Updated: Dec 5, 2008
Acute prostatitis presents as an acute urinary tract infection in men. It is much less common than chronic prostatitis but is easier to identify because of its more uniform clinical presentation. Chronic prostatitis, which now has several classifications, is poorly understood partly because of its uncertain etiology and lack of clearly distinguishing clinical features.
Acute prostatitis is usually associated with predisposing risk factors, including bladder outlet obstruction secondary to benign prostatic hyperplasia (BPH) or an immunosuppressed state. This review focuses on acute bacterial prostatitis (ABP).
In 1978-1979, symptoms due to acute and chronic prostatitis accounted for 25% of outpatient urinary conditions. In 1985, according to Nickel, acute and chronic prostatitis accounted for more office visits than BPH or prostate cancer. Most of these visits were for chronic prostatitis. In the early 1990s, the diagnosis of prostatitis resulted in slightly more than 2 million office visits per year.
Pathologically, prostatitis is defined as an increased number of inflammatory cells within the prostate gland. The inflammatory process may be infectious or inflammatory in origin. The most common histologic pattern is a lymphocytic infiltrate in the stroma immediately adjacent to the prostatic acini.1 Prostatitis occurs in distinct forms that have separate causes, clinical features, and outcomes. Four clinical entities have been described: acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial or abacterial prostatitis, and prostatodynia.
The National Institutes of Health (NIH) classification and definition of the categories of prostatitis are as follows:
Using data from the National Ambulatory Medical Care Surveys (NAMCS), Collins et al (1998) found that prostatitis was listed as the diagnosis in almost 2 million US physician visits annually from 1990-1994.2 Prostatitis is the most common urologic diagnosis in males younger than 50 years and the third most common diagnosis in men older than 50 years (after BPH and prostate cancer). However, acute prostatitis is rare. Approximately 5% of cases of acute bacterial prostatitis progress to chronic bacterial prostatitis.3
The international prevalence rate of prostatitis is similar to that in the United States. Of 600 men diagnosed with prostatitis, 5% had bacterial prostatitis, 64% had nonbacterial prostatitis, and 31% had pelvic-perineal pain syndrome or prostatodynia.
Most prostatic infections (82%) involve only a single bacterial organism. In some cases, 2 or 3 strains of bacteria may be involved. The organisms primarily responsible for acute bacterial prostatitis are also those responsible for most urinary tract infections.
The most common causal organisms of acute bacterial prostatitis include gram-negative members of the Enterobacteriaceae family. They include Escherichia coli, Proteus mirabilis, Klebsiella species, Enterobacter species, Pseudomonas aeruginosa, and Serratia species. Of these, E coli is involved most often and has been shown to increase biofilm formation.4
Obligate anaerobic bacteria and gram-positive bacteria other than enterococci rarely cause acute bacterial prostatitis. Enterococci account for 5-10% of documented prostate infections.5 Staphylococcus aureus infection due to prolonged catheterization may occur in the hospital. Other occasional causative organisms include Neisseria gonorrhea, Mycobacterium tuberculosis, Salmonella species, Clostridium species, and parasitic or mycotic organisms. N gonorrhea should be suspected in sexually active men younger than 35 years.
If recurrent urinary tract infections are confirmed, patients need to be evaluated for structural abnormality.
Several theories exist regarding the pathogenesis of acute bacterial prostatitis.
Acute bacterial prostatitis usually presents as an acute illness with moderate to severe fever, chills, low back and perineal pain, urinary frequency and urgency, nocturia, dysuria, and generalized malaise. Arthralgia and myalgia may accompany these symptoms. Acute bacterial prostatitis may also result in acute urinary retention due to varying degrees of bladder outlet obstruction. The diagnosis of acute bacterial prostatitis is based primarily on clinical findings, in association with positive results on urinalysis and urine culture.
