitis, chronic bacterial prostatitis, prostatic abscesses, and metastatic infection (eg, spinal or sacroiliac infection) [30]. Patients with underlying valvular heart disease or a valvular prosthesis are at risk for endocarditis when prostatitis is caused by certain bacterial pathogens, particularly gram-positive bacteria. These complications are more likely to occur if diagnosis and antimicrobial therapy are delayed.

Signs and symptoms of a prostatic abscess are similar to those of bacterial prostatitis in general but may persist despite appropriate antibiotic therapy; in addition, fluctuance of the prostate on gentle digital exam can suggest an underlying abscess. Risk factors for prostatic abscess are similar to those for acute bacterial prostatitis, including severe benign prostatic hypertrophy, neurogenic bladder, indwelling urinary catheter, and prostate biopsy [31]. Although diabetes mellitus, cirrhosis, and immunocompromising conditions are often reported risk factors for prostatic abscess in older literature [32,33], subsequent analyses have not clearly identified these as risk factors. As an example, in a retrospective study of 142 Korean patients with acute bacterial prostatitis, only voiding difficulties and symptom duration were independent risk factors for abscess development; diabetes mellitus was no associated with prostatic abscess in multivariate analysis [34].

DIAGNOSTIC EVALUATION

Clinical suspicion — The typical symptoms of acute bacterial prostatitis (systemic and urinary symptoms) overlap with those of complicated urinary tract infection, in general. Thus, the possibility of acute bacterial prostatitis should be considered in any male patient with acute complicated urinary tract infection (UTI), particularly if they have pelvic or perineal pain or if they present with fever or sepsis but have no other evidence of pyelonephritis or other infectious urinary source (eg, epididymitis). The threshold for suspicion for prostatitis should be lower in patients with risk factors, particularly those with a urinary catheter or with recent prostate instrumentation.

In patients who present with constitutional symptoms or leukocytosis only, the presence of pyuria, bacteriuria, or an elevated serum prostate specific antigen (PSA) level should also raise suspicion and prompt evaluation for acute bacterial prostatitis. However, elevated PSA is nonspecific and should not independently be used to establish the diagnosis of acute bacterial prostatitis [35].

Establishing the diagnosis by examination — Clinical suspicion for acute prostatitis should prompt evaluation of the prostate by digital rectal examination, which is key to making the diagnosis. An edematous and tender prostate on physical exam in patients with compatible symptoms establishes the diagnosis of acute prostatitis. The microbial etiology of acute bacterial prostatitis can be confirmed when a bacterial pathogen is identified, typically on urine culture, but also by testing for STI. (See 'Identifying the microbial etiology' below.)

Digital rectal examination should be performed gently. Although rectal examination in itself can be uncomfortable for the patient, the practitioner should specifically assess for tenderness of the prostate gland. However, vigorous prostate massage should be avoided since it is uncomfortable, allows no additional diagnostic or therapeutic benefit, and presumably increases the risk for bacteremia.

Identifying the microbial etiology — In order to establish the microbial etiology, urine testing is essential. Blood cultures are useful for febrile or septic patients or for those who have growth of S. aureus from urine cultures.

●Urine testing – A urine culture should be obtained in all patients with suspected acute bacterial prostatitis; a mid-stream urine specimen is generally sufficient. The urine culture should be obtained before starting antibiotics, if possible, as recovery of an organism is very helpful to guide treatment (see 'Antimicrobial therapy' below). Urine culture typically reveals a causative organism in acute bacterial prostatitis, unless antibiotics were recently used, the organisms is fastidious, or the colony counts are below the laboratory’s reporting threshold [15].

Urinalysis is also typically performed. Pyuria and a positive nitrite suggest inflammation and bacteriuria and support the diagnosis of acute bacterial prostatitis. However, urine testing that is negative for either pyuria or nitrites does not seem to have sufficient negative predictive value to exclude the possibility of acute bacterial prostatitis in the right clinical context [36,37].

In patients who may have a sexually transmitted infection (eg, recent exposure, new or multiple sexual partners, urethral discharge, testicular pain), we also submit urine for nucleic acid amplification testing (NAAT) for C. trachomatis and N. gonorrhoeae. Testing all sexually active men for these infections is also a reasonable management approach.

