Genitourinary tuberculosis (GUTB) is the second most common form of extrapulmonary tuberculosis after lymph node involvement (Kennedy 1980 kem 2000) and may account for 30 to 41% of non-pulmonary cases. Kidney is usually the primary organ infected in urinary disease, and other parts of urinary tract become involved by direct extension. Epididymis in men and fallopian tubes in women are the primary sites of genital infection ( Mohan A 2001) .
The usual frequency of organ involvememt is kidney, urinary bladder, fallopian tube and scrotum (Balasubramaniam IJP 2000). With the human immuno deficiency virus epidemic, an increasing number of extrapulmonary tuberculosis cases have been reported (Chaisson RE JID 1989, Wolf JS JU 1991). Genitourinary tuberculosis (GUTB) is a disease of young adults, with 60% of the affected patients being between the ages of 20 and 40 years (Heaton ND Br.Jun 1989) with a slight male predominence ( Kollm’s GA AJR 1974, Premkumar A). Renal involvement is rare before the age of 20 years, and signs and symptoms are usually found before the age of 40 years (Becker JA Urol. Radio 1988).
Urinary tuberculosis
Pathology
The kidney is the primary site of involvement in tuberculosis of the urinary tract. Renal tuberculosis progresses in 2 steps: (1) initial seeding and (2) reactivation. Diffuse hematogenous dissemination occurs at the time of initial pulmonary infection in approximately 25% of cases.1,6 The bacilli are trapped in the periglomerular capillaries and cause formation of numerous small abscesses in both kidneys. These cortical lesions are too small to be imaged.7,8 If the cellular immunity of the host is intact, or if antituberculous chemotherapy has been administered for clinically active primary tuberculosis, the organisms stay confined to the cortex with the subsequent formation of multiple small healed granulomas. If host immunity is impaired, reactivation may occur between 5 and 25 years after the initial pulmonary infection.1 Initial cortical foci reactivate and spill organisms into the renal tubules, and these propagate to the papillae through the loop of Henle. 9 In the renal medulla, bacillary proliferation leads to formation of granulomas, caseation, and cavitation.
Massive destruction may produce coalescent granulomas, which produce a mass lesion before they rupture into a calyx. Caseation and cavitation occurs in the mass, resulting in parenchymal cavities. More commonly, this papillary lesion ruptures into the calyceal system. Rarely the parenchymal cavity can extend outward and can rupture, producing a perinephric abscess and (Figure 8) later a fistula to skin. When the cavity ruptures into the calyx, 1 the disease can spread distally by seeding through the urothelial submucosa and lymphatic vessels to the infundibula, renal pelvis, ureter, and urinary bladder. The urothelium becomes inflamed, edematous, and ulcerated with multiple tiny granulomas in the mucosa and submucosa. The areas most severely affected are the sites of anatomic narrowings, such as the infundibula of the calyces, the pelvic ureteric junction, and the ureterovesical junction. 1,6,10 In the urinary bladder, initial changes are cystitis with ulceration, inflammation, and edema of the mucosa. With generalized involvement, the bladder capacity is reduced. Urinary tuberculosis is characterized pathologically by 2 basic processes : (1) destruction and (2) healing by fibrosis, granuloma formation, and calcification.1,10
Clinical features
Patients with tuberculosis of upper urinary tract are usually asymptomatic. Some of them may have recurrent or resistant UTI, sterile pyuria with or without hematuria (Wise GJ Urol. Clin.NA 2003). The hematuria may be gross or microscopic (Gupta NP Jurol 2006). Some may present with flank pain when there is hydronephrosis due to obstruction or perinephric abscess. One rare manifestation is a flank sinus due to a nephrocutaneous fistula. Very rarely a patient may present with renal failure when there is bilateral renal or ureteric involvement. Patients become symptomatic when the urinary bladder is involved. The common symptoms are dysuria, frequency, nocturia, suprapubic pain and heamaturia. The symptoms are chronic and intermittent running for months and years in some patients.