In patients with acute bacterial prostatitis, rectal palpation usually reveals an enlarged, exquisitely tender, swollen prostate gland, which is firm, warm, and, occasionally, irregular to the touch. Care must be taken to avoid vigorous prostatic massage in a patient with suspected acute bacterial prostatitis to prevent bacteremia and sepsis.
Sexual dysfunction is described as a symptom of chronic prostatitis and chronic pelvic pain syndrome. Pain associated with ejaculation (which translates to impaired overall quality of life) contributes to or causes erectile dysfunction.7
Prostatic abscess, which is an uncommon but well-described complication of acute bacterial prostatitis (ABP), is a potential indication for surgery. Medical management of prostatic abscess is often unsuccessful.Transrectal or perineal aspiration of the abscess is preferred and is often effective, especially if symptoms do not improve after 1 week of medical therapy. Transurethral resection of the prostate and drainage of the cavity is another approach. However, this approach is less desirable because of the potential hematogenic spread of bacteria.
The prostate is an extraperitoneal organ that encircles the neck of the bladder and urethra and weighs approximately 20 g in a healthy man. The adult prostate is divided into 4 distinct zones or regions: the periurethral, central, transitional, and peripheral zones. Carcinoma arises more often in the peripheral zone. However, the distribution of prostatic inflammation among the various zones is not clear.
Histologically, the prostate gland is composed of tubuloalveolar glands. The glandular spaces are lined by epithelium, which is composed of 2 layers of cells—a basal layer of low cuboidal epithelium covered by a layer of columnar mucus-secreting cells. The glands have a distinct basement membrane and are separated by a fibromuscular stroma.
Prostate biopsy is contraindicated in patients with suspected acute bacterial prostatitis (ABP) because of the potential complication of seeding the bacterial infection in adjacent organs. Furthermore, prostate biopsy is extremely painful without a prostatic nerve block. The current practice is to anesthetize the area prior to core biopsy sampling. Biopsy in the face of acute bacterial prostatitis may result in gram-negative sepsis.
Because of the potential for systemic infection and bacteremia, urethral instrumentation should be avoided in patients with acute bacterial prostatitis, especially if the patient is unstable or is already showing signs of sepsis, although placement of a small drainage catheter is safe in experienced hands. Pretreatment with appropriate antibiotics is mandatory.
Transurethral or perineal surgical approaches in the treatment of a prostatic abscess should be undertaken with caution and are currently not advised unless other drainage techniques have failed. Perineal incision can cause impotence due to nerve injury, and transurethral resection can elicit hematogenous spread of bacteria, leading to sepsis.8
Imaging studies, including CT scanning of the pelvis or transrectal ultrasonography, should be reserved for cases in which laboratory analysis findings are equivocal or when no improvement is observed following medical therapy. Ruling out complications of prostatitis (eg, prostatic abscess) is a strong indication to proceed to imaging studies. Transrectal ultrasonography and CT scanning of the pelvis can be very useful in diagnosing and draining prostatic abscesses.13 However, transrectal ultrasonography should be performed as gently as possible to prevent bacteremia.
Prostate biopsy is contraindicated in cases of suspected acute bacterial prostatitis because of the potential complication of seeding the bacterial infection in adjacent organs. Biopsy in the face of acute bacterial prostatitis may result in gram-negative sepsis.
A stromal leukocytic infiltrate may be accompanied by increased prostatic secretion or leukocytic infiltration within gland spaces. When complicated by abscess formation, focal or larger areas of the prostate become necrotic.
The intense inflammation in acute bacterial prostatitis (ABP) makes the prostate gland highly responsive to antibiotics, which otherwise penetrate poorly into the prostate. Hospitalization is required for patients in whom acute urinary retention develops and in those who require intravenous antimicrobial therapy.
