A 35-year-old HIV-positive man with a CD4 count of 70 cells/μL presents with fever, night sweats, and bilateral upper lobe infiltrates with cavitation on chest X-ray. Sputum culture grows acid-fast bacilli. The predominant mechanism of tissue destruction in pulmonary tuberculosis is:
- A Direct cytotoxicity by mycobacterial exotoxins
- B Antibody-dependent complement-mediated lysis
- C Type IV delayed-type hypersensitivity mediated by sensitized CD4+ T cells ✓
- D Neutrophil extracellular trap formation
Explanation
Tuberculosis tissue injury is primarily immunopathological, driven by CD4+ Th1 T-cell–mediated delayed-type hypersensitivity (Type IV reaction). Macrophages activated by IFN-γ from sensitized T cells form granulomas, and central caseation necrosis results from the local cytokine milieu combined with tissue ischemia. In immunocompromised patients like those with HIV, the T-cell response is blunted, leading to atypical presentations with less cavitation and more dissemination.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.