eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions

Prostatitis, Tuberculous

Vernon M Pais Jr, MD, Assistant Professor, Department of Surgery, Section of Urology, Dartmouth Medical School
Levi A Deters, MD, Staff Physician, Department of Urology, Dartmouth Hitchcock Medical Center; Jason R Bylund, MD, Resident, Division of Urology, University of Kentucky; Andrew A Wagner, MD, Staff Physician, Department of Surgery, Division of Urology, University of Massachusetts Medical Center

Updated: Jun 26, 2009

Introduction

Background

Tuberculosis (TB) has plagued humankind since antiquity. The effects of TB have been noted in skeletal remains from 4000 BC, and both Hippocrates and Galen described TB's clinical manifestations; however, prostatic TB was not described until the turn of the 20th century.

The most common site of TB infection is the pulmonary tract; however, the genitourinary tract is the most common extrapulmonary site of TB infection (33% of cases). Only 20% of TB prostatitis cases are accompanied by underlying pulmonary infection.¹

Despite optimistic predictions on the eradication of TB in developed nations, the disease continues to pose a major worldwide health problem. In 2006, the World Health Organization reported that more than 2 billion people, roughly one third of the world’s population, are infected with TB and a reported 1.7 million deaths per year are due to TB. Developing nations continue to carry a burden of the disease (83% of total cases), with 9.6 million new cases of TB reported worldwide during 2006. To compound the problem, in both developing and industrialized nations, rates of active TB associated with HIV infection are increasing (8% of total), and the incidence of multidrug-resistant TB is also increasing, with a reported 0.5 million cases during 2006.²

Pathophysiology

The causative agent in tuberculous prostatitis is Mycobacterium tuberculosis, a strictly aerobic nonmotile bacterium. The bacterium grows slowly, dividing only once every 24 hours, and is capable of surviving within immune cells after phagocytosis. Generally, tuberculous prostatitis results from hematogenous dissemination of the mycobacteria from the site of the primary infection. Theories of descending spread via infected urine have been abandoned, largely in light of animal studies demonstrating hematogenous spread and the scarcity of prostatic urethral TB in association with prostatic parenchymal TB.

Frequency

United States

Large autopsy studies from the first half of the 20th century report a 10%-12% incidence of prostatic involvement in men with TB.

International

Direct data are lacking, although extrapolation of the US autopsy data suggests that 10%-12% of men with TB might have prostatic involvement. More recent small series suggest a lower rate of clinically detected prostatic TB.

Mortality/Morbidity

• Mortality directly attributable to prostatic TB has not been reported in the recent literature. A case report described 2 patients with HIV infection who died of disseminated TB during hospitalization. Unsuspected tuberculous prostatic abscesses were noted in both patients during the postmortem examination.
• Male factor infertility, which manifests as decreased ejaculate volume, oligospermia, azoospermia, and leukocytospermia, has been observed in association with tuberculous prostatitis. A perineal urinary fistula may result from tubercular cavern formation within or behind the prostate. Reports note perineal swelling, pain, and discharge preceding the development of the urinary fistula. Prostatic tuberculous abscess formation has been noted, particularly in men with AIDS.

Race

Contemporary studies have not addressed racial distributions of tuberculous prostatitis. Autopsy data published in 1949 evaluated prostatic TB in white and nonwhite patients. Of 169 nonwhite patients with TB, 18 (10.7%) had prostatic involvement during autopsy, compared with 50 of 660 (7.6%) white patients.

Sex

Prostatic TB affects only males.

Age

In 1937, Moore presented the age distribution of 243 cases of prostatic TB. Seventy-nine percent of patients were younger than 50 years. Moore describes this as "a disease of young adults."³ The recent literature is unable to offer as large a view of the age distribution.

Kostakopoulos et al (1998) presented 5 cases of unsuspected prostatic TB, all in patients aged 60-71 years.⁴ Although this starkly contrasts with Moore's earlier data, all 5 cases were incidental findings at the time of transurethral resection of the prostate (TURP), and they do not necessarily reflect the age at which the disease first developed.

