I. What every physician needs to know.

Prostatitis refers to lower urinary tract symptoms caused by infection, inflammation, or irritation of the prostate gland. Prostatitis is a common presentation and occurs in men less than 50 years old. Most prostate disorders are managed in the ambulatory care setting. As few as 1% of cases of prostatitis are acute, and only a minority of these will be sufficiently ill to warrant hospital admission. The microbiology of prostate infection mirrors that of urinary tract infection, with a majority of cases caused by gram negative organisms. Complications of acute prostatitis include local abscess formation, bacteremia, and sexual dysfunction of nearby organs.

Recommendations for the duration of antibiotic therapy in acute prostatitis vary with the severity of presentation, causative organism(s), underlying host immune state, and presence of complications. In general, a 4-week course of therapy for acute infection is recommended.

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II. Diagnostic Confirmation: Are you sure your patient has Prostatitis?

Prostatitis is classified by the NIH in 1999 into four categories based on the presence or absence of white blood cell (WBC) and bacteria on midstream urine and urine obtained after prostate massage. The 2-or 4-glass tests have been used in the evaluation of chronic prostatitis to stratify patients. The 4-glass test compares WBC and bacterial counts in urethral, midstream, expressed prostatic secretions, and post-prostatic massage urine. It has been largely supplanted by the less cumbersome 2-glass test, in which urine is obtained before and after prostatic massage. The four categories are:

  • Acute bacterial prostatitis (ABP) – WBC in pre and post massage specimens, both cultures positive

  • Chronic bacterial prostatitis (CBP) – similar to ABP with lower WBC and bacterial colony counts

  • Chronic bacterial prostatitis/chronic pelvic pain syndrome (CP/CPPS)

    Inflammatory – WBC present, culture sterile in prostatic specimen

    Noninflammatory – absent WBC and sterile culture in both specimens

  • Asymptomatic inflammatory prostatitis (AIP) – small WBC count in midstream urine only

Approximately 10% of prostatitis cases are chronic, 80-90% CP/CPPS, and 10% AIP. This classification schema was developed to provide a common platform for investigation of these distinct clinical entities.

Working hospitalists will be caring primarily for patients with acute prostatitis but may see other prostate syndromes as a secondary diagnosis. This review will focus on management of acute bacterial prostatitis.

A. History Part I: Pattern Recognition:

Acute bacterial prostatitis can occur in the setting of urethritis, cystitis or other infections of the genital tract. Abnormalities in anatomy that can predispose to urogenital infection can increase the risk for prostatitis. The classic patient with ABP presents with the abrupt onset of lower urinary tract symptoms including dysuria and frequency. Systemic symptoms are typically present and often overshadow urinary complaints. Abdominal pain is often poorly localized. Obstructive symptoms may be present due to prostate edema.

A history of recent genitourinary instrumentation should always be obtained as post-procedural infections have been associated with resistant microorganisms such as Pseudomonas aeruginosa and extended spectrum beta-lactamase (ESBL)-producing E. coli. Human immunodeficiency virus (HIV) infected patients may be predisposed to infection with unusual microorganisms such as Salmonella typhi, and more susceptible to abscess formation and infection relapse. Other risk factors informally associated with acute prostatitis include sexual abstinence, perineal trauma, and dehydration, however, these factors have not been formally studied.

B. History Part 2: Prevalence:

It is estimated that two million visits annually occur for prostatitis. Acute bacterial prostatitis comprises about 4% of prostatitis diagnoses.

C. History Part 3: Competing diagnoses that can mimic Prostatitis.

The differential diagnosis of acute prostatitis includes cystitis and pyelonephritis. Benign prostatic hypertrophy and overactive bladder may also present with lower urinary tract symptoms, but are generally without signs of infection like fever or pyuria.

D. Physical Examination Findings.

Physical examination may demonstrate fever and, in severe cases, evidence of systemic inflammatory response syndrome (SIRS). The abdomen is usually unrevealing. Lower abdominal tenderness or suprapubic pain may be present if there is concomitant bladder infection or obstruction. Costovertebral tenderness should be sought. Genital examination should be performed to exclude epididymitis or orchitis complicating prostate infection.

Rectal examination in acute prostatitis discloses an exquisitely tender prostate. Localized fluctuance suggests a prostatic abscess. Avoid excessive palpation of the gland, which may provoke bacteremia. These findings are distinct from the minimal findings such as a ‘boggy’ prostate present in patients with CBP or CPPS.

E. What diagnostic tests should be performed?

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Patients should have urinalysis and culture performed. Prostatic massage is not indicated in acute prostatitis as this may provoke bacteremia.

Routine testing, including WBC with differential, and renal function tests, should be performed. Blood cultures should be obtained on systemically ill patients. Screening for sexually transmitted diseases such as Neisseria gonorrhea and Chlamydia trachomatis should be performed on at-risk patients. In the past the gonococcus was a common cause of prostatic abscess, but has been supplanted by common uropathogens. Gram stain of the urine may be helpful in guiding initial coverage for either gram negative or positive organisms.

