Lungs

2. Findings and Diagnosis

 

Reactivation Tuberculosis with Cavitating Pneumonia – Editorial Comment

• Pathophysiology of Reactivation TB and Cavitation

  • Reactivation tuberculosis (TB) occurs when latent Mycobacterium tuberculosis becomes active, typically in immunocompromised individuals or under conditions of stress, malnutrition, or aging.
  • Upper lung lobes (especially apical and posterior segments) are preferentially involved due to higher oxygen tension, which supports mycobacterial growth.
  • Cavitation occurs due to caseous necrosis, where infected lung tissue undergoes liquefactive destruction, drains via the airways, and leaves behind air-filled cavities with thick walls.

• Why Does TB Cause Caseous Necrosis?

  • Delayed hypersensitivity reaction (Type IV immune response) is triggered by Mycobacterium tuberculosis, leading to granuloma formation as an attempt to contain the infection.
  • Macrophages, T cells, and cytokines (TNF-α, IFN-γ) mediate a strong immune response, resulting in persistent inflammation and tissue destruction.
  • Mycobacterial antigens stimulate macrophage activation, but the bacteria’s ability to evade complete clearance leads to chronic immune activation.
  • Poor vascularization of granulomas limits oxygen and nutrient supply, causing central necrosis with a cheese-like appearance—hence the term caseous necrosis.
  • Liquefaction of necrotic material follows, allowing the formation of cavitating lesions, which provide a highly infectious reservoir for further spread of TB.

• Chest X-ray (CXR) Findings

  • Upper lobe predominant infiltrates with patchy consolidation.
  • Cavitating lesions, often with an air-fluid level if superinfected.
  • Volume loss in affected lung regions due to fibrosis and scarring.
  • Hilar or mediastinal lymphadenopathy is uncommon in reactivation TB (more common in primary TB).

• CT Findings in Cavitating TB Pneumonia

  • Thick-walled cavitary lesions with irregular inner margins, often in the apical or posterior upper lobes.
  • Satellite nodules and tree-in-bud opacities, representing bronchogenic spread of TB.
  • Bronchiectasis and fibrosis in chronic or treated cases.
  • Air-fluid levels suggest secondary bacterial superinfection.

• Why Does TB Cavitate?

  • Caseous necrosis results in liquefaction and destruction of lung parenchyma.
  • High oxygen tension in upper lobes promotes bacterial survival and tissue breakdown.
  • Drainage of necrotic material via airways leads to cavitation, which facilitates bacterial spread and high infectivity.

• Clinical and Imaging Implications

  • Cavitating TB is highly contagious due to high bacillary load in sputum.
  • Radiologic recognition of upper lobe cavitation is crucial for early TB diagnosis and infection control.
  • CT provides superior detection of small cavities and bronchogenic spread compared to CXR.
  • Persistent cavities post-treatment may indicate multi-drug resistant TB (MDR-TB) or fibrocavitary sequelae.

• Key Takeaways

  • Reactivation TB typically affects the upper lobes due to high oxygen availability.
  • Caseous necrosis occurs due to chronic immune activation and poor granuloma vascularization, leading to cavitation.
  • Chest X-ray and CT play complementary roles, with CT better defining cavities, satellite nodules, and endobronchial spread.
  • Early detection of cavitating TB on imaging is crucial for prompt treatment and containment of transmission.

Memory Images
The Red Snappers
Red Snappers = Mycobacteria Tuberculosis Stained with Ziehl Nielsen Stan Attacking the Left Lung Apex

 

The Snappers Go Especially for
The Weak and Immunocompromised