Over the last 15 years, case reports of prostatic TB in immunocompetent men note patient ages of 26-85 years. Reported cases of prostatic TB in men with HIV infection document presentation in men aged 30-47 years. Most recently, Kulchavenya and Khomyakov reported on a series of 58 Siberian men with prostatic TB; their mean age was 49 years.⁵

Clinical

History

• The often-incidental finding of tuberculosis (TB) in TURP chips suggests that many men may not have symptoms attributable to prostatic TB.
• Nonspecific symptoms, including irritative voiding, may be the only complaints. Of men with prostatic TB, 50% have dysuria and 40% have perineal pain. Renal TB, which is a common comorbidity, may manifest as flank pain. Significant differential diagnostic overlap requires maintaining a high index of suspicion for prostatic TB, particularly in men with a history of exposure to or infection with TB.
• Patients may present with male factor infertility, a well-described complication of prostatic TB.
• Sterile urethral discharge and terminal hematuria may herald tuberculous prostatitis.
• Perineal pain, swelling, and drainage can account for a less common but more overt presentation. Perineal urinary fistula has been reported.
• The most dramatic presentations of prostatic TB may be those in men with AIDS. To date, 6 cases of tuberculous prostatic abscesses have been reported in men with HIV infection. Unlike the more insidious presentations noted in immunocompetent men, these patients presented with fever, perineal pain, and urinary hesitancy; 2 of the patients also presented with mental status changes.

Physical

• Most patients with prostatic TB in contemporary series have a prostate that may be hard, irregular, nodular, or granular.
• In patients with a prostatic tuberculous abscess, a soft fluctuant mass has been noted.
• Tenderness varies with the acuity of the process.
• Prostatic TB should be suspected in patients who have a draining perineal fistula.

Causes

• Prior infection with TB is the most important risk factor. Historically, 10%-12% of men with TB had pathologic evidence of prostatic involvement during autopsy.
• HIV infection increases the risk for active TB and has been suggested to increase the risk for reactivation of dormant foci.
• Prolonged steroid use and immunosuppressive therapy may increase the risk of reactivation of dormant foci.
• Case reports have described prostatic TB as a complication of intravesical bacillus Calmette-Guérin immunotherapy.⁶

Differential Diagnoses

Other Problems to Be Considered

Fungal infections of the genitourinary tract
Postsurgical granulomatous prostatitis
Post–bacille Calmette-Guérin granulomatous prostatitis

Workup

Laboratory Studies

• Urinalysis: Findings that demonstrate microscopic hematuria, albuminuria, or sterile pyuria should raise suspicion for genitourinary tuberculosis (TB) but do not definitively establish the diagnosis.
• Culture of the urine and semen with drug-sensitivity profiling
  • Acid-fast bacilli (AFB) staining of urine and semen: Standard microbiological identification of prostatic involvement of M tuberculosis relies on culture and AFB staining results of semen and 3 early-morning urine specimens. AFB staining, while rapid, has a reported sensitivity of only 52%.
  • Culture: Although it is the criterion standard for mycobacterial identification, culture may require 10 days to 8 weeks for results. Because of the emergence of drug-resistant strains, sensitivities of the mycobacteria should be determined.
• Polymerase chain reaction (PCR): Genomic amplification of M tuberculosis –specific DNA allows rapid identification of TB. The reported sensitivity and specificity of PCR are 95.6% and 98.1%, respectively. Results can be available within 48 hours.
• Semen analysis: Although it is not a required test, semen analysis may be useful in the evaluation of male infertility associated with prostatic TB. The reported semen analyses of 53 patients with genital TB revealed low volume in 89% of patients and azoospermia or oligospermia in 53% of patients. Significant leukocytospermia was identified in 77.6% of patients with prostatic TB.
• Prostate-specific antigen (PSA): PSA levels are elevated in only one third of patients. In 18 patients from a contemporary series, the median PSA level was 2.7 ng/mL (range, 0.3-31 ng/mL).
• Sputum testing: Patients with confirmed prostatic TB should also undergo sputum testing.

Imaging Studies

• Transrectal ultrasonography (TRUS): In persons with a soft or fluctuant prostate in whom abscess is suspected, TRUS is particularly useful. TRUS allows demonstration and localization of the collection and can then guide transrectal aspiration and drainage of any fluid for culture and microscopic examination.
• Intravenous urography (IVU): An IVU or a CT scan should be obtained to determine the presence of concurrent renal TB. Of patients with prostatic TB, 72% have pathologic evidence of renal TB during autopsy.
• CT scanning/MRI
  • Although they are not first-line studies, descriptions of CT scan and MRI findings in TB prostatitis have been published.
  • On a contrast-enhanced CT scan, prostatic tuberculosis may appear as hypodense lesions within the prostate. Additionally, focal calcifications may be identified.
  • MRI may reveal low signal-intensity lesions suggestive of abscess. These studies may also be useful in delineating the extent of any renal disease.
• Radiography: A chest radiograph should be obtained to document active or chronic pulmonary involvement.