Appropriate antibacterial therapy should be administered after specimens have been obtained.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Abdominal computed tomography (CT) scan is indicated if there is concern for a gastrointestinal disorder presenting with lower urinary tract symptoms and sterile pyuria, e.g., diverticulitis adjacent to the bladder. A pelvic CT scan or prostate ultrasound to look for prostate abscess is also indicated if there is concern for failure of treatment despite urine culture tailored management.

F. Over-utilized or “wasted”adiagnostic tests associated with this diagnosis.

Elevation of prostate-specific antigen (PSA) has been noted in acute prostatitis but has no role at this time as a diagnostic test. Elective PSA screening for prostate cancer should be deferred one month following treatment of prostatitis. An elevated PSA obtained in the setting of acute prostatitis should not be reflexively attributed to prostatitis and requires ambulatory follow-up after acute hospitalization.

III. Default Management.

Initial management of acute prostatitis includes:

  • Initiation of antibiotic therapy.

  • Intravenous hydration as guided by hemodynamics, volume status, and ability of the patient to eat and drink.

  • Addressing urinary outflow obstruction if present.

A. Immediate management.


The most common pathogens associated with ABP are reflective of those that cause infections in the genitourinary system.

The reported pathogens in prostatitis are:

  • E. coli 50-80%

  • Proteus ~5%

  • Other Enterobacteriaecea (e.g., Klebsiella, Enterobacter, Serratia) ~3-11%

Pseudomonas spp ~5%

  • Staphylococcus aureus and epidermidis, streptococcus, enterococcus- uncommon

Although Staphylococcus aureus may be a primary uropathogen, its isolation should always prompt careful consideration of whether the urine has been seeded from a bacteremic staphlococcal infection of extraurinary origin (e.g., endovascular infection or osteomyelitis). Blood cultures should be obtained and careful examination for new murmurs and embolic stigmata performed. Echocardiography or additional body imaging may be indicated guided by examination and clinical evolution.

Unusual isolates from cases of acute prostatitis have been reported in HIV infected patients, such as Hemophilus parainfluenzae, Salmonella typhi, and Neisseria gonorrhoeae. HIV patients may be more prone to abscess formation complicating acute infection.

Uncommon pathogens that may present in more indolent fashion in patients with or without underlying immune defects include fungal causes including candida, cryptococcus, blastomycosis, and coccidioidomycosis. Mycobacterium tuberculosis is a well-described prostatic pathogen; Mycobacterium bovis has been reported in patients with a past history of intravesical Bacillus Calmette–Guérin (BCG) immunotherapy of bladder cancer. These pathogens typically produce granulomatous prostatitis.

Prostatitis has been reported as a presenting manifestation of Wegener’s granulomatosis, and has been rarely described in conjunction with sarcoidosis. Eosinophilic prostatitis caused by Churg-Strauss syndrome has also been reported.

Antibiotic Selection

There are no trials that compare which antibiotic is the best for ABP. Antibiotic choice should be selected based on the most likely pathogen(s) and most common. In addition to providing coverage for the most common uropathogens, selection of initial antibiotic therapy in prostatitis is also informed by consideration of antibiotic penetration into the prostate gland. In general, antibiotics penetrate poorly into the prostate gland. However, during acute inflammation, the entry of drugs is more permissive.

Antibiotics in prostatic capillaries must diffuse across the capillary endothelium and prostatic interstitium through the cuboidal epithelium into infected glandular acinar fluid. The capillary endothelium has no active antibiotic transport mechanism and none of the usual fenestrae that usually permit small molecules to pass between capillary endothelial cells. Most antibiotics are weak acids or bases, but only the non-ionized form can diffuse into the prostate. Thus, only non-protein bound lipophilic antibiotics achieve therapeutic intraacinar drug levels.

Gradient diffusion into the infected prostate may by further enhanced by the differing pH levels of capillary blood and prostate fluid. The pH of chronically infected prostatic fluid may be more alkaline than capillary blood, favoring the dissociation of weakly acidic antibiotics into an ionic form, which increases the gradient of non-ionized antibiotic between capillary and acinus, permitting additional diffusion.

Antibiotics achieving good levels in prostatic fluid include quinolones, trimethoprim-sulfamethoxazole, tetracyclines, and macrolides. Fosfomycin may achieve adequate prostate levels and may come to play an increasing role in the management of this condition in an area of increasing prevalence of multi-drug-resistant organisms. Other antimicrobials, such as beta-lactam agents and aminoglycosides, penetrate the acutely inflamed prostate and are also effective in the initial treatment of acute prostatitis.

Quinolones and trimethoprim-sulfamethoxazole are preferred initial therapy for gram negative pathogens, and ampicillin for suspect enterococcus. Pending identification and susceptibility testing, vancomycin therapy should be initiated if gram stain or preliminary culture results suggest staphylococcus.

