Hidden in plain sight: Extrapulmonary manifestations of tuberculosis in Asia

Nodal tuberculosis

Nodal tuberculosis is the most common form of extrapulmonary tuberculosis and can practically involve any region in the body, most commonly the cervical region. Contrast-enhanced CT is the most common modality in imaging thoracic and abdominal lymphadenopathy, allowing assessment of the lungs and solid organs as well. While nonspecific enlargement occurs in the acute stage, later caseous necrosis causes centrally hypodense nodes with peripheral rim enhancement characteristic for tuberculosis. In the chronic stage, nodes typically demonstrate coarse calcification. While differentials for thoracoabdominal lymphadenopathy are vast, features such as necrosis/rim enhancement, perinodal streaking and conglomeration raise suspicion for tuberculosis (Figures 1–2).

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Figure 1.

Coronal contrast-enhanced CT neck showing multiple, bilateral peripherally enhancing, necrotic cervical lymph nodes (white arrows) in a middle-aged man with tuberculosis.

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Figure 2.

Axial contrast-enhanced CT images showing enlarged mesenteric node with perinodal streaking (white arrow) in a young woman with gastrointestinal tuberculosis.

Tuberculous pleurisy

Tuberculous pleurisy is the second most common manifestation of extrapulmonary tuberculosis after lymphatic involvement. It is postulated to be directly inoculated from rupture of a subpleural infective focus in the lung into the pleural space. Imaging findings range from pleural effusion with minimal pleural thickening, empyema with nodular thickening or enhancing soft tissue, to late-stage fibrous tissue and calcification (fibrothorax). Rare complications such as empyema necessitatis (decompression through the chest wall or formation of a bronchopleural fistula) or pleural malignancy may occur in chronic tuberculous empyema ² (Figure 3).

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Figure 3.

Coronal contrast-enhanced CT images of a middle-aged man who presented with 1-month of cough, shortness of breath and pleuritic chest pain. CT shows large left pleural effusion, with multiple areas of pleural nodularity (white arrows).

Tuberculous pericarditis

Tuberculous pericarditis is relatively uncommon but can lead to heart failure, constrictive pericarditis or death. ³ It can manifest as pericardial effusion, constrictive pericarditis, or a combination of both. ⁴ Typical CT findings are pericardial effusion, thickening, enhancement and/or calcification. While 2D echocardiography is frequently used as first-line imaging in the evaluation of pericarditis, CT is superior in the context of suspected tuberculous pericarditis in that it offers higher sensitivity for subtle pericardial calcium frequently associated with constrictive pericarditis and simultaneously allows evaluation of the lungs for concomitant tuberculosis (Figure 4).

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Figure 4.

Axial contrast-enhanced CT image on the left (a) of a patient demonstrating nonspecific pericardial effusion (thin white arrow) without pericardial thickening. Contrast-enhanced CT image 4 months later on the right (b) demonstrating diffusely thickened pericardium and abnormal enhancement (thick white arrow).

Tuberculous aortitis

Infection of the aortic wall with tuberculosis is rare, but risk increases with underlying disease of the aorta such as atherosclerosis or trauma. There is a predisposition for infection in the distal aortic arch and the descending thoracic aorta, where the vessel may be involved through direct extension from adjacent mediastinal lymphadenopathy, empyema, or paraspinal abscesses. Mycotic aneurysms which demonstrate irregular saccular outpouchings and thickening of the aortic wall and “cold abscesses” may perforate and lead to mortality (Figure 5).

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Figure 5.

Axial contrast-enhanced CT of an elderly lady with disseminated tuberculosis. Thickening of the posterior wall of the descending thoracic aorta is inseparable from the adjacent “cold abscess”—an irregular rim-enhancing collection (white arrow) with minimal fat stranding extending into the adjacent left paravertebral musculature causing bony rib erosion (not pictured).