Other Tests

• Intradermal injection of tuberculin purified protein derivative (PPD): When prostatic involvement is suspected in patients without a previous diagnosis of TB, a PPD test is a standard means of documenting exposure. False-negative results are possible, particularly during the 4-6 weeks before hypersensitivity develops and in persons who are immunosuppressed owing to various sources.

Procedures

• Cystourethrography has been used to confirm and delineate the extent of a vesicoperineal fistula associated with prostatic TB.
• Transrectal ultrasound–guided needle biopsies have been used to obtain tissue for a definitive diagnosis of the disease, to monitor response to therapy, and to ensure eradication of the prostatic disease.

Histologic Findings

Upon microscopic examination of prostatic TB samples, characteristic granulomas composed of Langhans multinucleated giant cells and epithelioid cells are noted, usually in association with central regions of caseous necrosis. Note that similar histologic changes can be seen in the prostates of patients treated with intravesical bacillus Calmette-Guérin for transitional cell carcinoma of the bladder.

Treatment

Medical Care

Once the diagnosis of tuberculous prostatitis is confirmed, the treatment is similar to that of other tuberculous infections. Tuberculous prostatitis must be viewed as a systemic disease, and the treatment is primarily medical. Hospitalization is usually unnecessary but may be required to treat noncompliant patients. Patients should be isolated in a negative-pressure room, if available. In addition, the local health department should be notified to aid in identifying patient contacts. Drug susceptibility testing should be performed on the isolates obtained from the prostate.

Surgical Care

Some urologists advocate resection of the prostate, although only medical therapy is usually needed. In patients with obstructive symptomatology, resecting the prostate is reasonable. In addition, in resistant tuberculosis (TB), prostate resection can theoretically lessen the infected tissue burden. Surgical treatment should be undertaken only once antituberculous therapy has been initiated to reduce the risk of exposure to the surgical team.

In persons infected with HIV, prostatic TB can present as an abscess. Surgical drainage of an abscess collection is required. Wolf (1996) and Moreno (1988) have described TRUS-guided needle drainage.^7,8 Trauzzi et al (1994) successfully treated one such patient with transurethral unroofing of the collection.⁹ The surgeon should obtain intraoperative samples of any abscess fluid for AFB staining, culture, and PCR, if available.

Consultations

A consultation with an infectious disease specialist is indicated.

Activity

Advise patients to use condoms during intercourse. Sexual transmission of TB via infected semen has been reported to result in a vaginal tuberculous ulcer.

Medication

To prevent the emergence of resistant organisms, a multidrug regimen is the primary treatment. Resistance to primary antituberculous agents is increased in immigrants from Southeast Asia, China, the Indian subcontinent, and Central America. This has led to more complex empiric regimens. Compliance is difficult because of the length of therapy and the adverse effects; therefore, directly observed therapy is often recommended.

Isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and either ethambutol (EMB) or streptomycin (STP) should be the initial regimen. If the isolate is susceptible to INH and RIF, EMB or STP can be stopped and the 3-drug regimen of INH, RIF, and PZA can be continued for 8 weeks followed by 16 weeks of INH and RIF. Pyridoxine (vitamin B-6) at 25-50 mg/d should be considered in all patients to prevent neuropathy associated with INH use.

If INH resistance is documented, a 3-drug regimen of RIF, PZA, and either EMB or STP should be continued for at least 6 months. Multidrug-resistant tuberculosis (TB) has been isolated, and, if this is the case, patients should be referred to an expert in the treatment of TB disorders. In these cases, therapy usually consists of 3 drugs to which the organism is susceptible.

Initial therapy is similar to that used to treat pulmonary disease. Four drugs are used unless a drug resistance is improbable (eg, INH resistance in the community of <4%, no prior therapy for TB, no exposure to contacts with drug-resistant TB, patient is not from an area of increased resistance). Treatment is usually administered daily or, if a supervised regimen is used, twice weekly.

Successful treatment, documented with negative prostatic biopsy results upon follow-up following a triple-drug regimen of RIF, EMB, and INH for a duration of 6 months, has been reported.

In complicated cases, including recurrent genitourinary TB, prolonged therapy for a total of 9-12 months may be required.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Isoniazid (Laniazid)

Best combination of effectiveness, low cost, and minor adverse effects. First-line drug unless known resistance or another contraindication exists. Note that 50-70% of dose is excreted in urine in 24 h.

