Post-primary pulmonary tuberculosis

Last revised by Liz Silverstone on 22 Feb 2024

Post-primary tuberculosis is also known as reactivation tuberculosis or secondary tuberculosis. The typical upper zone predominant destructive pneumonia is due to an adaptive immune response in an immunocompetent host 1.

Pathology

Location

The upper zone predominance of pulmonary cavitation can explained by the relatively high oxygen tension and poor lymphatic drainage. Cavities commonly occur in:

  • the apical and posterior upper lobe

  • the superior segment of the lower lobe 

The location is puzzlingly different to that of primary TB. Recently, TB DNA has been isolated from bone marrow, and it seems possible that bacteria remain dormant in the hypoxic environment of bone marrow mesenchymal cells. These may migrate to the lung under certain circumstances such as respiratory infection. When the TB bacteria are in an oxygen-rich environment they proliferate.

The immunocompetent host has adaptive immunity from prior infection and the strong immune response results in destructive lung disease with cavitation. Tubercle bacilli proliferate in the cavities which communicate with the bronchial tree thereby facilitating endobronchial spread in the host and droplet spread to close contacts. Anti-tuberculous drugs do not enter the avascular cavities and treatment must be consistent and prolonged to effect cure. Without humans, there would be almost no transmission of TB 6,7.

Radiographic features

CT
Parenchymal disease
  • ill-defined patchy consolidation and cavitation with upper zone predominance

  • endobronchial spread with centrilobular nodules and tree-in-bud opacities

  • clustered parenchymal opacification with satellites may give rise to a galaxy sign

  • lymphadenopathy occurs only in 5% cases

  • healing results in fibro-calcific disease with volume loss and traction bronchiectasis

Airway disease

Central airway involvement may cause bronchial stenosis, broncholith, lobar collapse, traction bronchiectasis and mucoid impaction. 

Pleural disease
  • occurs in a minority of cases (18%)

  • small pleural effusion

  • empyema is less common

  • pleural thickening

  • pleural calcification

Chest wall involvement

Chest wall involvement occurring due to direct extension from pulmonary disease or empyema (empyema necessitans) manifests as bone and/or cartilage destruction and cutaneous fistula formation.

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Cases and figures

  • Case 1: pulmonary tuberculosis
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  • Case 2: tuberculous abscess
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  • Case 3
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  • Case 4
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  • Case 5
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  • Case 6
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  • Case 7
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  • Case 8
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  • Case 9
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  • Case 10
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  • Case 11
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