In granulomatous inflammation caused by Mycobacterium tuberculosis, the 'caseous necrosis' within granulomas is primarily due to:

• A Complement-mediated cytolysis of macrophages
• B Neutrophil elastase-driven proteolysis
• C TNF-mediated apoptosis of macrophages and T cells with high local lipid content from mycobacterial cell walls ✓
• D Liquefactive necrosis triggered by high bacterial load

Explanation

Caseous necrosis is a distinctive coagulative necrosis with 'cheese-like' gross appearance. It results from a combination of macrophage apoptosis/necroptosis driven by TNF-α and IFN-γ, and the high lipid content of mycobacterial cell walls (mycolic acids, cord factor/trehalose dimycolate) that prevents complete autolysis, leaving an amorphous eosinophilic debris. Mycobacterial cord factor is directly toxic to mitochondria. Complement cytolysis is not operative intracellularly. Neutrophil elastase causes liquefactive necrosis in abscesses. Liquefactive necrosis is the progression that occurs if caseous foci expand (cavitation), not the primary mechanism.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

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Written and medically reviewed by the StethoPrep medical team.