PULMONARY TUBERCULOSIS AND CHRONIC PULMONARY INFECTIONS

Pathology of Pulmonary Primary Tuberculosis (TB)

Primary tuberculosis refers to the initial infection caused by Mycobacterium tuberculosis in individuals who have not been previously exposed to the pathogen. The pathology of primary TB is characterized by a series of immune responses and tissue changes that occur after inhalation of the bacteria.

1. Initial Infection and Ghon Focus Formation:
   • When M. tuberculosis is inhaled, it typically lodges in the alveoli, most commonly in the middle or lower lobes of the lungs.
   • The bacteria are phagocytosed by alveolar macrophages but resist destruction due to their lipid-rich cell wall and ability to inhibit phagosome-lysosome fusion.
   • This leads to the formation of a localized area of inflammation known as a Ghon focus, which consists of granulomatous inflammation with central caseous necrosis.

2. Granuloma Formation:
   • A granuloma forms as part of the host’s immune response, involving macrophages, epithelioid cells, Langhans giant cells, and lymphocytes.
   • The granuloma aims to contain the infection but also serves as a site where bacteria can persist in a latent state.

3. Ghon Complex:
   • If nearby hilar lymph nodes are involved due to lymphatic drainage from the Ghon focus, this combination is termed a Ghon complex.
   • Over time, these lesions may calcify and become visible on chest radiographs as calcified nodules.

4. Outcome:
   • In most immunocompetent individuals, primary TB resolves with fibrosis and calcification, leading to latent TB infection.
   • However, in some cases (e.g., immunocompromised individuals), primary TB can progress directly to active disease or disseminate systemically (miliary TB).

Pathology of Secondary Tuberculosis

Secondary tuberculosis, also known as post-primary or reactivation TB, occurs when latent M. tuberculosis infection becomes reactivated or when there is reinfection in an individual with prior exposure. It typically affects adults and involves different pathological features compared to primary TB.

1. Location:
   • Secondary TB predominantly affects the apical or posterior segments of the upper lobes due to higher oxygen tension in these areas, which favors mycobacterial growth.

2. Pathological Features:
   • Reactivation leads to intense immune responses at sites where bacilli were dormant.
   • Granulomas form again but are more extensive than those seen in primary TB.
   • Central caseous necrosis becomes prominent within granulomas; over time, this necrotic material may liquefy and drain into airways, forming cavitary lesions.

3. Cavitation:
   • Cavities are thin-walled spaces filled with caseous material that communicate with bronchi.
   • These cavities facilitate bacterial proliferation and aerosolization during coughing, significantly increasing transmission risk.

4. Systemic Spread Risk:
   • Without treatment, secondary TB can spread locally within the lungs or disseminate hematogenously (e.g., miliary spread) or via lymphatics.

Pathology of Progressive Tuberculosis

Progressive tuberculosis refers to cases where either primary or secondary TB fails to resolve and instead advances into widespread disease due to inadequate immune control.

1. Uncontrolled Spread:
   • Progressive pulmonary TB involves extensive lung tissue destruction with coalescing areas of caseous necrosis.
   • Bronchial obstruction may occur due to compression by enlarged lymph nodes or fibrotic tissue.

2. Miliary Tuberculosis:
   • Hematogenous dissemination results in numerous small granulomas (1–3 mm) throughout multiple organs such as lungs, liver, spleen, bone marrow, and meninges.
   • These granulomas resemble millet seeds on gross examination (hence “miliary”).

3. Extrapulmonary Manifestations:
   • Progressive disease often extends beyond the lungs into other systems such as skeletal (Pott’s disease), genitourinary tract (renal TB), CNS (tuberculous meningitis), gastrointestinal tract (ileocecal involvement), or pericardium (granulomatous pericarditis).

4. Immune Response Failure:
   • The inability of macrophages and T-cells to contain bacterial replication leads to overwhelming inflammation and tissue damage.

Pathology of Chronic Pulmonary Infections

Chronic pulmonary infections refer broadly to long-standing infections that involve persistent inflammation and structural damage within lung tissues over time.

1. Tuberculosis-Related Chronic Pulmonary Infection:
   • Chronic pulmonary TB results from untreated or inadequately treated secondary/progressive TB.
   • Features include persistent cavitary lesions with fibrosis surrounding areas of caseation necrosis.
   • Bronchiectasis may develop due to repeated cycles of infection and scarring.

2. Non-Tuberculous Mycobacterial Infections (NTM):
   • Chronic infections caused by species like Mycobacterium avium-intracellulare complex often mimic chronic pulmonary TB but occur primarily in immunocompromised hosts.
3. Bronchiectasis Contribution: – Repeated cycles of inflammation lead to permanent dilation of bronchi/bronchioles associated with mucus stasis and recurrent infections.

4. Histopathological Findings Across Chronic Infections: – Granulomatous inflammation remains common but may vary depending on causative organisms; fibrosis dominates advanced stages leading eventually toward respiratory insufficiency if untreated.