●Blood cultures – We collect blood cultures in patients with suspected acute bacterial prostatitis who are febrile or have sepsis. In emergency departments, blood cultures are often drawn as part of initial laboratory workup for sepsis in febrile patients, whereas urine cultures are sometimes not collected until much later, particularly in patients who are dehydrated or experiencing urinary obstruction. Thus, the urine specimen is sometimes obtained after initial empiric antibiotic treatment, which may result in no growth of an organism. In such cases, the blood culture might provide the microbiological identity of the uropathogen. In a retrospective review of 261 men with acute bacterial prostatitis in whom blood cultures were collected, 55 (21 percent) had a positive blood culture [18].

When S. aureus grows from a urine culture in a patient without recent instrumentation or catheterization of the urinary tract, it is important to perform blood cultures to evaluate whether the bacteriuria reflects seeding of the prostate or urine from bacteremia. This is particularly important in patients with underlying conditions that may predispose them to complications of bacteremia (eg, endocarditis in patients with valvular disease or prostheses). (See "Clinical manifestations of Staphylococcus aureus infection in adults".)

Limited role for imaging — Imaging is not necessary to establish the diagnosis of acute bacterial prostatitis. The primary role of imaging is to identify complications, such as prostatic abscesses, which are generally not suspected unless patients have not responded appropriately to therapy. (See 'Evaluation of suboptimal response' below.)

However, imaging (in particular abdominal and pelvic computed tomography [CT]) is often performed during the initial evaluation of patients with sepsis in the emergency department, so prostatic abscesses are often identified at that point. (See 'Urologic intervention for complications' below.)

Evaluation for anatomical abnormalities — Following the acute episode, underlying anatomical abnormalities that may have predisposed to an acute prostatic infection (eg, urinary retention due to prostatic enlargement) should be identified and, if possible, addressed to decrease the risk of recurrence. Consultation with a urologist for this evaluation is useful.

DIFFERENTIAL DIAGNOSIS — 

The main differential diagnoses of acute bacterial prostatitis are other infections of the urogenital tract.

Among those who present with sepsis and/or fever of a presumed urinary source, infection of the upper urinary tract (pyelonephritis) is the main alternative diagnosis, but patients with acute pyelonephritis more commonly present with flank pain, costovertebral angle tenderness, and/or nausea/vomiting; lower urinary symptoms may be less prominent. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults", section on 'Clinical manifestations'.)

Otherwise, the most common alternative diagnosis to consider in a man without fever or sepsis who presents with dysuria, frequency, and/or urgency, and who has pyuria and bacteriuria, is an isolated lower urinary tract infection (UTI), or cystitis. Cystitis in males generally occurs in the presence of a predisposing functional or anatomic abnormality, such as prostatic hypertrophy or genitourinary instrumentation, which increases the risk of infection, although it can also uncommonly occur in otherwise healthy men. While isolated cystitis likely involves some amount of bacterial contamination along the prostatic ducts, this prostatic contamination may remain superficial without overt prostatic inflammation. In such cases, fever, chills, and constitutional symptoms are generally absent, and there is no prostatic tenderness on digital rectal exam. Men who lack such evidence of clinically significant prostatic involvement can be managed as having acute cystitis but should be monitored for lack of clinical response, which would warrant reevaluation for the possibility of underlying prostatitis. (See "Acute simple cystitis in male adults", section on 'Treatment'.)

Other urogenital infections (eg, urethritis, epididymitis) can also present with dysuria and coexist with prostatitis. Tenderness of the prostate on exam is generally not found with such infections in the absence of coexisting prostatitis. (See "Urethritis in adults and adolescents", section on 'Diagnosis' and "Acute epididymitis in adolescents and adults", section on 'Diagnostic approach'.)

Patients with certain urologic conditions, such as benign prostatic hyperplasia and overactive bladder, may also initially present with lower urinary tract symptoms but typically do not have fever, pyuria, and other signs or symptoms of infection. These conditions are discussed in detail elsewhere. (See "Clinical manifestations and diagnostic evaluation of benign prostatic hyperplasia" and "Lower urinary tract symptoms in males".)

