Acute Bacterial Prostatitis
- Author: Samuel G Deem, DO; Chief Editor: Edward David Kim, MD, FACS more...
Although 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 benign prostatic hyperplasia [BPH] and prostate cancer), acute prostatitis is rare. Acute prostatitis is easier to identify than chronic prostatitis, however, because of its more uniform clinical presentation.
Acute prostatitis presents as an acute urinary tract infection (UTI). It is usually associated with predisposing risk factors, including bladder outlet obstruction secondary to benign prostatic hyperplasia (BPH) or an immunosuppressed state. Approximately 5% of cases of acute bacterial prostatitis (ABP) progress to chronic prostatitis.
Pathologic definition of prostatitis
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 (see the image below).
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.
NIH classification and definition of prostatitis
The National Institutes of Health (NIH) classification and definition of the categories of prostatitis are as follows:
Category I – Acute bacterial prostatitis (ie, acute infection of the prostate)
Category II – Chronic bacterial prostatitis (ie, recurrent urinary tract infection and/or chronic infection of the prostate)
Category III – Chronic abacterial prostatitis/chronic pelvic pain syndrome (ie, discomfort or pain in the pelvic region for at least 3 mo with variable voiding and sexual symptoms and/or no demonstrable infection; by definition, the syndrome becomes chronic after 3 mo)
Category IIIA – Inflammatory chronic pelvic pain syndrome (ie, white blood cells in semen and/or expressed prostatic secretions and/or third midstream bladder specimen)
Category IIIB – Noninflammatory chronic pelvic pain syndrome (ie, no white blood cells in semen and/or expressed prostatic secretions)
Category IV – Asymptomatic inflammatory prostatitis (ie, evidence of inflammation in biopsy samples, semen and/or expressed prostatic secretions, but no symptoms)
Historical and epidemiologic data
In 1978-1979, symptoms due to acute and chronic prostatitis accounted for 25% of outpatient urinary conditions in the United States. 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.
The international prevalence rate of prostatitis is similar to that in the United States. In one report, of 600 men diagnosed with prostatitis, 5% had bacterial prostatitis, 64% had nonbacterial prostatitis, and 31% had pelvic-perineal pain syndrome or prostatodynia.
The prostate is an extraperitoneal organ that encircles the neck of the bladder and urethra. In an adult, this organ is divided into four distinct zones or regions: periurethral, central, transitional, and peripheral. Prostate carcinoma arises more often in the peripheral zone than the other zones. However, the distribution of prostatic inflammation among the various zones is not clear.
A normal prostate gland is approximately 20 g in volume, 3 cm in length, 4 cm wide, and 2 cm in depth. As men get older, the prostate gland often enlarges because of BPH.
The gland is located posterior to the pubic symphysis, superior to the perineal membrane, inferior to the bladder, and anterior to the rectum. The base of the prostate is in continuity with the bladder and the prostate ends at the apex before becoming the striated external urethral sphincter. The sphincter is a vertically oriented tubular sheath that surrounds the membranous urethra and prostate.
See Prostate Anatomy for more information.
See also the following:
Several theories exist regarding the pathogenesis of acute bacterial prostatitis, including intraprostatic urinary reflux, ascending urethral infection, direct invasion or lymphogenous spread from the rectum, and direct hematogenous infection.
Intraprostatic urinary reflux is the most widely accepted theory. Infected urine refluxes into the ejaculatory and prostatic ducts that empty into the posterior urethra. Because of the anatomy of the prostate gland, ducts that drain glands in the large peripheral zone are positioned more horizontally than other prostatic ducts and, thus, facilitate the reflux of urine into the prostate. Consequently, most infections occur in the peripheral zone.
In younger men, ascending urethral infection may occur following sexual intercourse. Meatal inoculation may occur during unprotected anal intercourse, instrumentation, and prolonged catheterization.
The organisms primarily responsible for acute bacterial prostatitis (ABP) are also those responsible for most urinary tract infections; these include gram-negative members of the Enterobacteriaceae family such as 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. Most prostatic infections (82%) involve only a single bacterial organism. In some cases, two or three strains of bacteria may be involved.
Obligate anaerobic bacteria and gram-positive bacteria other than enterococci rarely cause acute bacterial prostatitis. Enterococci account for 5-10% of documented prostate infections. Staphylococcus aureus infection due to prolonged catheterization may occur in the hospital. Other occasional causative organisms include Neisseria gonorrhoeae,Mycobacterium tuberculosis,Salmonella species, Clostridium species, and parasitic or mycotic organisms. N gonorrhoeae should be suspected in sexually active men younger than 35 years.
