Gross & microscopic appearance	Pathologic basis of disease	Clinical correlation	
Gross:
•	Early lesion: Ghon complex – small, white, soft nodule a few mm in diameter involving a lobule.
•	Late lesion: larger cheesy-yellow-white lesions characterized by extensive necrosis & cavitation dispersed in lung parenchyma.
•	Scarred apex
•	Fibrotic cavities
•	Walls of cavity contain ragged, white material housing millions of mycobacteria.
•	Thickened pleura with numerous adhesions to parietal pleura.
•	Bronchiectasis
•	Lung shrunken
•	Miliary spread: miliary tubercles resembling millet seeds; more numerous in upper lobes; at first translucent & gray, later become larger, opaque & yellow.
•	Late, healed lesions can be walled of by fibrosis & appear white & hard.
•	Dystrophic calcification – white chalky appearance. 

Microscopic:
•	Tubercles in walls of alveoli & blood vessel.
•	Caseating granulomas with central necrosis.
•	Spread of caseation to surrounding alveoli.
•	Cheesy-pink material scattered among lung parenchyma. 	Etiology:
•	Mycobacterium tuberculosis: most common cause
•	Mycobacterium avium-intracellulare: AIDS patients
•	Mycobacterium bovis: acquired through ingestion of contaminated milk.

Epidemiology:
•	Afflicts 33% of the world’s population & is responsible for 3 million deaths a year.
•	Incidence has increased in developed countries due to frequency of infection in AIDS patients.

Pathogenesis:
•	Bacterium enters individuals through inhalation of infectious sputum.
•	Bacterium is ingested by macrophages & multiply in it with subsequent lysis of host cell permitting spread of infection.
•	Development of an immune response aborts spread of infection & results in the formation of granulomas.
•	Mycobacteria are not killed within these granulomas & infection can be reactivated years later.

Primary tuberculosis:
•	Infection is by inhalation, followed by lymphatic spread to tracheobronchial & mediastinal nodes.
•	Combination of Ghon focus & hilar nodes is termed primary complex.
•	Commonest result: healing lead to fibrosis & calcification.
•	Infection of pleura results in tuberculous empyema.
•	Pressure on enlarged nodes on bronchi may lead to bronchial obstruction & collapse with retention of inflammatory consolidation.
•	Bronchiectasis & bronchopneumonia
•	Invasion of blood vessels leading to miliary tuberculosis.

Secondary tuberculosis:
•	Recurrence of tuberculous infection in later life due to reactivation of primary lesion or re-infection by tubercle bacilli.
•	Lesions tend to appear in upper part of lower lobes or apices.
•	Lesion may heal leaving a dense gray scar or spread via bronchial lumens leading to progressive cavity formation & widespread fibrosis.
•	Fibrosis occurs more diffusely throughout the lung.
•	Pleura is thickened with numerous adhesions to parietal pleura.	Symptoms:
•	Primary infection is usually asymptomatic.
•	Insidious fever
•	Night sweats
•	Weight loss
•	Productive cough with blood-streaked sputum
•	Hemoptysis due to erosion of vessels.

Complications:
•	Acute tuberculous bronchopneumonia
•	Acute miliary tuberculosis
•	Tuberculous ulcers of intestine & larynx due to direct infection from swallowed sputum.
•	Amyloidosis

Diagnosis:
•	Ziehl-Neelsen stain shows acid-fast bacilli.