MANAGEMENT — 

Treatment of acute prostatitis includes antimicrobial therapy and supportive measures to reduce symptoms. Rarely, more invasive intervention is indicated to manage complications.

Indications for hospitalization — Many, but not all, patients with acute bacterial prostatitis warrant hospitalization.

Potential reasons for hospitalization include severe illness or anticipated need for parenteral antibiotics, specifically:

●Sepsis or septic shock

●Inability to tolerate oral medications

●Unreliable intestinal absorption of oral medications

●History of a recent urinary tract infection with a pathogen for which oral antibiotics are not an option

Many patients with acute bacterial prostatitis have sepsis at presentation. However, those who have no major comorbidities and no signs or symptoms of sepsis, who can reliably take and tolerate oral antibiotics, and who are not expected to have an infection resistant to oral antibiotics can likely be managed appropriately in the outpatient setting. Nevertheless, for patients who would not otherwise be able to promptly return to medical care in the case of decompensation, a short hospital stay for monitoring purposes may be prudent.

As discussed elsewhere, acute urinary retention warrants prompt urological consultation; if managed successfully with bladder catheterization in the urgent or emergency setting, urinary retention does not necessarily warrant hospitalization in the absence of other indications. (See 'Urologic intervention for complications' below.)

Antimicrobial therapy

Empiric regimen selection — Acute bacterial prostatitis should be treated empirically pending culture results. Empiric antibiotic therapy should primarily target gram-negative organisms as the most likely infecting pathogens unless a prior urine culture suggests an alternate bacterial cause (see 'Microbiology' above). With urinary tract infection (UTI) in general, prior urine culture and susceptibility results are helpful to guide empiric therapy [38,39]; this principle likely applies to prostatitis as well.

A variety of antimicrobials can be used to treat acute bacterial prostatitis. Treatment data are limited, without comparative trials evaluating the optimal antimicrobial choice. Thus, antibiotic selection is informed by observational data and pharmacokinetic data on drug levels in the prostate. Although not all antibiotics equally penetrate into prostatic tissue, the presence of acute inflammation generally allows entry of drugs that would not otherwise achieve therapeutic levels.

Hospitalized patients — For patients who are hospitalized (see 'Indications for hospitalization' above), empiric antimicrobial selection depends on the severity of illness and the risk for resistant infection. Such risks include a resistant pathogen on prior urine cultures (eg, within the past two years), recent antibiotic exposure (eg, within the past three months), and recent history of prostate instrumentation (eg, biopsy).

●For patients who are not critically ill:

•If they have no risk factors for resistance, we generally suggest an empiric intravenous (IV) or oral fluoroquinolone (ciprofloxacin 400 mg IV twice daily or 500 to 750 mg orally every 12 hours; or levofloxacin 500 to 750 IV or orally once daily). A third-generation cephalosporin (eg, ceftriaxone 2 g IV daily) is another option and is preferred if local fluoroquinolone-resistant rates in gram-negative organisms are high, although prostate penetration by fluoroquinolones is better established than for cephalosporins.

•If they have risk factors for resistance, we typically choose between piperacillin-tazobactam 3.375 g IV every 6 hours and cefepime 2 g IV every 12 hours. A carbapenem (eg, ertapenem 1 g IV daily, meropenem 1 g IV every 8 hours) is another option, although we generally reserve this for patients who have a history of infection with an isolate resistant to the other options (eg, an extended-spectrum beta-lactamase [ESBL]-producing isolate) or who are severely ill and reside in a community with a high prevalence of ESBL-producing organisms. Rarely, patients have a history of extensively drug-resistant urinary tract infections and may warrant empiric therapy with an advanced beta-lactam antibiotic (eg, ceftazidime-avibactam, ceftolozane-tazobactam, cefiderocol); such patients should be managed in collaboration with an infectious diseases expert. (See "Carbapenem-resistant E. coli, K. pneumoniae, and other Enterobacterales (CRE)", section on 'Indications for empiric coverage of CRE'.)

