Specific inflammations

Specific Inflammations

Tuberculosis

Types of Inflammation

  • Chronic specific inflammation with proliferative-alterative granulomatous lesions with or without necrosis.

    • Primary TB: Initial infection.

    • Secondary TB: Reactivation in previously sensitized patients, often localized in lung apices, can lead to cavitations.

  • Lymphatics can lead to right heart and pulmonary arterial dissemination – miliary TB.

Etiology

  • Caused by Mycobacterium species:

    • Mycobacterium tuberculosis

    • Mycobacterium avium

    • Other species: Africanum, microti, pinnipedii, canettii, etc.

Pathogenesis

  • Granuloma formation is a type IV granulomatous hypersensitivity reaction.

  • Defends against poorly digestible antigens, e.g., Mycobacterium tuberculosis, causing tissue destruction.

Sequence in Granuloma Evolution

  1. Engulfment by macrophages.

  2. Antigen presentation to CD4+ T lymphocytes.

  3. Cytokines released:

    • IL-1, IL-2: Stimulate T cell proliferation.

    • Interferon-γ: Activates macrophages.

    • TNF-α: Promotes fibroblast growth and activates endothelium.

Mode of Transmission

  • Inhalation: Organisms in cough droplets or dried sputum from infected persons.

  • Ingestion: Leads to tonsillar or intestinal tuberculosis.

  • Inoculation: Rarely from infected tissues.

  • Transplacental: Congenital tuberculosis from infected mothers.

Characteristics of M. tuberculosis

  • Slender rod-like bacillus (0.5 to 3 μm), neutral in Gram staining.

  • Detection through:

    • Acid-fast (Ziehl-Neelsen) staining.

    • Fluorescent methods.

    • Culture (Lowenstein-Jensen medium).

    • Molecular methods (PCR).

    • Immunohistochemical staining with anti-MBP 64 antibody.

Diagnosis of Tuberculosis

  • Identification via:

    • Acid-fast stain (Ziehl-Neelsen).

    • Positive smears or cultures.

    • PCR tests.

Primary TB Features

  • Usually resolves spontaneously.

  • Symptoms: Lack of appetite, weight loss, asthenia, subfebrility, night sweats.

  • Ghon’s focus: Primary lesion, including lymphatic components and lymph nodes.

Ghon Complex

  • Location: Lower areas of the upper lobe and superior areas of the lower lobe.

  • Initial phase: Exudative alveolitis with monocytes and macrophages, leading to tuberculous pneumonia.

  • Dimensions: 1-1.5 cm, progressing to fibrosis and calcification over time.

Evolution of Primary TB

  • Healing occurs through fibrosis and calcification.

  • Primary Progressive Tuberculosis: Enlargement leading to bronchopulmonary dissemination.

  • Miliary Primary Tuberculosis: Hematogenous spread affecting the liver, spleen, kidneys, brain, bone marrow.

Secondary TB Overview

  • Arises from reactivation of dormant bacilli or reinfection.

  • Immediate symptoms can occur in immunocompromised patients, otherwise develops after 1-3 years.

  • Affected organs: Lungs, kidneys, bones, lymph nodes, meninges, genital tract.

Clinical Features of Secondary TB

  • Symptoms: Non-specific initially, including coughing (dry then mucopurulent), dyspnea, anemia, cachexia, difficulties with diabetes management.

  • Central caseous necrosis observed in gross pathology, resembling cheese; may form caverns if cleared through bronchi.

Histological Features of TB

  1. Kazanjian Method: Granulomas indicate type of inflammation.

  2. Cells Involved:

    • Epithelioid cells with radial disposition (mandatory feature).

    • Multinucleated giant cells (Langhans cells).

    • Peripherally arranged lymphocytes (mandatory feature).

Miliary Tuberculosis

  • Hematogenous spread to multiple organs: Liver, bone marrow, spleen, adrenal glands, meninges, kidney, salpinges, epididymis.

  • Nodules are small (1-3 mm), yellow matte, well-demarcated.

Differential Diagnosis

  • Lung Sarcoidosis: Non-caseous epithelioid granulomas, lacking lymphocyte wreath.

  • Other infections: Crohn's disease, Yersinia enterocolitis.

  • Skin: Lupus vulgaris, sarcoidosis.

Tuberculosis of the Lymph Node

  • Secondary extrapulmonary TB via lymphatic dissemination.

  • Clinical features include painless, mobile adenopathy in supraclavicular areas; may develop skin fistulas.

  • Known as Scrofula when severe.

Cytomegalovirus Sialadenitis

  • Gross features: Enlarged salivary glands, often appearing swollen and possibly with necrotic areas. May see focal areas of cystic degeneration.

  • Microscopy: Large cells (owl-eye cells) with intranuclear inclusions, inflammation in surrounding tissue, and possible necrosis.

Mycotic Pyelonephritis

  • Gross features: Swollen kidneys with possible abscess formation, and areas of necrosis.

  • Microscopy: Presence of fungal hyphae, inflammatory cells, and necrotic renal tissue.

Actinomycosis

  • Gross features: Hard, dense, yellowish granules (sulfur granules) visible in abscesses, which appear as raised lesions.

  • Microscopy: Characteristic actinomyces filamentous organisms, polymorphonuclear infiltrate, and necrotic areas with fibrosis.

Rheumatic Heart Disease

  • Gross features: Thickened and irregular heart valves, often with nodular vegetations (Aschoff bodies).

  • Microscopy: Presence of Aschoff bodies (granulomas) in the myocardium, and valve fibrosis with inflammatory infiltrate.

Luetic Aortitis

  • Gross features: Enlarged aortic wall with potential aneurysms, and calcification of the aortic wall.

  • Microscopy: Atypical inflammatory changes with plasma cell infiltration, and degeneration of vascular tissue (endarteritis obliterans).