Dosing

Adult

5 mg/kg/day PO; not to exceed 300 mg
Alternatively, 15 mg/kg PO 2 times/wk; not to exceed 900 mg

Pediatric

Not established

Interactions

Higher incidence of INH-related hepatitis can occur with daily alcohol ingestion; aluminum salts may decrease INH serum levels (administer 1-2 h before taking aluminum salts); may increase anticoagulant effects with coadministration; may inhibit metabolic clearance of benzodiazepines; carbamazepine toxicity or INH hepatotoxicity may result from concurrent use (monitor carbamazepine concentrations and liver function); coadministration with cycloserine may increase CNS adverse effects (eg, dizziness); acute behavioral and coordination changes may occur with coadministration of disulfiram; coadministration with RIF after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin

Contraindications

Documented hypersensitivity; previous INH-associated hepatic injury or other severe adverse reactions

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor patients with active chronic liver disease or severe renal dysfunction; periodic ophthalmologic examinations during INH therapy are recommended, even when visual symptoms do not occur; peripheral neuropathy, especially in persons predisposed to neuritis (eg, persons who are malnourished, have alcoholism, or have diabetes); pyridoxine deficiency is sometimes observed

Rifampin (Rifadin, Rimactane)

For use in combination with at least 1 other antituberculous drug. Inhibits DNA-dependent bacterial, but not mammalian, RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo or until 6 mo have elapsed from conversion to sputum culture negativity. Eliminated mostly through bile.

Dosing

Adult

10 mg/kg/day PO/IV; not to exceed 600 mg/day

Pediatric

Not established

Interactions

Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with INH may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFT results occur)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Obtain CBC counts and baseline clinical chemistries before and throughout therapy; in liver disease, weigh benefits against risk of further liver damage (monitor transaminases q4wk); interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur; doses >600 mg are not well tolerated; occasional GI, CNS, and cutaneous side effects occur; harmless orange discoloration of bodily secretions can occur

Pyrazinamide (Pyrazinamide)

Pyrazine analog of nicotinamide that may be bacteriostatic or bactericidal against M tuberculosis depending on concentration of drug attained at site of infection. Mechanism of action is unknown. Well absorbed from GI tract and hydrolyzed to active metabolite in liver. Note that 70% is excreted in urine within 24 h. Treat patients with drug-resistant disease with individualized regimens.

Dosing

Adult

15-30 mg/kg/day PO; not to exceed 2 g
Alternatively, 50-70 mg/kg PO 2 times/wk; not to exceed 4 g

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; severe hepatic damage; acute gout

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only in combination with other effective antituberculous agents; inhibits renal excretion of urates; may result in hyperuricemia (usually asymptomatic); perform baseline serum uric acid determinations; discontinue drug if signs of hyperuricemia with acute gouty arthritis occur; perform baseline LFTs (closely monitor in liver disease); discontinue PZA if signs of hepatocellular damage appear; caution in history of diabetes mellitus

Ethambutol (Myambutol)

Diffuses into actively growing mycobacterial cells, such as tubercle bacilli. Impairs cell metabolism by inhibiting synthesis of 1 or more metabolites, in turn causing cell death. No cross-resistance is demonstrated.
Mycobacterial resistance is common with previous therapy. Use in patients who were previously treated in combination with second-line drugs that have not been previously administered.
Absorption is not altered significantly by food. Excreted in urine and feces.

Dosing

Adult

15 mg/kg/day PO
Alternatively, 50 mg/kg PO 2 times/wk

Pediatric

Not established

Interactions

Aluminum salts may delay and reduce absorption (administer several hours before or after EMB dose)

Contraindications

Documented hypersensitivity; optic neuritis (unless clinically indicated)

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Decreased color perception and/or decreased visual acuity; a monthly eye examination should be performed; reduce dose in impaired renal function

Streptomycin

Aminoglycoside that interferes with protein synthesis. For treatment of susceptible mycobacterial infections. Use in combination with other antituberculous drugs (eg, INH, EMB, RIF).
Recommended when less potentially hazardous therapeutic agents are ineffective or contraindicated. Excreted in urine.

