eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions

Chronic Bacterial Prostatitis

Author: Sunil K Ahuja, MD, Chief of Minimally Invasive Urology, Department of Urology, Staff Urologist, Santa Teresa Community Hospital
Contributor Information and Disclosures

Updated: Mar 13, 2008

Introduction

Background

The symptoms of chronic bacterial prostatitis (CBP), which is category II in the 1995 NIH prostatitis classification system, are caused by bacterial infection. The nonbacterial form of chronic prostatitis is addressed in the eMedicine article Prostatitis, Nonbacterial. CBP causes an associated symptom complex and is characterized by recurrent urinary tract infections with a single organism that persists in the prostatic fluid.

The prostatitis symptom complex is very common. Approximately half of all men eventually develop symptoms consistent with prostatitis. This symptom complex accounts for approximately 25% of urologic evaluations in men, which is approximately 8% of all urology visits. In fact, the patient appointments for prostatitis outnumber those for cancer or benign prostatic hyperplasia (BPH).

Although the prostatitis symptom complex is not always caused by a bacterial infection, traditional teaching states that bacteria are the cause and require an antibiotic for treatment. This may explain why 50% of the patients with symptoms consistent with CBP are treated with antibiotics, yet only 5-10% of the men actually have a true bacteriologic condition that improves with treatment. Nonetheless, symptom improvement may also be due to a placebo effect or to an anti-inflammatory effect conferred by the antibiotic itself. 

A confounding factor is that fastidious organisms (eg, Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis) can cause prostatitis but do not grow in standard culture conditions; therefore, the condition may be interpreted as nonbacterial prostatitis. Continuing research, using sophisticated research methods, further elucidates that bacterial infection is the cause for more cases of prostatitis. Results from recent studies show that bacterial ribosomal ribonucleic acid (rRNA), by a reverse transcriptase–polymerase chain reaction (RT-PCR), assists in predicting a successful response to antibiotic treatment in patients with chronic prostatitis.

Pathophysiology

The prostate, because of its anatomic configuration, is the reservoir for the recurrent infections.

The normal prostate weighs approximately 18 g and measures 3 cm by 4 cm by 2 cm in length, width, and depth, respectively. It is located in the pelvis, underneath the symphysis pubis at the base of the bladder and on top of the rectum. The prostate is divided into 3 distinct zones, termed the central, transitional, and peripheral zones. These 3 zones fuse into a single glandular structure that completely surrounds the urethra. It is enclosed by a capsule composed of collagen, elastin, and smooth muscle.

The prostate is 70% glandular and 30% fibromuscular stroma. The glandular elements of the prostate are relatively simple tubuloalveolar glands and are lined with simple cuboidal or columnar epithelium. There are approximately 20 of these glands, and they branch out into the fibromuscular stroma. The prostate is innervated by sympathetic nerves from T-10 to L-1.

The peripheral zone of the prostate is composed of a system of ducts with a poor drainage system, which prevents the dependent drainage of secretions. As the prostate enlarges with age, causing obstructive symptoms, the urine refluxes into the prostatic ducts.

Urine reflux also may occur in urethral stricture disease. Refluxing urine, even when sterile, may cause chemical irritation and initiate tubule fibrosis and prostatic stone formation, which then lead to intraductal obstruction and stagnation of intraductal secretions. If trapped in these ducts, the infected material can serve as a nidus for relapsing infections, causing the symptoms of prostatitis. Infection of the prostate occurs via ascending urethral infection or reflux of infected urine into the prostatic ducts.

Infection often persists because antibiotics do not easily penetrate the prostate and no active transport mechanism exists whereby antibiotics can enter the prostatic ducts. Therefore, antibiotics depend on passive diffusion to enter the epithelial-lined prostatic glandular acini. The epithelial cells do not allow the free passage of antibiotics unless they meet certain criteria, ie, un-ionized, lipid-soluble, and not firmly protein-bound.

