- Author: Paul J Turek, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD more...
The different prostatitis categories are treated with various medical therapies, depending on the underlying pathology. Antibiotic therapy is essential in the treatment of acute bacterial prostatitis. If the patient is having systemic symptoms, then admission is warranted for intravenous antibiotics, hydration, and analgesia.
Therapy for chronic bacterial prostatitis varies with the type and duration of antibiotics used. Treatment typically consists of 4-8 weeks of prostate-penetrating antibiotics, such as fluoroquinolone or trimethoprim-sulfamethoxazole.
Chronic prostatitis, chronic pelvic pain syndrome, and asymptomatic inflammatory prostatitis may be treated with alpha-blocking agents or diazepam with sitz baths.
Empiric antibiotics should be tailored toward treating gram-negative pathogens. Sexually transmitted diseases (STDs), where Neisseria gonorrhoeae and Chlamydia trachomatis are the primary suspected pathogens, must also be considered, especially in patients younger than 35 years.
Current Centers for Disease Control and Prevention (CDC) updated treatment guidelines for gonococcal infection recommend single-dose IM ceftriaxone, plus single-dose oral azithromycin or 7 days of oral doxycycline. Cotreatment offers the benefits of hindering the development of antimicrobial resistant gonococci and providing coverage against C trachomatis infection, which often accompanies gonococcal infection. Fluoroquinolone antibiotics are no longer recommended to treat gonorrhea in the United States.
For the treatment of chronic bacterial prostatitis, where Enterobacteriaceae, enterococci, and Pseudomonas aeruginosa are common pathogens, consider trimethoprim/sulfamethoxazole (Bactrim) or fluoroquinolones for 28 days or more as empiric agents.
For nonbacterial prostatitis caused by Chlamydia and Ureaplasma species, which are difficult to culture, an empiric trial of doxycycline or erythromycin should be instituted.
This fluoroquinolone is indicated to treat acute and chronic bacterial prostatitis due to Escherichia coli, E faecalis, or Staphylococcus epidermidis. It has good concentration in the prostate. This is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. It provides good monotherapy with extended coverage against Pseudomonas species, as well as excellent activity against pneumococcus. Levofloxacin acts by inhibition of DNA gyrase activity.
Ofloxacin is a fluoroquinolone that is a pyridine carboxylic acid derivative with a broad-spectrum bactericidal effect.
This agent is a fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Ciprofloxacin has no activity against anaerobes. Continue treatment for at least 2 days (7-14 d typical) after signs and symptoms have disappeared.
Trimethoprim inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except P aeruginosa.
A third-generation cephalosporin with broad-spectrum, gram-negative activity, ceftriaxone has lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Its bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins.
This agent exerts its antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.
Ceftriaxone is highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of the dose excreted unchanged in urine, and remainder is secreted in bile and ultimately in feces as microbiologically inactive compounds. Ceftriaxone reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations of less than 25 mcg/mL to 85% bound at 300 mcg/mL.
Doxycycline inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. It may block dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Doxycycline is used to treat nonbacterial prostatitis caused by Chlamydia species. Chlamydia and Ureaplasma are difficult to culture; therefore, an empiric trial of doxycycline should be instituted.
These agents are used in the treatment of benign prostatic hypertrophy. Studies suggest that combining alpha-blockers with antibiotics may reduce the risk of prostatitis recurrence in chronic prostatitis. Alpha-blockers reduce bladder outlet obstruction and thus improve voiding dysfunction that may be associated with prostatic swelling with prostatitis. Alpha-blockers may also have role to improve symptoms in chronic pelvic pain syndrome.
Quinazoline compound that counteracts alpha1-induced adrenergic contractions of bladder neck, terazosin facilitates urinary flow in the presence of prostate inflammation.
An alpha-adrenergic blocker, specifically targeting the A1 receptors, tamsulosin has the advantage of causing relatively less orthostatic hypotension, and it requires no gradual up-titration from the initial introductory dosage. On the other hand, a higher incidence of ejaculatory dysfunction exists with this medication (8.4-18.1%).
Krieger JN, Nyberg L Jr, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA. 1999. 282:236-7. [Medline].
Murphy AB, Macejko A, Taylor A, Nadler RB. Chronic prostatitis: management strategies. Drugs. 2009. 69(1):71-84. [Medline].
Habermacher GM, Chason JT, Schaeffer AJ. Prostatitis/chronic pelvic pain syndrome. Annu Rev Med. 2006. 57:195-206. [Medline].
Mastroianni A, Coronado O, Manfredi R, Chiodo F, Scarani P. Acute cytomegalovirus prostatitis in AIDS. Genitourin Med. 1996 Dec. 72(6):447-8. [Medline].
Gebo KA. Prostatic tuberculosis in an HIV infected male. Sex Transm Infect. 2002 Apr. 78(2):147-8. [Medline].
Krieger JN, Dobrindt U, Riley DE, Oswald E. Acute Escherichia coli prostatitis in previously health young men: bacterial virulence factors, antimicrobial resistance, and clinical outcomes. Urology. 2011 Jun. 77(6):1420-5. [Medline].