Dosing

Adult

15 mg/kg/day IM; not to exceed 1.5 g
Alternatively, 25-30 mg/kg IM 2 times/wk; not to exceed 1.5 g

Pediatric

Not established

Interactions

Nephrotoxicity may be increased with aminoglycosides, cephalosporins, penicillins, amphotericin B, ethacrynic acid, furosemide, and mannitol

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index; not intended for long-term therapy; caution in patients with renal failure who are not on dialysis; caution with myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; vestibular ototoxicity, rash, fever, and urticaria may occur; baseline audiometric tests are advisable with extended therapy

Follow-up

Further Outpatient Care

• Periodically check semen cultures to monitor treatment, and, if results are positive after 3 months, bacterial resistance to the current drug regimen or patient noncompliance should be strongly suspected.
• Histologic follow-up via repeat transrectal ultrasound–guided prostate biopsies has been recommended to ensure the efficacy of treatment.

Inpatient & Outpatient Medications

• See Medication.

Deterrence/Prevention

• Condom use is encouraged to prevent possible transmission to sexual partners.

Complications

• Infertility
• Abscess
• Perineal sinus or fistula
• Sexual transmission

Prognosis

• Most patients with prostatic tuberculosis (TB) can be cured with early treatment with a multiple-drug regimen.

Patient Education

• Condom usage
• For excellent patient education resources, visit eMedicine's Prostate Health Center and Bacterial and Viral Infections Center. Also, see eMedicine's patient education articles Tuberculosis and Prostate Infections.

Miscellaneous

Medicolegal Pitfalls

• Nonspecific symptoms, including irritative voiding, may be the only complaints associated with tuberculous prostatitis. Significant differential diagnostic overlap requires maintaining a high index of suspicion for prostatic tuberculosis (TB), particularly in men with a history of exposure to or infection with TB.
• To prevent the emergence of resistant organisms, a multidrug regimen is the primary treatment. Because of the length of therapy and the adverse effects, maintaining patient compliance is difficult; therefore, directly observed therapy is often recommended.

References

1. Wise GJ, Shteynshlyuger A. An update on lower urinary tract tuberculosis. Curr Urol Rep. Jul 2008;9(4):305-13. [Medline].

2. Tuberculosis facts 2008. 2008. World Health Organization; 2008.

3. Moore R. Tuberculosis of the prostate gland. J Urol. 1937;37:372-384.

4. Kostakopoulos A, Economou G, Picramenos D, et al. Tuberculosis of the prostate. Int Urol Nephrol. 1998;30(2):153-7. [Medline].

5. Kulchavenya E, Khomyakov V. Male genital tuberculosis in Siberians. World J Urol. Feb 2006;24(1):74-8. [Medline].

6. Aust TR, Massey JA. Tubercular prostatic abscess as a complication of intravesical bacillus Calmette-Guérin immunotherapy. Int J Urol. Oct 2005;12(10):920-1. [Medline].

7. Wolf LE. Tuberculous abscess of the prostate in AIDS. Ann Intern Med. Jul 15 1996;125(2):156. [Medline].

8. Moreno S, Pacho E, Lopez-Herce JA, et al. Mycobacterium tuberculosis visceral abscesses in the acquired immunodeficiency syndrome (AIDS). Ann Intern Med. Sep 1 1988;109(5):437. [Medline].

9. Trauzzi SJ, Kay CJ, Kaufman DG, Lowe FC. Management of prostatic abscess in patients with human immunodeficiency syndrome. Urology. May 1994;43(5):629-33. [Medline].

10. Angulo JC, Ramirez JC, Esteban M, et al. Perineal fistulization of genital tuberculosis. J Urol. May 1999;161(5):1576-7. [Medline].

11. Cek M, Lenk S, Naber KG, Bishop MC, Johansen TE, Botto H. EAU guidelines for the management of genitourinary tuberculosis. Eur Urol. Sep 2005;48(3):353-62. [Medline].

12. Fujikawa K, Matsui Y, Fukuzawa S, et al. A case of tuberculosis of the prostate. Scand J Urol Nephrol. Aug 1999;33(4):268-9. [Medline].

13. Gonzalez Tuero J, Alonso de la Campa J, Perez Lacort L, et al. Granulomatous prostatitis. Urol Int. 1988;43(2):97-101. [Medline].

14. Gow JG. Genitourinary tuberculosis. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED, eds. Campbell's Urology. 1998. 7^th ed. Philadelphia, Pa: WB Saunders; 1998:807-836.

15. Hemal AK, Aron M, Nair M, Wadhwa SN. 'Autoprostatectomy': an unusual manifestation in genitourinary tuberculosis. Br J Urol. Jul 1998;82(1):140-1. [Medline].