Empiric therapy of patients with SIRS physiology, recent antibiotic recipients, frequent health care system exposure, or recent genitourinary (GU) instrumentation should include coverage for resistant gram negative rods with a third-generation cephalosporin or carbapenem. Addition of vancomycin pending culture results is also indicated if no gram stain is available. Therapy can be tailored to the causative pathogen when microbiologic results have returned. Local microbiologic resistance patterns, if available, can guide the selection of gram negative coverage.

Supportive Care

Urinary outflow obstruction should be managed in consultation with a urologist. A urinary catheter may obstruct the drainage of infected prostatic secretions into the urethra and exacerbate the infection. This can be avoided with the use of a suprapubic catheter. Alpha blockers have been used in acute prostatitis to ameliorate obstructive and irritative voiding symptoms, but should probably be avoided in the acutely systemically ill patient. Nonsteroidal anti-inflammatory agents (NSAIDs) may be used to ameliorate pain if not otherwise contraindicated (e.g., renal insufficiency, heart failure). Narcotics should be avoided because of the risk of urinary retention.

B. Physical Examination Tips to Guide Management.

Lower urinary tract and systemic symptoms should gradually resolve within several days of antibiotic initiation. Persistence of symptoms or laboratory abnormalities may be due to:

  • Local complication of infection-prostatic abscess, epididymitis

  • Incorrect antibiotic selection

  • Bacteremia with metastatic infection

  • Endocarditis in patients with underlying valvular disease or prosthesis

  • Other nosocomial infection or drug fever

Urine culture and sensitivity results should inform any change in initial antibacterial therapy. In the event that the patient was pretreated and cultures are negative, empiric change of antibiotics to a carbapenem and vancomycin may be necessary to cover epidemiologically likely resistant flora once local complications are excluded.

Abdominal CT scan or transrectal ultrasound should be performed to exclude a prostatic abscess. If present, and >1 centimeter, drainage should be considered. Drainage techniques include transrectal aspiration, transurethral drainage, and ultrasound-guided placement of a transrectal drainage tube. Consultation with urology is warranted.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) may return to normal more slowly than the resolution of symptoms.

D. Long-term management.

Duration of therapy and follow up:

There are no randomized trials to guide the duration of therapy in acute prostatitis. In general, because of concerns about antibiotic penetration of the gland, particularly as acute inflammation subsides, longer courses of therapy are recommended. Although 2 week courses of therapy may suffice in uncomplicated patients (quinolone sensitive organism, prompt response to antibiotics, no comorbidities), most experts recommend at least 4 weeks of therapy.

Common Pitfalls and Side-Effects of Management.


IV. Management with Co-Morbidities.


A. Renal Insufficiency.


B. Liver Insufficiency.


C. Systolic and Diastolic Heart Failure.


D. Coronary Artery Disease or Peripheral Vascular Disease.


E. Diabetes or other Endocrine issues.


F. Malignancy.


G. Immunosuppression (HIV, chronic steroids, etc).


H. Primary Lung Disease (COPD, Asthma, ILD).


I. Gastrointestinal or Nutrition Issues.


J. Hematologic or Coagulation Issues.


K. Dementia or Psychiatric Illness/Treatment.


V. Transitions of Care.

A. Sign-out considerations While Hospitalized.


B. Anticipated Length of Stay.


C. When is the Patient Ready for Discharge.

In general, healthy patients without co-morbidities or signs of sepsis that are reliable to follow-up and can tolerate outpatient antibiotics can generally be managed in the outpatient setting. This is usually seen 24-48 hours after antibiotics are initiated when there is improvement clinically.

D. Arranging for Clinic Follow-up.

1. When should clinic follow up be arranged and with whom.

Clinic follow-up should be arranged in one week with a primary care doctor.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Urine culture can be repeated within 7 days after antibiotics. Studies suggest that if using quinolones, a negative culture at 7 days usually predicts there will be cure after full antibiotic course. If the culture remains positive, antimicrobial therapy should be switched based on the culture results of the new isolate. There should be suspicion in patients with repeatedly positive blood cultures for chronic bacterial prostatitis.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Complete blood count, basic metabolic panel, urinalysis, and urine culture.

E. Placement Considerations.


F. Prognosis and Patient Counseling.

The development of acute to chronic bacterial prostatitis is not well understood. Those patients who take a shorter course of antibiotics may be at risk for higher failure rates.

Immunocompromised patients including alcoholics and diabetics may also be at risk for higher failure rates.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.


VII. What's the Evidence?

Collins, MM, Stafford, RS, O’Leary, MP, Barry, MJ. “How common is prostatitis? A national survey of physician visits”. J Urol. vol. 159. 1998. pp. 1224

McGowan, CC, Krieger, J, Bennett, JE. “Prostatitis, epididymitis, and orchitis”. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 2015.

Shigehara, K, Miyagi, T, Nakashima, T. “Acute bacterial prostatitis after transrectal prostate needle biopsy: clinical analysis”. . vol. 14. 2008. pp. 40-43.

Cornia, PB, Takahashi, TA, Lipsky, BA. “The microbiology of bacteriuria in men: a 5-year study at a Veterans' Affairs hospital”. . vol. 56. 2006. pp. 25-30.

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