| Thoracic | |
| Primary TB | |
| Lymphadenopathy | Usually unilateral; commonly paratracheal, hilar or subcarinal; usually > 2 cm in diameter; can feature “rim-sign”: enhancing rim of granulomatous tissue and a low-attenuation necrotic center |
| Parenchymal involvement | Ghon focus: dense consolidation; preferentially in lower and middle lobes; may heal with residual calcified granuloma; Ghon focus + ipsilateral hilar lymphadenopathy = Ghon’s complex; calcified Ghon’s complex = Ranke complex |
| Miliary TB | Pulmonary hematogenous dissemination: 1 - 4 mm granulomata, randomly distributed throughout lungs |
| Pleural effusion | Commonly on the side of the primary pulmonary focus; pleural thickening/enhancement can be seen with TB empyema; TB empyema may be complicated by broncho-pleural fistula or extension to the chest wall—empyema necessitans; can result in pleural thickening and calcification; may lead to fibrothorax |
| Post-primary pulmonary TB | |
| Parenchymal involvement | Poorly-defined consolidation; apical and posterior segments of upper lobes and superior segments of lower lobes predominance; cavitations are common; endobronchial spread results in “tree-in-bud” appearance; cavities can lead to TB empyema, broncho-pleural fistula, spread to the chest wall and pulmonary arterial pseudoaneurysm |
| Airway involvement | 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 |
| Pleural effusion | Less common than in primary TB; usually small, associated with parenchymal disease |
| Cardiac | |
| Pericardial effusion and irregular pericardial thickening of more than 3 mm | |
| Abdominal | |
| Lymphadenopathy | Most common presentation of abdominal TB; often bulky; can feature “rim-sign” |
| Peritoneal | Wet ascetic (most common): large amounts of slightly hyperattenuating peritoneal free fluid, peritoneal enhancement common; fibrotic type: large omental and mesenteric masses; dry plastic type (less common): mesenteric thickening, peritoneal caseous nodules and fibrous adhesions |
| Gastrointestinal | Vast majority of cases occur at ileo-cecal junction (90%), often extending to terminal ileum and cecum; CT usually shows concentric thickening of the bowel |
| Renal | Parenchymal hypodense lesions, nodules, abscesses; urothelial thickening/enhancement; caliectasis, infundibular strictures, hydronephrosis; may lead to renal cortical thinning, scarring and calcifications |
| Musculoskeletal | |
| Tuberculous spondylitis (Pott’s disease) | Most common in thoracic spine > lumbar spine; usually begins in anterior vertebral body, adjacent to the end-plate and spreads to intervertebral disk; associated paravertebral abscesses are common |
| Tuberculous arthritis | Monoarticular, affecting large weight-bearing joints; imaging findings: osteopenia, synovitis, soft-tissue swellings, marginal erosions, cartilage destruction |
| Tuberculous osteomyelitis | Most common in metaphysis of long bones, pelvis, small bones of hands and feet; common features: osteopenia, relative lack of periostitis or sclerosis around lytic lesions |
| Central nervous system | |
| Tuberculous meningitis | Abnormal meningeal enhancement, predominantly in basal cisterns; may lead to deep infarcts, hydrocephalus, cranial nerve involvement; spinal meningitis: obliteration of spinal subarachnoid space, matting of nerve roots in lumbar region, nodular and linear intradural enhancement |
| CNS parenchymal | tuberculomas: may be solitary, multiple or military; CT and MRI: round or lobulated masses with surrounding edema, can enhance homogeneously or in a ring-like fashion |