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    Subjects/Pathology/Tuberculosis Pathology
    Tuberculosis Pathology
    easy
    microscope Pathology

    Which of the following is the characteristic histological hallmark of tuberculosis?

    A. Non-caseating granuloma with central fibrin deposition and neutrophilic infiltration
    B. Suppurative abscess with liquefactive necrosis and polymorphonuclear leukocytes
    C. Caseating granuloma with central acellular necrosis surrounded by epithelioid macrophages and Langhans giant cells
    D. Granuloma with central calcification and surrounding fibroblasts without epithelioid differentiation

    Explanation

    ## Histological Hallmark of Tuberculosis **Key Point:** The pathognomonic lesion of tuberculosis is the **caseating granuloma** (also called tubercle), characterized by central caseous (cheese-like) necrosis surrounded by epithelioid macrophages and Langhans giant cells. ### Structural Components | Component | Characteristics | |-----------|------------------| | **Central necrosis** | Acellular, amorphous, eosinophilic caseous material (pathognomonic) | | **Epithelioid macrophages** | Activated macrophages with elongated nuclei, arranged in palisade | | **Langhans giant cells** | Multinucleated giant cells with nuclei arranged in a horseshoe pattern at the periphery | | **Outer zone** | Lymphocytes, fibroblasts, and collagen forming a fibrous capsule | **High-Yield:** The presence of **caseous necrosis** (not suppurative/liquefactive) is the key distinguishing feature of TB granulomas from other granulomatous diseases like sarcoidosis (which are non-caseating). **Clinical Pearl:** Acid-fast bacilli (AFB) are typically found at the periphery of the caseous center, where macrophages are still viable and contain organisms. The necrotic center is relatively acellular and organism-poor. **Mnemonic:** **CELT** — **C**aseating, **E**pithelioid macrophages, **L**anghans giant cells, **T**uberculosis. ### Why Caseation Occurs Caseation is thought to result from: 1. Hypersensitivity reaction to mycobacterial antigens 2. Tumor necrosis factor (TNF)-α-mediated macrophage activation 3. Mycobacterial lipids triggering tissue-damaging immune response [cite:Robbins 10e Ch 8]

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