Tuberculosis (TB) results from infection by Mycobacterium tuberculosis and can involve any organ or tissue, affecting notably the lungs, heart, bones and joints, central nervous system and intra-abdominal viscera. TB is one of the top ten causes of death overall and the leading cause of death from a single infectious agent [1]. Millions of people continue to contract TB each year. In 2017, TB caused an estimated 1.3 million deaths [1]. Early diagnosis of TB is essential for timely initiation of therapy in order to decrease transmission rate and avoid severe morbidity [1] [2].

As radiologic imaging constitutes an essential part of modern-day TB diagnostic pathway, radiologists’ and clinicians’ ability to promptly recognize various radiological manifestations of tuberculous infection becomes paramount. In the hope to promote physicians’ awareness of the multitude of imaging manifestations of TB throughout the body, we have attempted to provide a concise and yet reasonably comprehensive review of major radiological manifestations of TB in various organs, as summarized in Table 1, using illustrative examples compiled from our collections of clinical cases.

Tuberculosis most commonly affects the lungs [2] [3] [4]. Pulmonary TB is divided into primary and post-primary [5] [6]. Differentiating these two forms can be challenging, as some of their clinical and radiological features overlap.

Primary pulmonary TB occurs when exposure to M. tuberculosis occurs for the first time. Primary pulmonary TB has four most common radiological presentations:

1) Lymphadenopathy, which is usually unilateral and commonly occurs in the paratracheal, hilar and subcarinal regions [4]. On CT, lymphadenopathy is usually more than 2 cm in diameter, with a characteristic “rim-sign”, consisting of an enhancing rim, due to granulomatous inflammatory tissue, and a low-attenuation center resulting from caseous necrosis [5] [6] (Figure 1).

2) Lung parenchymal involvement, frequently presenting as a dense, homogeneous consolidation, preferentially involving lower and middle lobes [7] (Figure 2). Multi-lobar consolidations are seen in 25% of cases [5]. TB consolidations are indistinguishable from consolidations of bacterial pneumonia.

The site of primary TB lung involvement is known as a Ghon focus, which commonly heals with residual calcified granuloma. If a Ghon focus is associated with ipsilateral hilar lymphadenopathy, it is known as the Ghon’s complex or primary complex. Calcified Ghon’s complex is known as a Ranke complex and its presence is strongly suggestive of previous TB [6] (Figure 3).

3) Pleural effusion, which is commonly unilateral and complex. Tuberculous effusions are more often found in primary (25%) than in post-primary TB (18%) [2]. Pleural effusion is commonly on the same side as the primary focus of TB (Figure 4). Pleural thickening and pleural enhancement can be seen with TB empyema [8]. If not treated, TB empyema may be complicated by broncho-pleural fistula or extension to the chest wall, the latter known as empyema necessitans [8]. After treatment, residual pleural thickening with calcification can develop and may lead to formation of fibrothorax [2] (Figure 5).

4) Miliary TB, which represents pulmonary dissemination of the disease by hematogenous spread, occurring in 1% - 7% of patients with all forms of TB, and presenting as granulomata 1 - 4 mm in diameter, randomly distributed throughout lungs [8] (Figure 6).

Post-primary pulmonary TB occurs as either reactivation of a latent primary infection or as a repeated infection. The classic features of post-primary TB include upper lung zones distribution, cavitation and absence of lymphadenopathy. Post-primary TB can have the following radiologic presentations:

1) Pulmonary parenchymal involvement, presenting as a poorly-defined consolidation with predominance in the apical and posterior segments of the upper lobes and superior segments of the lower lobes [5] (Figure 7). Cavitations are seen in 20% - 45% of post-primary TB patients [8] and can be multiple [5] (Figures 8-10). The most common complication of cavitation is endobronchial spread of infection, resulting in typical “tree-in-bud” appearance, characterized by small centrilobular nodules with concomitant branching opacities [3] (Figure 9). Cavities can rupture into the pleural space, resulting in TB empyema, broncho-pleural fistula or spread to the chest wall. Cavitary lesions can occasionally erode into a pulmonary artery, causing a pseudoaneurysm, called Rasmussen aneurysm [5] (Figure 10).

2) Airway involvement can occur from direct extension from TB infected lymph nodes, endobronchial spread or lymphatic dissemination [5]. Imaging features of airway involvement include long segments of airway narrowing with irregular wall thickening, luminal obstruction resulting in lobar collapse, hyperinflation, obstructive pneumonia, mucous impaction and tree-in-bud opacities (Figure 5).

3) Pleural effusion can occur in 18% of patients with post-primary tuberculosis, is usually small and associated with parenchymal disease [5].