For patients who are not critically ill, we typically do not include broad-spectrum gram-positive coverage (eg, vancomycin or linezolid) as part of empiric therapy since gram-positive acute bacterial prostatitis is much less common than gram-negative infection. However, such therapy should be added if early results from blood or urine culture suggest gram-positive growth.

●For patients who are critically ill (eg, with septic shock), empiric therapy generally includes broad-spectrum coverage for gram-negative and gram-positive organisms (see "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Choosing a regimen'). We typically choose a gram-negative agent used for patients with risk factors for resistance, as outlined above. Options for gram-positive coverage include vancomycin and linezolid, although published trials of these agents for acute bacterial prostatitis are lacking; case reports have described use of these agents for prostatic abscesses caused by methicillin-resistant S. aureus [40,41].

Comparative data are limited, but observational studies have mainly described successful initial inpatient treatment with fluoroquinolones or cephalosporins (either with or without an aminoglycoside) [42,43]. Inappropriate empiric therapy (ie, that is not active against the isolate that ultimately grew out) has been associated with an increased risk of relapse, but a particular drug class has not been implicated [42].

Outpatients — For empiric treatment of most outpatients, we suggest a fluoroquinolone or trimethoprim-sulfamethoxazole, depending upon local bacterial-resistance patterns. Doses and the choice between them are discussed elsewhere. (See 'Directed therapy' below.)

We typically choose one of these antimicrobial agents because they achieve high levels in prostatic tissue. Although this may not be an issue in the acute setting, where prostatic inflammation allows penetration of a broader range of antibiotics, the ability of an antibiotic to penetrate prostate tissue is thought to be important during prolonged therapy, while inflammation is resolving [44]. Additionally, use of other agents for directed therapy of acute bacterial prostatitis has been associated with a higher risk of relapse [42], as discussed elsewhere. (See 'Directed therapy' below.)

However, resistance to both fluoroquinolones and trimethoprim-sulfamethoxazole in urinary isolates is widespread (see "Acute simple cystitis in female adults", section on 'Resistance trends in E. coli'). If the patient has had a urinary isolate resistant to both fluoroquinolones and trimethoprim-sulfamethoxazole within the past two years, we choose a regimen based on the susceptibility profile of that organism. (See 'Directed therapy' below.)

If a sexually transmitted infection is suspected based on sexual history or presence of urethral discharge, the empiric regimen should also cover N. gonorrhoeae and C. trachomatis (table 2), while awaiting results of testing for these particular organisms [44]. Doxycycline and macrolides, which are used to treat C. trachomatis, penetrate the prostate well [45]. (See "Treatment of uncomplicated gonorrhea (Neisseria gonorrhoeae infection) in adults and adolescents", section on 'Preferred regimen' and "Treatment of Chlamydia trachomatis infection in adults and adolescents", section on 'Doxycycline as preferred agent'.)

Directed therapy — Once culture and susceptibility data are available, the empiric regimen should be tailored to those results.

●Tailoring parenteral therapy – For hospitalized patients, the empirically chosen IV regimen can be narrowed to target the recovered isolate. If a patient was initiated on a carbapenem and had an isolate that was susceptible to other agents, the regimen should be switched (eg, to a more narrow-spectrum beta-lactam or a fluoroquinolone).

●Switching to an oral regimen – Patients who initiated parenteral therapy can switch to an oral regimen if the patient is clinically improving, source control has been achieved (if applicable), the target isolate is susceptible to an oral regimen that achieves adequate levels in the prostate, as discussed below, there are no concerns about oral absorption of antimicrobial therapy, and there are no logistical reasons that preclude oral antimicrobials [46].

If no oral options are appropriate, then a parenteral regimen should be used for the duration of treatment. (See 'Duration of therapy' below.)

●Choosing an oral regimen – If the isolate is susceptible, we use a fluoroquinolone (ciprofloxacin 500 to 750 mg orally every 12 hours or levofloxacin 500 to 750 mg orally once daily) or trimethoprim-sulfamethoxazole (one double-strength tab orally every 12 hours) to complete the course for acute bacterial prostatitis. The choice between these should take into account anticipated potential adverse effects and other patient-specific considerations (such as impaired renal function, which makes trimethoprim-sulfamethoxazole less attractive, or risk for prolonged QTc, which makes fluoroquinolones less attractive), in addition to susceptibility testing results. If ciprofloxacin or levofloxacin is chosen for the duration of therapy, we usually use a 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 [47]. 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.