Peritoneal tuberculosis

Peritoneal tuberculosis is the most common presentation of abdominal tuberculosis. ⁵ It is classically classified into three types according to its macroscopic aspects: [1] Wet type, with predominant findings of free or loculated ascites, associated with diffuse and smooth peritoneal thickening. [2] Dry type, with predominance of nodular peritoneal and mesenteric thickening, lymph node enlargement and fibrinous adhesions. [3] Fibrous type, predominance of marked omental thickening and clustering of bowel, which may present as a mass on clinical palpation.

Peritoneal carcinomatosis is the main differential and is frequently radiologically indistinguishable from tuberculosis. Tuberculosis should be considered in the presence of necrotic lymph nodes or absence of a known primary tumor in young patients. Smooth peritoneal thickening favors tuberculosis, while nodular, irregular peritoneal thickening and omental caking are more common in peritoneal carcinomatosis. However significant overlap in imaging and clinical findings typically requires histology or definitive microbiology to confirm the diagnosis ⁵ (Figures 6–7).

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Figure 6.

Axial CT images of an elderly man who presented with unintentional loss of weight, demonstrating diffuse peritoneal nodular thickening with discrete peritoneal nodules (white arrows). Peritoneal biopsy found granulomatous inflammation.

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Figure 7.

Contrast-enhanced axial CT of a young female patient showing wet-type peritoneal disease, with free fluid in the pelvis (thin white arrow) and smooth peritoneal thickening (thick white arrow). Bilateral adnexa are notably normal. Omental biopsy demonstrated necrotizing granulomatous inflammation with acid fast bacilli, compatible with tuberculosis.

Gastrointestinal tuberculosis

Though tuberculosis may involve any segment of the gastrointestinal tract, the ileocecal region is affected in up to 90% of cases. ⁶ This is likely attributable to the abundance of lymphoid tissue and relative stasis. ⁷ Main imaging findings of gastrointestinal tuberculosis include ileocecal involvement, diffuse wall thickening, mesenteric thickening, skip lesions in the bowel, and necrotic abdominal lymphadenopathy. Complications include obstruction, perforation, fistulation, intestinal bleeding, and rarely intussusception. ⁷ The differentials include Crohn’s disease, lymphoma, adenocarcinoma and amebiasis (Figure 8).

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Figure 8.

Coronal oblique contrast-enhanced CT images (arterial phase) (a) of a young patient with recurrent subacute intestinal obstruction. Segmental thickening and hyperenhancement of the ascending colon (white arrowhead), ileocecal valve (black arrow), terminal ileum (thin white arrow), compatible with inflammation. Multiple enlarged pericolic and mesenteric nodes (b) (circle). A skip lesion in the splenic flexure is also seen (thick white arrow).

Hepatobiliary tuberculosis

Broadly, imaging findings of hepatic tuberculosis may be categorized into [1] miliary pattern, [2] macronodular pattern (>2 cm) with tuberculomas, [3] abscesses and [4] biliary tuberculosis. ⁸

On CT, miliary lesions appear as microabscesses in the form of multiple small foci with low attenuation, and can be challenging to differentiate from metastases, lymphoma or other granulomatous diseases.

Macronodular tuberculomas appear as hypodense lesions with no or minimal enhancement on CT. Calcification may be present in chronic tuberculomas, typically coarse and occasionally involving the entire lesion. On MRI, tuberculomas are typically T1w hypointense, with variable T2w signal.

Frank caseous necrosis and liquefaction of macronodular tuberculomas leads to the formation of abscesses. Rupture may be complicated by infective peritonitis or portal vein thrombus. ⁹

Biliary tuberculosis can either be due to primary involvement of the biliary tree or secondary to compression by enlarged periportal nodes. Imaging findings can vary from bile duct thickening, biliary dilatation and strictures to frank obstructive biliopathy. Miliary calcifications along the bile ducts have been described as one of the characteristic features of tubercular cholangitis. ¹⁰ As findings overlap with cholangiocarcinoma, follow-up for resolution after treatment is typically advised (Figures 9–10(b)).

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Figure 9.