The choice of antibiotic is based on results of the initial culture and sensitivity. However, initial therapy should be directed at gram-negative enteric bacteria. Useful agents include fluoroquinolones, trimethoprim-sulfamethoxazole, and ampicillin with gentamicin. Antipyretics, analgesics, stool softeners, bed rest, and increased fluid intake provide supportive therapy. A Foley catheter can be inserted gently for drainage if severe obstruction is suspected. A punch suprapubic tube can be used if a catheter cannot be passed easily or is not tolerated by the patient. The catheter can be removed 24-36 hours later.
If the initial clinical response to therapy is satisfactory and the pathogen is susceptible to the chosen antibiotic, treatment is continued orally for 30 days to prevent sequelae such as chronic bacterial prostatitis and prostatic abscess formation.
For intravenous therapy, use trimethoprim-sulfamethoxazole (Bactrim), 8-10 mg/kg/d (based on the trimethoprim component) in 2-4 intravenous doses bid, tid, or qid until the culture and sensitivity results are known. An alternate regimen is gentamicin with ampicillin 3-5 mg/kg/d IV (gentamicin dose divided tid and 2 g ampicillin divided qid). After the patient is afebrile for 24 hours, an appropriate oral agent can be substituted for an additional 30 days.
For oral therapy, use trimethoprim-sulfamethoxazole (Bactrim), 160 mg of trimethoprim and 800 mg of sulfamethoxazole, PO bid for 30 days. Use levofloxacin (Levaquin) 500 mg PO bid; ciprofloxacin, 500 mg PO bid; norfloxacin, 400 mg PO bid; ofloxacin, 400 mg PO bid; or enoxacin, 400 mg PO bid for 30 days when clinical response is favorable.
Alpha-blocker therapy should also be considered. Because the bladder neck and prostate are rich in α receptors, alpha blockade may improve outflow obstruction and diminish intraprostatic urinary reflux (terazosin 5 mg/d PO for 4-52 wk).14 Tamsulosin (Flomax), alfuzosin (UroXatral) and doxazosin (Cardura) are acceptable alternatives.
Because of the limitation of alpha-blockers, clinical trials are ongoing using combination of alpha-blockers and 5-alpha-reductase inhibitors.15
A prostatic abscess can be surgically drained with either transrectal or perineal aspiration, transurethral resection, or transrectal ultrasound–guided placement of a transrectal drainage tube.3 Drainage of some kind should be performed if the abscess is larger than 1 cm.16,17 Because of the potential for systemic infection and bacteremia, urethral instrumentation should be avoided in patients with acute bacterial prostatitis, especially if the patient is unstable or already showing signs of sepsis. In patients with sepsis, transurethral resection may be life-saving and should be considered if they are not responding to conservative therapy.
In patients with acute urinary retention, a Foley catheter may be attempted first as tolerated by the patient. However, it may cause extreme discomfort. In some cases, the transurethral catheter may obstruct drainage of an acutely inflamed prostate and cause bacteremia or prostatic abscess. If the catheter is not easy to pass, a suprapubic punch cystostomy is indicated.
For excellent patient education resources, visit eMedicine's Prostate Health Center. Also, see eMedicine's patient education articles Understanding the Male Anatomy and Prostate Infections.
Prostatic abscess is an uncommon but well-described complication of acute bacterial prostatitis (ABP). Although very rare, it usually occurs in patients who are immunocompromised, patients who have diabetes, patients with urethral instrumentation or prolonged indwelling urethral catheters, or patients on maintenance dialysis. Coliform bacteria, especially E coli, cause more than 70% of prostatic abscesses. A prostatic abscess should be suspected when worsening clinical symptoms follow an initial favorable response to treatment of acute bacterial prostatitis or a fluctuant mass is developing in the prostate gland. The presence of the abscess is confirmed with transrectal ultrasonography and noncontrast CT scanning of the pelvis.