Cardiac tuberculosis is rare and only accounts for 0.5% of extra-pulmonary TB [3]. Most common presentation is pericardial involvement and can be demonstrated by CT as pericardial effusion and irregular pericardial thickening of more than 3 mm [3] (Figure 11).

Abdominal TB can have the following radiologic presentations:

1) Lymphadenopathy, which can be necrotic, is the most common presentation of abdominal TB, accounting for 55% - 66% of cases [9] (Figure 12).

2) Peritoneal tuberculosis, which can present as either wet ascitic, fixed fibrotic and dry plastic types. The most common type, wet ascitic (90% of cases of peritoneal TB) is associated with large amounts of slightly hyperattenuating peritoneal free fluid, often accompanied by peritoneal enhancement [2]. The fibrotic type (60% of cases of peritoneal TB), is characterized by large omental and mesenteric cake-like masses [2] (Figure 13). The dry plastic type is less common, and presents as mesenteric thickening, peritoneal caseous nodules and fibrous adhesions [2].

3) Gastrointestinal tuberculosis is rare. Although it may occur anywhere along the gastrointestinal tract, the vast majority of cases involve the ileo-cecal junction (90%), often extending to the terminal ileum and cecum [9]. CT usually shows concentric thickening of the bowel [3] (Figure 14).

4) Solid organs tuberculosis can involve any visceral organ; however, the genitourinary system is most commonly affected, accounting for 15% - 20% of extra-pulmonary TB [10]. CT findings may include renal parenchymal hypodense lesions, nodules and abscesses, urothelial thickening and enhancement, caliectasis, infundibular strictures and hydronephrosis [10] (Figure 15). Chronic cases may show renal cortical thinning, scarring and calcifications (Figure 16).

Musculoskeletal (MSK) TB is rare, reported in 1% - 3% of cases [3]. The main route of infection is via hematogenous spread from the lungs or activation of latent infection in bone or joint post-trauma [9]. MSK TB is classified into three subclasses:

1) Tuberculous spondylitis (Pott’s disease) is the most common type of skeletal TB, accounting for 25% - 60% of MSK cases [11]. It most commonly affects the thoracic spine and, to a lesser degree, lumbar spine. Infection normally begins in the anterior part of the vertebral body, adjacent to the end-plate and spreads to the intervertebral disk. It then may progress to additional spinal segments and paraspinal tissues and result in formation of paravertebral abscesses [2] [12] (Figure 17).

2) Tuberculous arthritis is characteristically monoarticular, affecting large weight-bearing joints. The imaging findings are nonspecific and include osteopenia, synovitis, soft-tissue swelling, marginal erosions, and cartilage destruction [13] (Figure 18).

3) Tuberculous osteomyelitis is most commonly seen in the metaphysis of long bones, in the pelvis, and small bones of the hands and feet [13] (Figure 19). TB osteomyelitis is difficult to differentiate from chronic pyogenic osteomyelitis, but the presence of osteopenia and relative lack of periostitis or sclerosis around lytic lesions may favor diagnosis of TB. Tuberculous dactylitis, a form of tubercular osteomyelitis (“spina ventosa”), refers to painless involvement of the short tubular bones of hands and feet [14].

Central neural system (CNS) involvement occurs in about 5% of patients with TB and MRI is considered the imaging modality of choice for its diagnosis [3]. TB can involve the CNS in the following ways:

1) Tuberculous meningitis is the most common presentation of CNS TB and usually occurs by haematogenous spread of pulmonary TB. Typical MRI finding is abnormal meningeal enhancement, predominantly involving the basal cisterns [15] (Figure 20). Complications of TB meningitis include deep infarcts due to occlusion of penetrating lenticulo-striate vessels, hydrocephalus and cranial nerve involvement. Spinal TB meningitis can present on MRI as obliteration of the spinal subarachnoid space, and matting of the nerve roots in the lumbar spine region. Contrast-enhanced MRI can show nodular, thick and linear intradural enhancement [15].

2) CNS parenchymal tuberculosis is usually manifested by tuberculomas, which may be solitary, multiple or miliary. On CT and MRI, tuberculomas usually appear as round or lobulated masses with surrounding edema, and can enhance either homogeneously or in a ring-like fashion [15] (Figure 21).

Tuberculosis is still impacting millions of people worldwide. The intention of this review is to familiarize radiologists and clinicians with common radiologic manifestations of TB in various body systems.

The authors declare no conflicts of interest regarding the publication of this paper.

Semionov, A., Lebel, K., Diouf, A. and Pressacco, J. (2022) Tuberculosis: A Head to Toe Radiological Review. Open Journal of Radiology, 12, 207-221. https://doi.org/10.4236/ojrad.2022.124021