Updated: Nov 21, 2008
Tuberculosis has plagued humankind since before recorded history. The story of humankind's battle against tuberculosis parallels that of the development of the practice of medicine in general. Although largely controlled in developed countries, tuberculosis remains a significant worldwide health problem because of the incidence in developing countries. Genitourinary tuberculosis represents 2-4% of cases of tuberculosis or approximately 15% of nonpulmonary manifestations of tuberculosis. Genitourinary tuberculosis is the most common extrapulmonary site of tuberculosis.1
The spread of tuberculosis to the epididymis is thought to occur hematogenously or by retrocanalicular descent of organisms from the hematogenously infected prostate. Because epididymal tuberculosis is more common than prostatic tuberculosis, hematogenous spread is likely more common. Distal spread through the genitourinary tract from a renal source is also possible.
In very rare cases, tuberculous epididymitis has been reported following intravesical bacille Calmette-Guérin (BCG) therapy for superficial bladder tumors, presumably due to retrocanalicular descent of organisms from the prostatic urethra.2,3,4
The formation of granulomas in the epididymis is responsible for the clinical manifestations of epididymal tuberculosis, as in other organ systems.
Approximately 4000 cases of extrapulmonary tuberculosis are reported annually in the United States. This incidence is stable, despite a decreasing incidence of pulmonary tuberculosis. Much of the increase in the relative incidence of genital tuberculosis can be attributed to tuberculosis in men with HIV infection, which apparently predisposes to tuberculosis.
The incidence of tuberculosis in some developing countries is 30 times greater than that in the United States. In developing countries, the percentage of cases of tuberculosis with genitourinary involvement is approximately double that in developed areas.
In developed countries, most cases of tuberculosis are observed in the immigrant population. Only 20% occur in white people.
Epididymal tuberculosis most commonly develops in sexually active young men. Before the age of antituberculous chemotherapy, the typical patient was aged 16-40 years. Now, more than 70% of men with genital tuberculosis are older than 35 years, and 15-20% are older than 65 years.
| Epididymitis | Testicular Seminoma |
| Hydrocele | Testicular Torsion |
| Scrotal Trauma | Testicular Trauma |
| Spermatocele | Testicular Tumors: Nonseminomatous |
Testicular teratocarcinoma
Histologic findings of tuberculous epididymitis are similar to those of tuberculosis elsewhere in the body (granuloma formation, nonspecific inflammatory infiltrate). Additionally, mycobacteria are present.
Consultation with an infectious disease specialist is recommended for physicians who are not familiar with the treatment of tuberculosis.
The chemotherapy used to treat tuberculosis has changed over the past few decades. Currently, a 4-month course generally is recommended for genitourinary tuberculosis. Two alternative regimens are provided, as follows:
Any regimen must contain multiple drugs to which the Mycobacterium tuberculosis (MTB) is susceptible. In addition, the therapy must be taken regularly and continued for a sufficient period.
This pyrazine analogue of nicotinamide is absorbed well from the GI tract. Its half-life is 9-10 h with normal renal and hepatic function. May be bacteriostatic or bactericidal against MTB, depending on the concentration of drug attained at site of infection.
25 mg/kg/d PO; not to exceed 2 g PO qd
Administer as in adults
Reported to produce a pink-brown color with some urine test strips
Documented hypersensitivity; severe hepatic damage; acute gout
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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 pyrazinamide if signs of hepatocellular damage appear; caution in history of diabetes mellitus
The hydrazide of isonicotinic acid. Within 1-2 h of oral administration, produces peak blood levels, which decline to 50% or less within 6 h. Isoniazid acts against actively growing tubercle bacilli. Isoniazid-resistant MTB bacilli develop rapidly when isoniazid monotherapy is administered.
5 mg/kg PO/IM up to 300 mg qd or 15 mg/kg up to 900 mg/d 2-3 times/wk
10-15 mg/kg PO/IM up to 300 mg qd or 20-40 mg/kg up to 900 mg/d 2-3 times/wk
Higher incidence of isoniazid-related hepatitis can occur with alcohol ingestion on daily basis; aluminum salts may decrease isoniazid 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 isoniazid 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 rifampin after halothane anesthesia may result in hepatotoxicity and hepatic encephalopathy; may inhibit hepatic microsomal enzymes and increase toxicity of hydantoin
Documented hypersensitivity; previous isoniazid-associated hepatic injury; severe adverse reactions to isoniazid such as drug fever, chills, or arthritis; acute liver disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor patients with active chronic liver disease or severe renal dysfunction; periodic ophthalmologic examinations during isoniazid therapy are recommended even when visual symptoms do not occur
Semisynthetic antibiotic derivative of rifamycin SV. Readily absorbed from gastrointestinal tract. In healthy adults, half-life of rifampin in serum averages 3-4 h after a 600-mg oral dose, with increases up to 4-6 h reported after a 900-mg dose. With repeated administration, the half-life decreases and reaches average values of approximately 2-3 h. Has bactericidal activity against both intracellular and extracellular MTB organisms.
10 mg/kg PO/IV qd; not to exceed 600 mg/d
10-20 mg/kg PO/IV; not to exceed 600 mg/d
Rifampin is known to induce certain cytochrome P-450 enzymes, adjusting the dosages of the following drugs may be necessary: anticonvulsants, antiarrhythmics, oral anticoagulants, antifungals, barbiturates, beta-blockers, calcium channel blockers, chloramphenicol, clarithromycin, corticosteroids, cyclosporine, cardiac glycoside preparations, clofibrate, oral or other systemic hormone contraceptives, dapsone, diazepam, doxycycline, fluoroquinolones, haloperidol, oral sulfonylureas, levothyroxine, methadone, narcotic analgesics, nortriptyline, progestins, quinine, tacrolimus, theophylline, tricyclic antidepressants, and zidovudine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Obtain CBCs and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; 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
A water-soluble aminoglycoside derived from Streptomyces griseus. Following intramuscular injection of 1 g of streptomycin as sulfate, a peak serum level of 25-50 mcg/mL is reached within 1 h, diminishing slowly to about 50% after 5-6 hours. Excreted by glomerular filtration. Streptomycin sulfate is a bactericidal antibiotic active against many organisms, including MTB.
15 mg/kg IV qd maximum 1 g
20-40 mg/kg IV qd maximum 1 g
Nephrotoxicity may be increased with aminoglycosides, cephalosporins, penicillins, amphotericin B, and loop diuretics
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Narrow therapeutic index; not intended for long-term therapy; caution in renal failure not on dialysis; caution with myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission
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epididymal tuberculosis, epididymal TB, tuberculous epididymitis, genital tuberculosis, genital TB, genitourinary tuberculosis, genitourinary TB, mycobacterial tuberculosis, Mycobacterium tuberculosis, MTB, granulomas, extrapulmonary tuberculosis, nonpulmonary tuberculosis, extrapulmonary TB, nonpulmonary TB, male genital tuberculosis, male genital TB
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
Martha K Terris, MD, FACS, Professor, Department of Surgery, Medical College of Georgia
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Urological Association, New York Academy of Sciences, and Society of University Urologists
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
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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