Sonographic features
The various lesions of urinary tuberculosis are seen on sonography and the features are well seen on high resolution sonogragphy using the high frequency probe from 5 to 12 MHz utilizing recent techniques like compound imaging and harmonics. The sonographic features of urinary tuberculosis reflect the pathological process. The salient feature of urinary tuberculosis on sonography is involvement of multiple areas of the urinary tract and visualization of the different stages of the disease in the same patient. The coalescent granumlomas in the renal parenchyma are seen as masses of variable size and echogenicity (2-5). Usually they are seen as masses of mixed echogenicity, with or without necrotic areas of caseation ( Fig.1 and 2).
Some of the granulomas may show punctuate calcifications (Fig.3). Caseation and cavitation in the granuloma is seen as parenchymal cavities of varying size (Fig. 4 -6). Some of them are very close to the calyces distorting them (Fig.4). When the cavity ruptures into the calyx, the communication seen as an echoic tract, between the parenchymal cavity and the calyx (Fig.5A). When there is marked destruction of the papilla, the resulting cavity is seen in continuity with the calyx with a broad communication (Fig.5B). Rarely the sloughed necrosed papilla is seen in the cavity (Fig.7). Very occasionally the cavity extends externally and ruptures into perinephric space, which is seen as a perinephric abscess on sonography (Fig.8). This abscess may extend further into the abdominal wall (Fig.8) and rupture externally resulting in a neurocutaneous fistula (Fig 8), which is seen as a hypoechoic tract (Fig.9) from perinephric space to skin.
The involvement of the collecting system is seen as varying degrees of irregular mucosal thickening in calyces and pelvis (Fig. 6,9 and 10). It is due to inflammation, granulomas, caseation and ulceration of the urothelim .The lesions are seen at sites of anatomic narrowing such as the infundibula of the calyces, the pelviureteric junction and the ureterovesical junction. In the ureter the lesions are seen as mucosal thickening with narrowing of lumen and proximal dilatation (Fig.11). If multiple sites of ureter are involved the lumen of the ureter gives a beaded appearance due to alternate areas of the mucosal thickening (Fig.12) with intervarying dilatation.
Along with these features due to destruction, features due to healing by fibrosis and calcification are also seen which is characteristic of tuberculosis. There are parenchymal scars with or without calcification (Fig. ). The fibrous scarring of the collecting system usually involves the sites of anatomic narrowing. Narrowing of the infundibulum of the calyx produces focal caliectasis. If there is stricture of the pelvis , the characteristic feature seen is uneven or asymmetric caliectasis, which means that some calyces are grossly dilated, some are slightly dilated, and some are not dilated. If all the calyces are involved, there is asymmetric or symmetric dilatation of all the calyces without renal pelvis dilatation (Figure 13).
The fibrosis of the infundibulum and pelvis results in the retraction of some part of the kidney and dilatation of the other part resulting in kinking and distortion of the renal pelvis (Figure 14).11,12 Fibrotic healing of the pelvic ureteric junction results in hydronephrosis (Figure 10) or pyonephrosis (Figure 15). In the ureter, fibrosis leads to single or multiple strictures with hydronephrosis. In the lower ureter, it can result in a straight, rigid tube with a patulous ureteric orifice and vesicoureteric reflux (Figure 16). 9,11.
In the urinary bladder, mucosal tubercles coalesce and produce ulceration and edema, (the common situs at involvement are around the ureteric orifices). Edema of the trigonal mucosa can cause ureteral obstruction (Figure 18). Extensive involvement of bladder mucosa results in a potentially reversible decrease in the capacity of the urinary bladder, most probably due to spasm.
The inflammation progresses to involve the muscular layer, and mural fibrosis causes the bladder to become markedly thickened and contracted resulting in a tumble bladder (Fig. ) . Fibrosis in the region of the trigone may produce a gaping of a ureteric orifice and vesicoureteric reflux (Figure 16).9,11 Calcification of the lesions occurs as part of healing. In the renal parenchyma, this is seen as clumps of punctuating calcification (Figure 3) or a lobar type of calcification deep to a scar (Fig. ).