16. Kochi A. The global tuberculosis situation and the new control strategy of the World Health Organization. Tubercle. Mar 1991;72(1):1-6. [Medline].

17. Lanjewar DN, Maheshwari MB. Prostatic tuberculosis and AIDS. Natl Med J India. Jul-Aug 1994;7(4):166-7. [Medline].

18. Lee Y, Huang W, Huang J, et al. Efficacy of chemotherapy for prostatic tuberculosis-a clinical and histologic follow-up study. Urology. May 2001;57(5):872-7. [Medline].

19. Lubbe J, Ruef C, Spirig W, et al. Infertility as the first symptom of male genitourinary tuberculosis. Urol Int. 1996;56(3):204-6. [Medline].

20. Medical Economics Staff. Physicians' Desk Reference. 55^th ed. Montvale, NJ: Medical Economics Co; 2001.

21. Medlar EM, Spain DM, Holliday RW. Post-mortem compared with clinical diagnosis of genito-urinary tuberculosis in adult males. J Urol. 1949;61:6.

22. Moussa OM, Eraky I, El-Far MA, et al. Rapid diagnosis of genitourinary tuberculosis by polymerase chain reaction and non-radioactive DNA hybridization. J Urol. Aug 2000;164(2):584-8. [Medline].

23. Mundy LM, L'Ecuyer PB. Treatment of infectious diseases. In: The Washington Manual of Medical Therapeutics. 29^th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1998:279-81.

24. Orakwe JC, Okafor PI. Genitourinary tuberculosis in Nigeria; a review of thirty-one cases. Niger J Clin Pract. Dec 2005;8(2):69-73. [Medline].

25. Saw KC, Hartfall WG, Rowe RC. Tuberculous prostatitis: nodularity may simulate malignancy. Br J Urol. Aug 1993;72(2):249. [Medline].

26. Selwyn PA, Hartel D, Lewis VA, et al. A prospective study of the risk of tuberculosis among intravenous drug users with human immunodeficiency virus infection. N Engl J Med. Mar 2 1989;320(9):545-50. [Medline].

27. Sporer A, Auerbach O. Tuberculosis of prostate. Urology. Apr 1978;11(4):362-5. [Medline].

28. Tanagho EA. Specific infections of the genitourinary tract. In: Tanagho EA, McAnich JW, eds. Smith's General Urology. 15^th ed. New York, NY: McGraw-Hill Professional Publishing; 2000:265-81.

29. Veenema RJ, Lattimer JK. Genital tuberculosis in the male: clinical pathology and effect on fertility. J Urol. Jul 1957;78(1):65-77. [Medline].

30. Wang LJ, Wong YC, Chen CJ, Lim KE. CT features of genitourinary tuberculosis. J Comput Assist Tomogr. Mar-Apr 1997;21(2):254-8. [Medline].

Keywords

tuberculous prostatitis, tuberculosis, TB, prostatic TB, prostatic tuberculosis, consumption, phthisis, Mycobacterium tuberculosis, M tuberculosis, prostatic urethral tuberculosis, prostatic urethral TB, prostatic parenchymal tuberculosis, prostatic parenchymal TB, tuberculous prostatic abscess, genitourinary tuberculosis, GU tuberculosis, genitourinary TB

Contributor Information and Disclosures

Author

Vernon M Pais Jr, MD, Assistant Professor, Department of Surgery, Section of Urology, Dartmouth Medical School
Vernon M Pais Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Urological Association, Endourological Society, Sigma Xi, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Levi A Deters, MD, Staff Physician, Department of Urology, Dartmouth Hitchcock Medical Center
Disclosure: Nothing to disclose.

Jason R Bylund, MD, Resident, Division of Urology, University of Kentucky
Disclosure: Nothing to disclose.

Andrew A Wagner, MD, Staff Physician, Department of Surgery, Division of Urology, University of Massachusetts Medical Center
Andrew A Wagner, MD is a member of the following medical societies: American Urological Association
Disclosure: Nothing to disclose.

Medical Editor

Richard A Santucci, MD, FACS, Chief of Urology, Detroit Receiving Hospital; Specialist-in-Chief of Urology, Detroit Medical Center; Chief of Urologic Trauma Surgery, Sinai Grace Hospital; Director, The Center for Urologic Reconstruction; Clinical Professor of Urology, Michigan State College of Medicine
Richard A Santucci, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, and Société Internationale d'Urologie (International Society of Urology)
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

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
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; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching

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