Brede CM, Shoskes DA. The etiology and management of acute prostatitis. Nat Rev Urol. 2011 Apr. 8(4):207-12. [Medline].
Feneley M, Kirby RS, Parkinson C. Clinico-pathological findings simulating prostatic malignancy following sclerotherapy: a diagnostic pitfall. Br J Urol. 1996 Jan. 77(1):157-8. [Medline].
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].
Nickel JC, Downey J, Hunter D, Clark J. Prevalence of prostatitis-like symptoms in a population based study using the National Institutes of Health chronic prostatitis symptom index. J Urol. 2001 Mar. 165(3):842-5. [Medline].
Schaeffer AJ. Clinical practice. Chronic prostatitis and the chronic pelvic pain syndrome. N Engl J Med. 2006 Oct 19. 355(16):1690-8. [Medline].
Awadh B, Watson K, Abdou NI. Wegener prostatitis presenting with acute urinary retention. J Clin Rheumatol. 2006 Feb. 12(1):50-1. [Medline].
Huong DL, Papo T, Piette JC, Wechsler B, Bletry O, Richard F, et al. Urogenital manifestations of Wegener granulomatosis. Medicine (Baltimore). 1995 May. 74(3):152-61. [Medline].
Middleton G, Karp D, Lee E, Cush J. Wegener's granulomatosis presenting as lower back pain with prostatitis and ureteral obstruction. J Rheumatol. 1994 Mar. 21(3):566-9. [Medline].
Donovan DA, Nicholas PK. Prostatitis: diagnosis and treatment in primary care. Nurse Pract. 1997 Apr. 22(4):144-6, 149-56. [Medline].
[Guideline] Grabe M, Bishop MC, Bjerklund-Johansen TE, et al. Prostatitis and chronic pelvic pain syndrome. Guidelines on the management of urinary and male genital tract infections. Arnhem, The Netherlands: European Association of Urology (EAU). 2008 Mar. 79-88. [Full Text].
Loeb S, Gashti SN, Catalona WJ. Exclusion of inflammation in the differential diagnosis of an elevated prostate-specific antigen (PSA). Urol Oncol. 2009 Jan-Feb. 27(1):64-6. [Medline].
de la Rosette JJ, Giesen RJ, Huynen AL, Aarnink RG, van Iersel MP, Debruyne FM, et al. Automated analysis and interpretation of transrectal ultrasonography images in patients with prostatitis. Eur Urol. 1995. 27(1):47-53. [Medline].
[Guideline] Fall M, Baranowski AP, Elneil S, Engeler D, Hughes J, Messelink EJ, et al. General treatment of chronic pelvic pain. Guidelines on chronic pelvic pain. Arnhem, The Netherlands: European Association of Urology (EAU). 2008 Mar. 84-97. [Full Text].
Centers for Disease Control and Prevention. Update to CDC's sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. 2007 Apr 13. 56(14):332-6. [Medline]. [Full Text].
Yoon BI, Han DS, Ha US, Lee SJ, Sohn DW, Kim HW. Clinical courses following acute bacterial prostatitis. Prostate Int. 2013. 1(2):89-93. [Medline].
Le BV, Schaeffer AJ. Genitourinary pain syndromes, prostatitis, and lower urinary tract symptoms. Urol Clin North Am. 2009 Nov. 36(4):527-36, vii. [Medline].
Berghuis JP, Heiman JR, Rothman I, Berger RE. Psychological and physical factors involved in chronic idiopathic prostatitis. J Psychosom Res. 1996 Oct. 41(4):313-25. [Medline].
Sindhwani P, Wilson CM. Prostatitis and serum prostate-specific antigen. Curr Urol Rep. 2005 Jul. 6(4):307-12. [Medline].
Mehik A, Hellström P, Sarpola A, Lukkarinen O, Järvelin MR. Fears, sexual disturbances and personality features in men with prostatitis: a population-based cross-sectional study in Finland. BJU Int. 2001 Jul. 88(1):35-8. [Medline].
Wise GJ, Shteynshlyuger A. How to diagnose and treat fungal infections in chronic prostatitis. Curr Urol Rep. 2006. 7(4):320-8. [Medline].
Kim JW, Oh MM, Bae JH, Kang SH, Park HS, Moon du G. Clinical and microbiological characteristics of spontaneous acute prostatitis and transrectal prostate biopsy-related acute prostatitis: Is transrectal prostate biopsy-related acute prostatitis a distinct acute prostatitis category?. J Infect Chemother. 2015 Jun. 21 (6):434-7. [Medline].
Etienne M, Pestel-Caron M, Chapuzet C, Bourgeois I, Chavanet P, Caron F. Should blood cultures be performed for patients with acute prostatitis?. J Clin Microbiol. 2010 May. 48 (5):1935-8. [Medline].
Gill BC, Shoskes DA. Bacterial prostatitis. Curr Opin Infect Dis. 2016 Feb. 29 (1):86-91. [Medline].
Breyer BN, Van den Eeden SK, Horberg MA, Eisenberg ML, Deng DY, Smith JF, et al. HIV status is an independent risk factor for reporting lower urinary tract symptoms. J Urol. 2011 May. 185 (5):1710-5. [Medline].