When the dystrophic calcifications are diffuse and uniform, they are called putty-like calcification, a hallmark of renal tuberculosis. In the collecting system, when focal, it is seen as speckled or curvilinear calcifications in the wall of the calyx (Figure 6), pelvis (Figure 19), and ureter. When large, they produce a cast of most of or the entire kidney.1.6 There may be extensive dystrophic calcification of the hydronephrotic nonfunctioning kidney, resulting in a cast of the kidney, referred to as an autonephrectomy. Confirmation of the diagnosis of urinary tract is by seeing the bacille in smear of urine, growth of bacille in culture of the urine or by biopsy of lesions in urinary bladder. If there is obstruction, eg. ureteric structure, the sample of urine has to be collected proximal to the obstruction.
Differential Diagnosis :
Thus, sonography can visualize a myriad of conditions caused by urinary tuberculosis, and each of these can be caused by other disease processes, such as other forms of papillary necrosis, malignant lesions of the kidney and collecting system, and bacterial cystitis. The major distinguishing feature of urinary tuberculosis on sonography is involvement of multiple areas of the urinary tract and visualization of different stages of the disease in the same patient along with chronic nature of the symptoms.
Genital Tract
The primary site for infection of the genital tract is often the epididymis in men and fallopian tubes in women. The spread is by haematogeneous mode. The infection then spreads to adjacent organs by direct extension (Campell). The sexual transmission of genital tuberculosis (TB) is very rare despite the fact that a man with genital tuberculosis (TB) can have the organisms in the semen (Sutherland et al 1982).
Male genital tract
Prostate
Prostate gland is the next organ in male to be most commonly affected by tuberculosis. The spread is usually hematogeneous. Direct extension of disease from urinary tuberculosis has not been established ( Smith annual urology 13th ed). The disease is characterized pathologically by focal necrosis with caseation and cavitation. The lesions may heal by fibrosis and calcification ( Auerbach O NIC 1940).
The fibrosis around the ejaculatory ducts can result in their obstruction, leading to dilatation of the proximal ductal system including the vas deferens and seminal vesicles ( Rajeevkumar IJU 2000). Rarely, particularly in immuno-compromised patients like AIDS, there may be tuberculous abscess which can proceed to the peri-prostatic region or fistula formation. ( Raksh Kapoor IJU 2009). Most of the patients with tuberculosis of prostate are asymptomatic.
Some of them may have hemospermia. A rare manifestation is fever due to an abscess. Many of them present with infertility, mostly with azoospermia. Sonography of the prostate is done by trans-rectal route. In many patients, sonography fails to reveal any lesion in the prostate. Some may show focal areas of decreased echogenicity. ( Hamrick – Tumor JAJR 1992 Wolf LE Anm. Int.Med.1996).
There may be dystrophic calcifications. Rarely, there may be an abscess in the prostate with or without peri-prostatic collection, which will mimic a pyogenic abscess, particularly in an immuno-compromised state (Tikkakoski J.Cli.Urol. 1993). Very rarely there may be a fistulous tract to the perineum or an air-filled tract extending from prostate to the anal canal indicating an ano-urethral fistula. When patients present with infertility due to obstruction to ejaculatory ducts, sonography will show dilated seminal vesicles associated with dilated tubules in the epididymis.
There may be ectasia of rete testis and epididymal cysts. The appearance of prostatic lesions is nonspecific and may mimic appearances of malignancy or nonspecific infection. A biopsy may not be necessary if the symptoms are chronic or there are additional features of urinary tuberculosis. Otherwise a guided biopsy or aspiration is necessary to prove tuberculosis. In the chronic type of lesions like fibrosis and calcifications, it is almost impossible to prove the infection and it may not be necessary as the treatment is directed towards the effects like relieving the obstruction or correcting the fistula and not tuberculosis.
Epididymal and testicular tuberculosis
Tuberculosis of epididymis results from retrograde extension from the prostate and seminal vesicles or from hematogeneous spread. Less frequently it may be transmitted sexually or due to intra-vesical Bacilli Calmette – Guerin therapy for superficial bladder cancer (4,6,7,10-13) (Aysel JCU 2004). The infection affects the tail of the epididymis first, either because the tail has greater blood supply or because it is the first portion involved by reflux along the vas deference.11,14,16 But Chung et at.7 suggested that the infection more frequently involves the entire epididymis or its head. The testis may become involved secondarily by direct extension, but hematogeneous spread to the testis is rarely possible (2,10,14,15) (JCU 2004).
