Tuberculosis

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Pathophysiology

Tubercle bacilli initially produce a primary infection, followed by a latent (dormant) phase and, in some cases, by active disease. Infection is not transmissible in the primary and latent phases.

Primary infection:

Airborne droplet nuclei lodge in subpleural terminal airspaces, predominantly in the lower lung, usually in only one site. Tubercle bacilli replicate inside macrophages, ultimately killing them; inflammatory cells are attracted to the area, causing a tubercle and sometimes pneumonitis. In the early weeks of infection, some infected macrophages are borne to regional lymph nodes (eg, hilar, mediastinal).

Hematogenous spread to any part of the body, particularly the apical-posterior portion of the lungs, epiphyses of the long bones, kidneys, vertebral bodies, and meninges, may occur. In 95% of cases, after about 3 wk of uninhibited growth, the immune system suppresses bacillary replication before symptoms or signs develop. Foci of infection in the lung or other sites resolve into epithelioid cell granulomas, which may have caseous and necrotic centers; tubercle bacilli can survive in this material for years, the host's resistance determining whether the infection ultimately resolves without treatment, remains dormant, or becomes active. Foci may leave nodular scars in the apices of one or both lungs (Simon foci), calcified scars from the primary infection (Ghon foci), or calcified hilar lymph nodes. The tuberculin skin test (see BCG page) is positive.

Rarely, the primary focus immediately progresses, causing acute illness with pneumonia (sometimes cavitary), pleural effusion, and marked mediastinal or hilar lymph node enlargement (which in children may compress bronchi). Small pleural effusions are predominantly lymphocytic, typically contain few organisms, and clear within a few weeks. Primary extrapulmonary TB at any site can sometimes present without evidence of lung involvement. TB lymphadenopathy is the most common extrapulmonary presentation; however, meningitis is the most feared because of its high mortality in the very young and very old.

Active disease: In about 10% of patients overall, latent infection develops into active disease, although the percentage varies significantly by age and other risk factors. In 50 to 80% of those who develop active disease, TB reactivates within the 1st 2 yr, but it can occur decades later. Any organ initially seeded may be a site of reactivation, but reactivation occurs most often in the lung apices, where O₂ tension is highest. Ghon foci and affected hilar lymph nodes are much less likely to be sites of reactivation. Extrapulmonary TB is discussed in the Extrapulmonarypage.

TB damages tissues through delayed hypersensitivity (see Allergic and Other Hypersensitivity Disorders: Introduction), typically producing granulomatous necrosis with a caseous histologic appearance. Lung lesions are cavitary. Pleural effusion is less common than in progressive primary TB but may occur from direct extension or hematogenous spread. Rupture of a large tuberculous lesion into the pleural space may produce empyema with or without bronchopleural fistula; it sometimes causes pneumothorax. In the prechemotherapy era, TB empyema sometimes complicated medically induced pneumothorax therapy and was usually rapidly fatal.

The course varies greatly, depending on the virulence of the organism and the state of host defenses. The course may be rapid among blacks and American Indians who have not had as many centuries of selective pressure to develop innate or natural immunity.

Acute respiratory distress syndrome, which appears to be due to hypersensitivity to TB antigens, develops rarely after diffuse hematogenous spread or rupture of a large cavity with spillage into the lungs.

(posted with kind permission of MERCK  WHERE THE PATIENT COMES FIRST  http://www.merck.com/mmpe/)

Atypical TB