If the isolate is resistant to both fluoroquinolones and trimethoprim-sulfamethoxazole (or the patient cannot use them because of allergies), options are limited. For Enterobacterales, we suggest checking susceptibility to fosfomycin and using that agent if the isolate is susceptible. Fosfomycin achieves therapeutic levels in the prostate [48] and is often active against isolates that are resistant to other agents. However, data on its use for acute prostatitis are scant and optimal dosing is uncertain, with regimens of 3 g every 24, 48, or 72 hours reported [49,50].

Otherwise, 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, amoxicillin 1 g three times daily, 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 [42]. Step-down therapy with oral beta-lactams following initial parenteral therapy has been associated with a higher rate of relapse compared with step-down oral fluoroquinolones in some [42] but not all [43] observational studies. The prostate penetration of beta-lactams (including cephalosporins) varies [51], and it is uncertain whether higher doses can overcome these challenges. In some studies of patients with gram-negative bacteremia from a urinary source, step-down therapy with higher-than-typical doses of oral beta-lactams has been associated with comparable rates of clinical success as fluroquinolones and trimethoprim-sulfamethoxazole [52-54]; however outcomes related to prostatitis, specifically, are unknown. Ultimately, for acute bacterial prostatitis caused by a pathogen susceptible only to beta-lactams, the risks of using an intravenous antibiotic for several weeks may still outweigh the potentially increased risk of relapse with an oral agent at a higher dose, depending on the severity of the initial infection and other specific patient circumstances.

Nitrofurantoin should not be used as it does not achieve adequate levels in the prostate [55].

Duration of therapy — The optimal duration of antimicrobial therapy for acute bacterial prostatitis is uncertain. Consistent with other expert opinion, we suggest at least a two-week course of therapy and extend it to four weeks if symptoms have not fully resolved by then [19,56,57]. Symptoms that might suggest a need to continue antibiotics for four weeks include lower urinary tract irritative symptoms that have not returned to baseline.

Prospective randomized controlled trials evaluating the duration of therapy for acute bacterial prostatitis are lacking. In a trial evaluating the duration for febrile UTI in males, 78 percent of the 125 participants who received 14 days of a fluoroquinolone had treatment success, defined as clinical and microbiological response with no need for retreatment within six weeks; all participants had clinical response [58]. Although patients with acute bacterial prostatitis would have met the inclusion criteria for the trial, the number of patients with prostatitis in the trial is unknown.

In the absence of higher-quality data, some experts may suggest a minimum of four weeks duration. Older literature recommended a four- to six-week duration of therapy for acute bacterial prostatitis [59], citing concerns for poor antimicrobial penetration into the prostate, particularly with agents other than fluoroquinolones, and development of protected microcolonies deep within the gland. The main concern was that shorter durations would increase the risk of progression to chronic prostatitis and recurrent UTIs. In an observational study among 437 men with acute bacterial prostatitis in Korea, progression to chronic infectious or inflammatory prostatitis at three months occurred in 12 percent and was associated with a shorter mean duration of antibiotic therapy (28 versus 37 days) [43]. Although this study has been widely cited to support a treatment duration longer than four weeks, the retrospective design with no adjustment for relevant variables such as urinary retention substantially reduce confidence in these findings. Thus, this study does not provide adequate evidence that longer antibiotic treatment reduces the risk of subsequent chronic bacterial prostatitis. (See 'Prognosis' below.)

Urologic intervention for complications — Patients with acute prostatitis may present with or develop urinary retention. Urgent consultation with a urologist is advised to restore urinary drainage. Passage of a catheter through the inflamed urethra into the bladder in a patient with acute prostatitis risks the possibility of precipitating septic shock. Nevertheless, some experienced urologists do cautiously attempt urethral catheterization; the alternative is to place a suprapubic catheter. (See "Acute urinary retention", section on 'Urethral catheterization in most patients'.)