Seventy percent of patients with tuberculous epididymits have a previous history of tuberculosis 6,17,19. Although earlier reports suggested more incidence of bilateral involvement, recent reports have documented more of unilateral disease 7,11,16,21. The most common symptoms of scrotal tuberculosis are scrotal pain and swelling. Some are insidious and chronic, with painless or only slightly painful, epididymal swelling. 2,4,10,22. Rarely there may be acute presentation 4,9,23. Constitutional symptoms are rare 4,9. The presence of an abscess or sinus formation indicates advanced and wide spread disease 18.
Pathologically, there is necrosis of the tubules followed by caseation and fibrosis. There will be lesions in various stages of development ie. exudative, granulomatous and fibrosis. 9,10 Later there is calcification. When the tunica vaginalis is invaded there is hydrocele.
Sonography of scrotum shows marked heterogenicity in correlation with pathologic components namely caseous necrosis, fibrosis, granulomas and calcifications 9. Tuberculous epididymitis appears as diffusely enlarged heterogeneously hypoechoic epididymis or there may be nodular heterogeneous hypoechoic lesions in epididymis. Rarely the epididymis is diffusely enlarged and homogeneously hypoechoic 2,7,15,16,24. In aggressive infection, there may be an abscess mimicking a pyogenic infection. The abscess may extend into the scrotal wall. When there is a scrotal sinus there may be an echo poor or fluid filled tract extending from epididymis, mostly tail, into the scrotal wall up to the skin 7.
There may be thickening of the scrotal skin, hydrocele, calcification of epididymis and tunica vaginalis 2,7,16. On Colour Doppler Study, there are a few vessels seen in the periphery of epididymis with absence of flow in the focal lesions. In tuberculosis orchitis the common appearance is enlarged testis with multiple small, hypoechoic nodules 7,14. Another feature is blurred separation between the testis and epididymis. Rarely there may be diffuse enlargement of testis with homogeneous or heterogeneous hypoechoic texture. The differential diagnosis for scrotal tuberculosis includes acute nonspecific infection and tumors 2,26,28.
The presence of both epididymal and testicular lesions is suggestive of an infection. In nonspecific infection the clinical feature is acute and involvement is diffuse and homogeneous as opposed to chronic nature and focal heterogeneous lesion of tuberculosis. Occasionally the differentiation may be difficult. The presence of a sinus tract, the lack of response to nonspecific antimicrobial agents and evidence of tuberculosis of rest of the genitourinary system might help to differentiate the two conditions ( long etal JCU 1997). When there is isolated lesion in testis it has to be differentiated from a tumor by biopsy Demsy JCU 1992).
Tuberculosis of Seminal vesicles and vasa deferntia
The tuberculous involvement of seminal vesicles is the rarest from of extra-pulmonary tuberculosis (Estham JA South Med.J 1999). It occurs as a hematogeneous spread or as a secondary involvement from prostatic infection. The course is insidious and patients are usually asymptomatic. Eventually, there is fibrosis and calcification. The disease is usually bilateral and also involves the vasa deferentia because of contiguity, in which case patients present initially with low volume ejaculate and then with infertility and reveal aspermia.
Transrectal Ultrasonography reveals small solid seminal vesicles with or without calcifications. There may be calcification of the vas deferens. There may be single or multiple hypoechoic masses in the vas seen in the spermatic cord. Fibrotic, atrophic seminal vesicles with aspermia have been considered a diagnostic feature of tuberculosis and these patients need not be further evaluated and treated with assisted reproduction (12 Paick J Br.J Uro 2000).
The only condition to be considered in differential diagnosis is congenital absence of vas deferens, which will show an absent seminal vesicle and vas deferens on transrectal ultrasonography and good clinical examination. Kumar R AV 2005. Rarely when there is severe infection particularly in immuno- compromised patients there is abscess of the seminal vesicle, usually involving the prostate also. These patients may present with fever and irritative voiding symptoms. In such patients, transrectal ultrasonography will reveal an abscess of seminal vesicle seen as enlarged seminal vesicle with fluid and debris filled areas in it with or without involvement of prostate and loss of interface between seminal vesicle and prostate.
