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Specific infections are those caused by particular organisms, each of which cause a clinically unique disease with identifiable pathologic tissue reactions.

Tubercle bacilli may invade one or more (or even all) of the organs of the genitourinary tract and cause a chronic granulomatous infection that shows the same characteristics as tuberculosis in other organs. Urinary tuberculosis is a disease of young adults (60% of patients are between the ages of 20 and 40) and is more common in males than in females.


The infecting organism is Mycobacterium tuberculosis, which reaches the genitourinary organs by the hematogenous route from the lungs. The primary site is often not symptomatic or apparent.

The kidney and possibly the prostate are the primary sites of tuberculous infection in the genitourinary tract. All other genitourinary organs become involved by either ascent (prostate to bladder) or descent (kidney to bladder, prostate to epididymis). The testis may become involved by direct extension from epididymal infection.

Pathogenesis (Figure 15–1)

Figure 15–1.

Pathogenesis of tuberculosis of the urinary tract.

Kidney and Ureter

When a shower of tubercle bacilli hits the renal cortex, the organisms may be destroyed by normal tissue resistance. Evidence of this is commonly seen in autopsies of persons who have died of tuberculosis; only scars are found in the kidneys. However, if enough bacteria of sufficient virulence become lodged in the kidney and are not overcome, a clinical infection is established.

Tuberculosis of the kidney progresses slowly; it may take 15–20 years to destroy a kidney in a patient who has good resistance to the infection. As a rule, therefore, there is no renal pain and little or no clinical disturbance of any type until the lesion has involved the calyces or the pelvis, at which time, pus and organisms may be discharged into the urine. It is only at this stage that symptoms (of cystitis) are manifested. The infection then proceeds to the pelvic mucosa and the ureter, particularly its upper and vesical ends. This may lead to stricture and obstruction (hydronephrosis).

As the disease progresses, a caseous breakdown of tissue occurs until the entire kidney is replaced by cheesy material. Calcium may be laid down in the reparative process. The ureter undergoes fibrosis and tends to be shortened and therefore straightened. This change leads to a “golf-hole” (gaping) ureteral orifice, typical of an incompetent valve.


Vesical irritability develops as an early clinical manifestation of the disease as the bladder is bathed by infected material. Tubercles form later, usually in the region of the involved ureteral orifice, and finally coalesce and ulcerate. These ulcers may bleed. With severe involvement, the bladder becomes fibrosed and ...

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