Another inhibiting factor is that prostatic fluid is acidic (pH of 6.4) compared with plasma (pH of 7.4), thus creating a pH gradient that further inhibits diffusion of acidic antibiotics into the prostatic fluid. Basic antibiotics are able to dissociate and concentrate in the prostatic fluid because of ion trapping within the prostatic fluid due to the pH gradient. Therefore, the best antibiotics for use in prostatitis have high dissociation constants (ie, measure of acid strength), are basic instead of acidic, and are not tightly protein-bound. This combination can allow up to a 6-fold higher concentration of antibiotic in the prostatic fluid compared to plasma.

Natural host defenses that prevent prostatitis include the flushing of the prostatic urethra by emptying the bladder, ejaculation, and the presence of a zinc-rich antibacterial polypeptide that has antibacterial effects against gram-positive and gram-negative bacteria. The prostate has the highest level of zinc concentration of any organ. Healthy men have very high zinc levels, whereas men with CBP have low prostatic zinc levels and normal serum zinc levels. Interestingly, oral zinc supplementation does not increase the prostatic zinc levels in men with CBP.

Spermine and spermidine are also natural host defenses in prostatic fluid. These impart the characteristic odor on ejaculate, and their antibacterial activity is directed mainly at gram-positive bacteria.

Frequency

United States

At some point in their lives, 35-55% of men have prostatitis symptoms. This accounts for approximately 25% of the men evaluated for a urologic problem, which is approximately 8% of all urology visits.

Mortality/Morbidity

  • Prostatitis impairs the patient's quality of life to the same degree as coronary artery disease or Crohn disease.
  • Recent studies show that prostatitis has the same effect on a patient's mental health as does diabetes mellitus and congestive heart failure.1

Age

  • Symptoms of prostatitis are very common in men aged 36-50 years.
  • Prostatitis is the most common urologic problem in men younger than 50 years and the third most common in older men.
  • Recent studies using the US National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) found that the prevalence of prostatitis symptoms was 10% in a population of men aged 20-74 years. See Image 1.

Clinical

History

Patients with chronic bacterial prostatitis (CBP) often present with myriad subjective complaints. Only a few of these complaints offer diagnostic clues for CBP because the complaints are often not of an unusual nature and are not specific for CBP. If culture results are positive, an expressed prostatic secretion (EPS) that contains bacteria or more than 10 WBCs per high-power field (WBCs/hpf) confirms the diagnosis.

  • Genitourinary pain occurs in the perineal area, penile tip, testicles, rectum, lower abdomen, and back.
  • Patients can also have irritative or obstructive urologic symptoms such as frequency, urgency, dysuria, decreased force of the urinary stream, nocturia, and postvoid dribbling.
  • Other symptoms include a clear-to-milky urethral discharge, ejaculatory pain, hematospermia, and sexual dysfunction.

Physical

Physical examination findings are often nonspecific.

  • The classic presentation in a symptomatic patient is an enlarged, soft, or, boggy gland that is moderately-to-severely tender upon palpation.
  • In some cases, an examiner is able to palpate prostatic stones. Because stones may be a nidus for recurrent infections, they may offer a significant clue to the cause of the recurrences.

Causes

Causative organisms include following:

  • Escherichia coli
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
  • Proteus species
  • Staphylococcus species
  • Enterococcus species
  • Trichomonas species
  • Candida species
  • C trachomatis
  • U urealyticum
  • M hominis

More on Chronic Bacterial Prostatitis

Overview: Chronic Bacterial Prostatitis
Differential Diagnoses & Workup: Chronic Bacterial Prostatitis
Treatment & Medication: Chronic Bacterial Prostatitis
Follow-up: Chronic Bacterial Prostatitis
Multimedia: Chronic Bacterial Prostatitis
References
Further Reading

References

  1. McNaughton Collins M, Pontari MA, O'Leary MP, Calhoun EA, Santanna J, Landis JR, et al. Quality of life is impaired in men with chronic prostatitis: the Chronic Prostatitis Collaborative Research Network. J Gen Intern Med. Oct/2001;16(10):656-62. [Medline].