Axial contrast-enhanced CT image (a) of a middle-aged female presenting with painless jaundice and weight loss. CT demonstrates subcapsular segment V hypodensity with coarse central calcification compatible with tuberculoma (white arrowhead). Bilobar tubular structures are compatible with dilated intrahepatic ducts (thin white arrows). Low-density necrotic periportal nodes were also present (not pictured). ¹⁴ T2w coronal MRCP (b) showing dilated intrahepatic ducts and multiple biliary strictures (thick white arrows).

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Figure 10.

(a) Axial contrast-enhanced CT images (A) of an elderly man demonstrating a hypoenhancing hepatic mass (thick black arrow) centered in the caudate lobe. T2w axial MRI image (B) showing corresponding predominantly T2w isointense hepatic mass (thin white arrow) in the caudate lobe. T2w MRCP (C) demonstrating biliary obstruction at the level of the hepatic duct confluence (thick white arrow) from the caudate lobe lesion. Subsequent percutaneous transhepatic cholangiogram (D) demonstrates corresponding obstruction at the common hepatic duct (thin black arrow). Biliary fluid PCR tested positive for tuberculosis. This stricture was successfully crossed with a drainage catheter. (b) Follow-up MRCP 3 months after placement of biliary stent and tuberculosis treatment shows improvement in stricture and reduced dilatation of the right hepatic ducts (white arrow).

Renal tuberculosis

Renal parenchymal involvement in tuberculosis in the acute phase may have similar appearances as pyelonephritis caused by other organisms, showing ill-defined edema or striation. Parenchymal granulomas may demonstrate minimal to no enhancement; when mass-like, these may mimic renal neoplasms. ¹¹ Tuberculous “cold abscesses” may present with much milder perilesional edema compared to bacterial abscesses and may mimic cysts or cystic neoplasms.

Chronic tuberculous glomerulonephritis leads to healing and fibrosis and may eventually lead to autonephrectomy. Dystrophic calcifications typically appear, ranging from punctate foci to complete replacement of the renal parenchyma, referred to as “putty kidney” ¹¹ (Figure 11).

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Figure 11.

Coronal CT image on the left (a) demonstrating atrophic left kidney with coarse parenchymal calcifications in the “putty kidney” appearance of end stage renal tuberculosis. Similar calcification at the right midpole. 3D coronal CT reconstruction of the same patient on the right (b).

Ureteric tuberculosis

Ureteric tuberculosis typically results from contiguous spread of renal tuberculosis down the collecting systems from the renal pelvis. Early infection can cause ulcerations leading to mucosal irregularity, wall thickening and enhancement with periureteral stranding, similar to infectious ureteritis. However, tuberculous ureteritis may cause intraluminal filling defects from mucosal tuberculomas and typically has a more indolent onset. Fibrosis occurring in late stages can result in multifocal strictures, leading to a beaded appearance which is characteristic of ureteric tuberculosis (Figure 12). Another important differential to consider in the setting of ureteric wall thickening is transitional cell carcinoma, which typically manifests as focal asymmetric wall thickening without significant periureteral fat stranding, compared to the long-segment nodular involvement in ureteric tuberculosis. ¹¹

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Figure 12.

Coronal contrast-enhanced CT image on the left (a) of a patient with long-segment circumferentially thickened right ureter with irregular beading (thin white arrow), causing right hydronephrosis. Axial image on the right (b) of the same patient demonstrating and delayed enhancement in the right kidney (thick white arrow).

Male genitourinary tuberculosis

Isolated male lower genital tract involvement by tuberculosis is exceedingly rare and usually due to spread from renal or pulmonary tuberculosis. Special risk factors include intravesical infusion of Bacillus Calmette-Guérin (BCG) vaccine for bladder urothelial cancer and prostatic interventions (e.g., TURP). MRI is the modality of choice for prostatic evaluation and further can illustrate nodular and diffuse morphologies of tuberculosis. In the diffuse type, streaky low T2w signal intensity is seen in the peripheral zone, described as the watermelon skin sign. ¹¹

In the nodular type, granulomas show low T2w signal intensity and restricted diffusion and enhancement, which are indistinguishable from prostatic adenocarcinoma.