Urologic consultation is also warranted for prostatic abscess or other indication for surgical intervention. Abscesses greater than 2 cm generally warrant drainage [34]. Other indications for surgical intervention would be persistent prostatitis symptoms and persistence of the abscess on imaging. These recommendations are based on retrospective data [34].

FOLLOW-UP

Monitoring during therapy — In most cases, fever abates within two to six days after the start of therapy [60-62]. Patients should be followed for resolution of symptoms attributable to prostatitis.

No laboratory test offers validated proof of cure. In particular, we recommend not performing a test of cure with repeated urine cultures for individuals who are improving; this is generally not recommended for urinary tract infections in general, as asymptomatic bacteriuria does not merit antibiotic treatment or change in management [19,35].

Although treatment of acute bacterial prostatitis has been associated with a normalization of prostate-specific antigen (PSA) in patients who had an elevated level on presentation [63,64], there is no clearly established role for following PSA to evaluate for response to treatment of acute bacterial prostatitis. If PSA testing is being performed for prostate cancer screening, it should be deferred until the infection has completely resolved. (See "Screening for prostate cancer", section on 'Approach to screening'.)

Evaluation of suboptimal response — For patients without expected response to antibiotic therapy (eg, with persistently high or increasing fever after 48 hours of appropriate antibiotics), further evaluation is warranted to identify potential complications that may need additional intervention.

In such cases, we obtain blood cultures to evaluate for bacteremia, which in turn would prompt evaluation for an undrained source of infection, such as a prostatic abscess.

Imaging is the best diagnostic modality for prostatic abscess, including transrectal ultrasound, CT, and magnetic resonance imaging (MRI) [31,65]. On transrectal ultrasound, abscesses appear as hypoechoic or anechoic areas with thick walls or peripheral edema [33,66]. CT findings include nonenhancing fluid-density collections that can be multiseptated or rim-enhancing lesions. MRI may be helpful in early stages of abscess formation, particularly when transrectal ultrasound is inconclusive.

For patients with suspected sexually transmitted infectious prostatitis, persistent symptoms could reflect reinfection and suggest a need to test and treat the patient’s sexual partner(s).

Recurrent bacterial urinary tract infections (UTIs) with the same organism should prompt evaluation for chronic bacterial prostatitis. (See "Chronic bacterial prostatitis".)

PROGNOSIS — 

Most males recover from acute bacterial prostatitis without any lasting sequelae. Progression from acute to chronic bacterial prostatitis or inflammatory chronic pelvic pain syndrome (CPPS) is poorly understood. In a prospective cohort of 437 Korean men who presented with a confirmed diagnosis of acute bacterial prostatitis, 82 percent recovered without subsequent development of chronic infection three months or longer after treatment [43]. Development of chronic bacterial prostatitis or inflammatory CPPS was observed in 1.3 and 10.5 percent, respectively.

PREVENTION — 

Apart from minimizing unnecessary urogenital instrumentation, antibiotic prophylaxis prior to selected procedures involving the prostate (eg, transrectal prostate biopsy) is the main preventive strategy. This is discussed in detail elsewhere. (See "Prostate biopsy", section on 'Prophylactic antibiotics' and "Surgical treatment of benign prostatic hyperplasia (BPH)", section on 'Antibiotic prophylaxis'.)

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 5^th to 6^th 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 10^th to 12^th 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 – Acute bacterial prostatitis is an acute infection of the prostate. It can occur in the setting of urinary tract infection; functional or anatomic lower urinary tract obstruction, bladder catheterization, and prostate biopsy are risk factors. It is generally caused by typical uropathogens, most commonly the gram-negative Enterobacterales (typically Escherichia coli or Proteus species). Pseudomonas aeruginosa is associated with urinary tract instrumentation. Sexually transmitted pathogens, such as Neisseria gonorrhoeae and Chlamydia trachomatis, are also possible etiologies in sexually active men, who may have concomitant urethritis or epididymitis. (See 'Epidemiology' above and 'Microbiology' above.)