  2. Nickel JC, Shoskes D, Wang Y, Alexander RB, Fowler JE Jr, Zeitlin S, et al. How does the pre-massage and post-massage 2-glass test compare to the Meares-Stamey 4-glass test in men with chronic prostatitis/chronic pelvic pain syndrome?. J Urol. Jul 2006;176(1):119-24. [Medline].

  3. Kaplan SA, Volpe MA, Te AE. A prospective, 1-year trial using saw palmetto versus finasteride in the treatment of category III prostatitis/chronic pelvic pain syndrome. J Urol. Jan 2004;171(1):284-8. [Medline].

  4. Dennis LK, Lynch CF, Torner JC. Epidemiologic association between prostatitis and prostate cancer. Urology. Jul 2002;60(1):78-83. [Medline].

  5. Roberts RO, Bergstralh EJ, Bass SE, Lieber MM, Jacobsen SJ. Prostatitis as a risk factor for prostate cancer. Epidemiology. Jan 2004;15(1):93-9. [Medline].

  6. Association of Genitourinary Medicine, Medical Society for the Study of Venereal Diseases. National guideline for the management of prostatitis. Clinical Effectiveness Group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect. Aug 1999;75 Suppl 1:S46-50. [Medline].

  7. Britton JJ, Carson CC. Prostatitis. AUA Update Series. 1998;17:154-9.

  8. Collins MM, Stafford RS, O'Leary MP, Barry MJ. How common is prostatitis? A national survey of physician visits. J Urol. Apr 1998;159(4):1224-8. [Medline].

  9. Kirby RS, ed. An Atlas of Prostatic Diseases. Boca Raton, Fla: CRC Press; 1997:11-24.

  10. Lipsky BA. Prostatitis and urinary tract infection in men: what's new; what's true?. Am J Med. Mar 1999;106(3):327-34. [Medline].

  11. Litwin MS, McNaughton-Collins M, Fowler FJ Jr, Nickel JC, Calhoun EA, Pontari MA, et al. The National Institutes of Health chronic prostatitis symptom index: developmentand validation of a new outcome measure. Chronic Prostatitis Collaborative Research Network. J Urol. Aug 1999;162(2):369-75. [Medline].

  12. Meares EM. Prostatitis: a review. Urol Clin North Am. 1975;2:3-27.

  13. Nickel JC. Prostatitis. In: Mulholland SG, ed. Antibiotic Therapy in Urology. Philadelphia, Pa: Lippincott-Raven; 1996:57-69.

  14. Schaeffer AJ, Landis JR, Knauss JS, Propert KJ, Alexander RB, Litwin MS, et al. Demographic and clinical characteristics of men with chronic prostatitis: the national institutes of health chronic prostatitis cohort study. J Urol. Aug 2002;168(2):593-8. [Medline].

  15. Shoskes DA, Shahed A. Presence of Bacterial Signal in Expressed Prostatic Secretions Predicts Response to Antibiotic Therapy in Men with the Chronic Pelvic Pain Syndrome. J Urol. 2000;163(4):99A.

  16. Spaine DM, Mamizuka EM, Cedenho AP. Microbiological Aerobic Studies of the Normal Male Urethra. J Urol. 1998;161(4):33A.

Further Reading

For additional information, see Medscape’s Prostatitis Resource Center.

Keywords

chronic bacterial prostatitis, chronic prostatitis, CBP, urinary tract infection, UTI, prostatitis symptom complex, nonbacterial prostatitis, non-bacterial prostatitis, urethral stricture, acute prostatitis, prostatic stones, prostate cancer, urinary stricture disease, bladder neck obstruction

Contributor Information and Disclosures

Author

Sunil K Ahuja, MD, Chief of Minimally Invasive Urology, Department of Urology, Staff Urologist, Santa Teresa Community Hospital
Sunil K Ahuja, MD is a member of the following medical societies: American Urological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf, Jr, MD, FACS, David A Bloom Professor of Urology, Director, Division of Minimally Invasive Urology, Department of Urology, University of Michigan Medical Center
J Stuart Wolf, Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, and Society of University Urologists
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting

Chief Editor

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
Disclosure: Lilly Consulting fee Consulting

 
 
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