There may thickening of adjacent wall of urinary bladder. ( Dilip Kumar Pcl IJ Jun 2003). The findings mimic a pyogenic abscess and ultrasound guided aspiration will give proof of tuberculosis.
Female Genital tract tuberculosis
The fallopian tube is the primary site of infection in the female genital tract and the usual route is hematogeneous. Occasionally it may be by lymphatic spread from peritoneal implants or direct extension from an intestinal lesion ( Siegler AM. sem Romit 1979) . The fallopian tubes are affected in 94% of women with genital TB. In most of the patients, there is bilateral tubal involvement but not symmetrically.
The fallopian tubes are thickened with caseous ulceration of the mucosa resulting in ragged contours and diverticular outpouchings of both the isthmus and ampulla (4). As it heals, the tube becomes encased in connective scar tissue and the lumen develops a beaded appearance due to multiple strictures or rigid pipe stem appearance (5). Obstruction of the tube may result in hydrosalphinx (7). In the late stage of diseases, there may be calcification of the tubes – in the form of linear streaks or tiny nodules.
The tubal tuberculosis spreads to the endometrium in about 50 % of cases (5). Pathologically there are two types of female pelvic tuberculosis – the wet and dry (adhesive) types1,5,6. In the ‘wet’ type there is ascites. The peritoneum of the parietal wall and viscera is covered with innumerable small tubercles. The Genitourinary tuberculosis Fallopian Tubes, in addition to being covered with miliary tubercles on the sersoal surface, are usually slightly enlarged and distended.
In Contrast to other forms of salpingitis, the fimbriae may be patent. Within the tubal wall and mucosa, the histology is typical of tuberculosis with tubercle formation, multi-nucleated giant cells and epithelioid reaction. In advanced cases, frank caseation is present. ‘Dry’ (adhesive) tuberculosis may represent the healed fibroitc end result of the wet ascitic pattern. The pelvic organs show evidence of tuberculous salpingitis with enlargement of the tubes and occasionally pyosalpinges and even tubo-ovarian abscess formation. Clinical presentations of female pelvic tuberculosis are extremely varied. They may present with ascites, pelvic pain or pelvic mass with or without constitutional symptoms. Some of them come with infertility.
On Sonography, there is ascites, which is usually septated1,6. The septation may show lattice like appearance. It may show echogenic particles. There may be thickening of greater omentum and parietal as well as visceral peritoneum. With adhesions the ascites may be loculated with thick speta, mimicking an ovarian tumor or tuboovarian abscess. In the dry type, Fallopian tube may show thick walls. It may show distended lumen with irregular thick walls with preserved patency on saline infusion sonohysterography. There may be hydrosalphinx. The involvement of Fallopian Tube is usually bilateral.
Most of these features are seen in ovarian carcinoma or other infections. The occurrence of the combination of these features particularly with septated ascites is in favour of tuberculosis1,6. Laparoscopy and biopsy will confirm tuberculosis. When a patient presents with infertility, Sonography may reveal hydrosalphinx. When Endovaginal Sonography, does not reveal any abnormally saline infusion sonohysterography may reveal either tubal block or abnormal Fallopian Tubes.
Endometrial Tuberculosis
Uterine endometrium is involved in 50% of patients who have tubal tuberculosis12,65 (Premkumar A book – see book Xerox (Siegler Am Semi Roent 1979). It is involved by extension of disease from the Fallopian Tube . It is seen in 11.5% of patients with pulmonary tuberculosis (PK Mukerjee IJTB 1991). The pathology involves granulomas and caseation necrosis, Genitourinary tuberculosis. It later results in shrunken cavity due to adhesions and calcification. The patients present with infertility ( 45 to 55%) and menstrual disturbances (20%) or amenorrhea. Some patients are asymptomatic (Choudry JIMH 1996 Dawn CS Text Brh of G & C 1998). Saline Infusion Sonohysterography is the technique of sonography that can reveal some features of endometrial tuberculosis.
The features which suggest tuberculosis are irregular contour of endometrium, endometrial polyp, synechia and scarred cavity. D & C or Hysteroscopic biopsy has to be done for histological diagnosis. Endometrial calcification is seen as tiny specks of bright echoes in the endometrium. If extensive it can mimick endometrial osseous metaplasia.