If recurrent urinary tract infections are confirmed, patients need to be evaluated for any structural abnormality.
Another source of acute prostatitis is following transrectal ultrasound-guided prostate needle biopsy. In this instance, the acute prostatitis is iatrogenic in nature but presents similarly and is treated as acute bacterial prostatitis.
A study comparing the multiresistant ST131 E coli pathogen found after transrectal ultrasound-guided prostate biopsy to non-ST131 E coli from patients with spontaneous urosepsis showed that the ST131 E coli had fewer virulence-associated genes than the non-ST131 group. The finds suggest that antimicrobial resistance, rather than virulence genotype, is the most important trait associated with an increased risk of infection following transrectal biopsy.
The following are risk factors for acute bacterial prostatitis (all allow bacterial colonization):
Intraprostatic ductal reflux
Phimosis and redundant foreskin
Specific blood groups 
Unprotected anal intercourse
Urinary tract infections
Indwelling Foley catheter and condom catheter
Altered prostatic secretions
Recent transrectal ultrasound-guided prostate needle biopsy
If the initial response to medical therapy for acute bacterial prostatitis (ABP) 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, has been reported in samples that contained more than 106 colony-forming units (CFU)/mL of bacteria.
Prostatic abscess is an uncommon but well-described complication of acute bacterial prostatitis. Although very rare, it usually occurs in patients who are immunocompromised, who have diabetes, who have urethral instrumentation or a prolonged indwelling urethral catheters, or who are on maintenance dialysis. Coliform bacteria, especially E coli, cause more than 70% of prostatic abscesses.
Other potential sequelae of acute bacterial prostatitis include progression to chronic prostatitis, septicemia, pyelonephritis, and epididymitis. Recently, it has been shown that nearly 10% of patients with acute bacterial prostatitis develop chronic prostatitis and another 10% develop chronic pelvic pain syndrome.
Nickel JC. Inflammatory conditions of the male genitourinary tract: prostatitis and related conditions, orchitis, and epididymitis. Wein. AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. 9th ed. Philadelphia, Pa: WB Saunders: 2005; Chapter 9.
Nickel JC. 5 alpha reductase therapy for chronic prostatitis. Nickel JC, ed. Textbook of Prostatitis. Oxford, UK: ISIS Medical Media; 1999. 333-7.
Collins MM, Stafford RS, O'Leary MP, Barry MJ. How common is prostatitis? A national survey of physician visits. J Urol. 1998 Apr. 159(4):1224-8. [Medline].
Kanamaru S, Kurazono H, Terai A, Monden K, Kumon H, Mizunoe Y, et al. Increased biofilm formation in Escherichia coli isolated from acute prostatitis. Int J Antimicrob Agents. 2006 Aug. 28 Suppl 1:S21-5. [Medline].
Bergman B. On the relevance of gram-positive bacteria in prostatitis. Infection. 1994. 22 Suppl 1:S22. [Medline].
Williamson DA, Freeman JT, Porter S, Roberts S, Wiles S, Paterson DL, et al. Clinical and molecular correlates of virulence in Escherichia coli causing bloodstream infection following transrectal ultrasound-guided (TRUS) prostate biopsy. J Antimicrob Chemother. 2013 Dec. 68(12):2898-906. [Medline].
Lomberg H, Cedergren B, Leffler H, Nilsson B, Carlström AS, Svanborg-Edén C. Influence of blood group on the availability of receptors for attachment of uropathogenic Escherichia coli. Infect Immun. 1986 Mar. 51(3):919-26. [Medline]. [Full Text].
Wagenlehner FM, Pilatz A, Bschleipfer T, Diemer T, Linn T, Meinhardt A, et al. Bacterial prostatitis. World J Urol. 2013 Mar 22. [Medline].
Nagy V, Kubej D. Acute bacterial prostatitis in humans: current microbiological spectrum, sensitivity to antibiotics and clinical findings. Urologia Internationalis. October/2012. 89 (4):445-450. [Medline].
Nickel JC. The Pre and Post Massage Test (PPMT): a simple screen for prostatitis. Tech Urol. 1997 Spring. 3(1):38-43. [Medline].