Once an abscess is diagnosed, anaerobic antimicrobial therapy should be added to the treatment regimen. Clindamycin intravenously at 600-900 mg q8h or orally at 150-450 mg q8h is a good choice. However, medical management is often unsuccessful. Transrectal or perineal aspiration of the abscess is preferred and is often effective, especially if symptoms do not improve after 1 week of medical therapy. Transurethral resection of the prostate and drainage of the cavity is another approach. Recurrent abscesses are rare. The abscess should be allowed to drain and should be monitored closely if a spontaneous rupture occurs into the urethra.
Other potential sequelae of acute bacterial prostatitis include progression to chronic prostatitis, septicemia, pyelonephritis, and epididymitis.
If the initial response to medical therapy is favorable, the patient’s prognosis is very good. Decreased fertility has been reported, but only in cases of massive bacterial inoculation. Decreased sperm viability, including impaired motility and agglutination, was reported in samples that contained more than 106 colony-forming units (CFU)/mL.
Despite the fact that prostatitis syndromes are common urologic disease processes, little is known about prostatitis and the factors associated with the condition. Several important questions need to be answered, including the following:
The first question is important considering the recent efforts to find the most accurate and most expedient method of diagnosing and treating prostate cancer. Prostatitis is more common in younger men, whereas BPH and prostate cancer are more common in men older than 50 years. An important research question is whether prostatitis in younger men leads to BPH or prostate cancer later, since approximately 5% of acute bacterial prostatitis (ABP) cases lead to chronic prostatitis. Although one study reported that nearly 50% of prostate specimens resected for prostate cancer showed evidence of prostatitis, no causal association has been demonstrated.18
The exact public health burden of prostatitis should also be addressed. Most urologists agree about the ever-growing need for both community-based cross-sectional and longitudinal epidemiological prostatitis studies. Active research and a more aggressive effort are needed to generate hypotheses regarding the etiology of prostatitis.
Formulating risk factors associated with prostatitis is important. For example, the incidence of prostatitis among men with a history of a prostatic biopsy requires investigation. With increased screening for prostate cancer, more men are undergoing biopsy based on elevated serum PSA levels. These biopsies may trigger an inflammatory response in the prostate, leading to prostatitis, or, alternatively, a biopsy may be a source of transmission of organisms into the prostate gland.
These examples outline potential research directions in the field of prostatitis. Results of these and other studies could promote an increased awareness of the disease and increase the knowledge about prostatitis. This research should improve diagnosis and treatment, promote an appropriate allocation of resources to the management of the disease, and reduce the incidence and public health burden of prostatitis.
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acute bacterial prostatitis, prostatic abscess, ABP, acute prostatitis, prostatitis, prostate disease, bladder outlet obstruction, benign prostatic hyperplasia, chronic bacterial prostatitis, nonbacterial prostatitis, abacterial prostatitis, prostatodynia, male urinary tract infection, Escherichia coli, Proteus mirabilis, Klebsiella species, Enterobacter species, Pseudomonas aeruginosa, Serratia species, acute infection of the prostate, recurrent urinary tract infection, chronic infection of the prostate, chronic abacterial prostatitis, chronic pelvic pain syndrome, inflammatory chronic pelvic pain syndrome, noninflammatory chronic pelvic pain syndrome, asymptomatic inflammatory prostatitis, intraprostatic urinary reflux
Jonathan J Rhee, MD, Staff Physician, Department of Urology, University of Virginia
Jonathan J Rhee, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.
Michael Piesman, MD, Staff Physician, Department of Internal Medicine, Madigan Army Medical Center
Michael Piesman, MD is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.
Raymond A Costabile, MD, Jay Y Gillenwater Professor of Urology, University of Virginia Health System
Raymond A Costabile, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Andrology, American Urological Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Edmund S Sabanegh, MD, Director, Center for Male Fertility, Glickman Urological and Kidney Institute, Cleveland Clinic Foundation
Edmund S Sabanegh, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, Society for the Study of Male Reproduction, Society of Reproductive Surgeons, and Southwest Oncology Group
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
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Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association
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