Caseous necrosis of prostatic tuberculomas can form abscesses, which are demonstrable on both CT and MRI, with irregular and peripherally enhancing cystic foci seen on CT. On MRI, abscesses demonstrate “dirty” high T2w signal, restricted diffusion and rim enhancement (Figure 13).

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Figure 13.

Axial contrast-enhanced CT image (a) of an elderly man with recurrent sterile pyuria not responsive to antibiotics. CT showed focal hypodensity within the posterolateral right prostatic lobe (white arrow), worrying for abscess. Follow-up multiparametric MRI prostate was performed. Post-contrast T1w fat saturated axial MRI image (b) more clearly illustrating the irregular peripheral enhancement of the right prostatic lobe abscess (white arrowhead). Axial T2w MRI image (c) show corresponding dirty high signal in the right posterior peripheral zone (thin black arrow). The rest of the peripheral zone demonstrates streaky low T2w hypointensities suggestive of prostatitis. Diffusion weighted imaging (DWI) (d) and corresponding apparent diffusion coefficient (ADC) (e) shows multifocal areas of restricted diffusion in the right posterior peripheral zone abscess (white chevrons). Other smaller foci of disease, for example, anterior left lobe (thick white arrows), were not detected on the other sequences. Granulomatous prostatitis was raised as a differential, and the patient was empirically treated with Rifampicin, Isoniazid, Ethambutol and Pyrazinamide (RHEZ). Follow-up MRI 6 weeks later of the same patient demonstrating resolution of abscesses on DWI (f) (thick black arrow).

Tuberculous involvement of the epididymis and testes occurs from hematogenous seeding, lymphatic spread, or contiguous extension from the lower urinary tract. Owing to its rich blood supply, tuberculous epididymitis typically begins at the tail of the epididymis, and gradually invade the body and head, and if left untreated, may spread to the testes. Sonographic features of tuberculous epididymitis may include heterogeneously hypoechoic and nodular lesions of the involved segment due to formation of caseating granulomas, and in late stages may present as abscesses (Figure 14). Other associated sonographic findings include thickened scrotal skin, hydrocele and intrascrotal extra testicular calcification. ¹²

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Figure 14.

Grayscale ultrasound examination of the scrotum in the top row (a), (b) shows a heterogeneous hypoechoic lesion in the right epididymal tail (white arrows). On Color flow Doppler ultrasound examination of the scrotum in the bottom row (c), (d) there are areas of peripheral vascularity (white arrowheads). Cross-sectional imaging of the same patient found hydronephrosis and ureteric strictures (not shown). The reporting radiologist raised genitourinary tuberculosis with epididymal granulomatous abscesses due to chronicity of disease and lack of response to prior antibiotic treatment.

Spinal tuberculosis

Radiologic manifestations of spinal tuberculosis include intraosseous and paraspinal abscess formation, subligamentous spread of infection, vertebral body destruction and collapse, and extension into the spinal epidural space. The relatively avascular intervertebral disc can be spared until late stages of the disease, as tuberculous bacilli do not produce proteolytic enzymes, in contrast to pyogenic infection where the disc is typically involved early in the disease.

Common conditions that mimic spinal tuberculosis include pyogenic spondylitis, Andersson’s lesion in ankylosing spondylitis, rheumatoid arthritis, and metastases. Important features favoring metastases include history of malignant tumor, posterior element destruction, absence of sequestrum, and absence of subligamentous spread ¹³ (Figure 15).

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Figure 15.

Sagittal T1w MRI image of an elderly man who presented with chronic back pain, demonstrating generalized hypointense signal of the L3 and L4 vertebrae (a) (thin white arrows), that demonstrates florid enhancement on T1w post-contrast image (b) (thick white arrows). Small epidural enhancing collection is seen at the level of L3 (white arrowhead) with associated narrowing of the spinal canal. Sagittal STIR MRI image (c) demonstrates marrow edema in the L3 and L4 vertebrae (white chevrons). Subsequent tissue histology from the L3/4 disc space yielded granulomatous inflammation with acid fast bacilli present.