●Clinical manifestations – Patients with acute bacterial prostatitis are typically acutely ill, and many have sepsis at presentation. The most common symptoms and signs include fevers, chills, dysuria, and pelvic or perineal pain. Obstructive symptoms, such as dribbling of urine, can also occur. On exam, the prostate is often firm, edematous, and exquisitely tender. Common laboratory findings include an elevated white blood cell count, pyuria, and bacteriuria. (See 'Clinical manifestations' above.)

Secondary complications include bacteremia, prostatic abscess, and metastatic infection (eg, spinal or sacroiliac infection). Failure of symptom resolution on appropriate antibiotics could indicate prostatic abscess. (See 'Complications (including prostatic abscess)' above.)

●Diagnosis – In males with typical symptoms or with suspicion for acute complicated urinary tract infection (UTI), an edematous and tender prostate on physical exam usually establishes the diagnosis. Prostate tenderness is generally not found in isolated UTIs or other acute causes of dysuria (eg, urethritis, epididymitis) in the absence of coexisting prostatitis. Digital rectal examination should be performed gently; vigorous prostate massage should be avoided. A urine culture should be obtained to identify the bacterial etiology; we also obtain blood cultures in those who are systemically ill or in those who are unable to void urine. (See 'Diagnostic evaluation' above and 'Differential diagnosis' above.)

●Limited role for imaging – Imaging studies are generally not needed in acute bacterial prostatitis. Their main role is to evaluate for prostatic abscess in patients with persistent symptoms despite appropriate antimicrobial therapy. (See 'Limited role for imaging' above.)

●Indications for hospitalization – Severe illness (including sepsis) or anticipated need for parenteral antibiotics generally warrant hospitalization. Patients without sepsis who can reliably take and tolerate oral antibiotics and are not expected to have an infection resistant to oral antibiotics (eg, based on prior urine cultures) can generally be managed appropriately in the outpatient setting. (See 'Indications for hospitalization' above.)

●Empiric antibiotic therapy – Empiric antibiotic therapy should primarily target gram-negative organisms, as the most likely infecting pathogens.

•Hospitalized patients – Regimen selection depends on the severity of illness and the risk for resistant infection. Such risks include a resistant pathogen on prior urine cultures, recent antibiotic exposure, and recent prostate instrumentation. For patients who are not critically ill and have no risk factors for resistance, we suggest an intravenous or oral fluoroquinolone (ciprofloxacin or levofloxacin) (Grade 2C). Ceftriaxone or another third-generation cephalosporin is an alternative. For those who have risk factors for resistance or for those who are critically ill, we suggest piperacillin-tazobactam or cefepime (Grade 2C). A carbapenem (eg, meropenem) is an alternative when the risk of an extended-spectrum beta-lactamase-producing organism is high (eg, because of prior cultures or community prevalence). Critically ill patients also generally warrant empiric broad-spectrum gram-positive coverage. (See 'Hospitalized patients' above.)

•Outpatients – For empiric treatment of outpatients, we suggest an oral fluoroquinolone (ciprofloxacin or levofloxacin) or trimethoprim-sulfamethoxazole (Grade 2C). These agents achieve high levels in uninflamed prostatic tissue, which may be important after the initial days of therapy, while inflammation is resolving. (See 'Outpatients' above.)

●Directed antibiotic therapy and duration – Once culture and susceptibility tests return, the antibiotic regimen should be narrowed to target the isolate. A parenteral regimen can be transitioned to an oral one once the patient is clinically improving and source control has been achieved, if applicable. If the isolate is susceptible to fluoroquinolones or trimethoprim-sulfamethoxazole, we suggest one of those agents (Grade 2C). Fosfomycin is a potential option for resistant isolates. We reserve high-dose oral beta-lactams for patients who have no other options. (See 'Directed therapy' above.)

We treat for at least two weeks of antibiotic therapy. If lower urinary tract symptoms persist at two weeks, we extend the duration to four weeks. (See 'Duration of therapy' above.)

●Adjunctive measures – Adjunctive therapies include management of complications, such as acute urinary retention and prostatic abscesses. Passage of a catheter through the inflamed prostate into the bladder is potentially dangerous; urologic consultation is warranted to resolve acute urinary retention. (See 'Urologic intervention for complications' above.)

ACKNOWLEDGMENT — 

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