Magri V, Cariani L, Bonamore R, Restelli A, Garlaschi MC, Trinchieri A. Microscopic and microbiological findings for evaluation of chronic prostatitis. Arch Ital Urol Androl. 2005 Jun. 77(2):135-8. [Medline].
Meares EM, Stamey TA. Bacteriologic localization patterns in bacterial prostatitis and urethritis. Invest Urol. 1968 Mar. 5(5):492-518. [Medline].
Terrone C, Poggio M, Bollito E, Cracco CM, Scarpa RM. [Asymptomatic prostatitis: a frequent cause of raising PSA]. Recenti Prog Med. 2005 Jul-Aug. 96(7-8):365-9. [Medline].
Granados EA, Riley G, Salvador J, Vincente J. Prostatic abscess: diagnosis and treatment. J Urol. 1992 Jul. 148(1):80-2. [Medline].
Barbalias GA, Nikiforidis G, Liatsikos EN. Alpha-blockers for the treatment of chronic prostatitis in combination with antibiotics. J Urol. 1998 Mar. 159(3):883-7. [Medline].
Aravantinos E, Kalogeras N, Zygoulakis N, Kakkas G, Anagnostou T, Melekos M. Ultrasound-guided transrectal placement of a drainage tube as therapeutic management of patients with prostatic abscess. J Endourol. 2008 Aug. 22(8):1751-4. [Medline].
Chou YH, Tiu CM, Liu JY, Chen JD, Chiou HJ, Chiou SY, et al. Prostatic abscess: transrectal color Doppler ultrasonic diagnosis and minimally invasive therapeutic management. Ultrasound Med Biol. 2004 Jun. 30(6):719-24. [Medline].
Barozzi L, Pavlica P, Menchi I, De Matteis M, Canepari M. Prostatic abscess: diagnosis and treatment. AJR Am J Roentgenol. 1998 Mar. 170(3):753-7. [Medline].
Zowawi HM, Harris PN, Roberts MJ, Tambyah PA, Schembri MA, Pezzani MD, et al. The emerging threat of multidrug-resistant Gram-negative bacteria in urology. Nat Rev Urol. 2015 Oct. 12 (10):570-84. [Medline].
Campeggi A, Ouzaid I, Xylinas E, Lesprit P, Hoznek A, Vordos D, et al. Acute bacterial prostatitis after transrectal ultrasound-guided prostate biopsy: epidemiological, bacteria and treatment patterns from a 4-year prospective study. Int J Urol. 2014 Feb. 21(2):152-5. [Medline].
Song W, Choo SH, Sung HH, Han DH, Jeong BC, Seo SI, et al. Incidence and management of extended-spectrum beta-lactamase and quinolone-resistant Escherichia coli infections after prostate biopsy. Urology. 2014 Nov. 84 (5):1001-7. [Medline].
Wagenlehner FM, Pilatz A, Waliszewski P, Weidner W, Johansen TE. Reducing infection rates after prostate biopsy. Nat Rev Urol. 2014 Feb. 11(2):80-6. [Medline].
Kaye KS, Pogue JM. Infections Caused by Resistant Gram-Negative Bacteria: Epidemiology and Management. Pharmacotherapy. 2015 Oct. 35 (10):949-62. [Medline].
Meares EM Jr. Prostatitis. Med Clin North Am. 1991 Mar. 75(2):405-24. [Medline].
Kabay S, Kabay SC, Yucel M, Ozden H. Efficiency of posterior tibial nerve stimulation in category IIIB chronic prostatitis/chronic pelvic pain: a Sham-Controlled Comparative Study. Urol Int. 2009. 83(1):33-8. [Medline].
Lee SH, Lee BC. Electroacupuncture relieves pain in men with chronic prostatitis/chronic pelvic pain syndrome: three-arm randomized trial. Urology. 2009 May. 73(5):1036-41. [Medline].
Liu L, Yang J. Physician's practice patterns for chronic prostatitis. Andrologia. 2009 Oct. 41(5):270-6. [Medline].
Ludwig M. Diagnosis and therapy of acute prostatitis, epididymitis and orchitis. Andrologia. 2008 Apr. 40(2):76-80. [Medline].
Nickel JC, Shoskes D. Phenotypic approach to the management of chronic prostatitis/chronic pelvic pain syndrome. Curr Urol Rep. 2009 Jul. 10(4):307-12. [Medline].