PATHOGENESIS OF PULMONARY TUBERCULOSIS
Tuberculosis is spread from infected individuals through the air by tiny droplets that contain Mycobacterium tuberculosis. These droplets are aerosolized when an infected patient coughs, sneezes, or speaks. Particles larger than this size are deposited in the upper air-way and tend not to cause infection. After inhalation, droplets are deposited in the respiratory bronchioles or the alveoli, where the organisms can multiply. They can then spread via the lymphatics to the hilar lymph nodes and through the bloodstream to more distant sites. Multiplication continues until the replicating mycobacteria are of a sufficient size to elicit a host immune response. In normal individuals, the growth of M. tuberculosis is halted once cell-mediated immunity develops. This usually requires 2 to 12 weeks and corresponds temporally with the development of reaction to the tuberculin skin test. Once cell-mediated immunity develops, granulomas consisting of macrophages and activated T lymphocytes can form and arrest the growth of the organisms. A small number of viable mycobacteria may persist inside the granulomas, typically in the necrotic center. Often, this primary infection is clinically silent, but it may manifest as a mild pneumonic illness. Primary infection can occasionally overcome the host defenses, resulting in primary progressive disease. In most patients, however, the mycobacteria remain arrested inside the granulomas, with the potential for reactivate in the future. Reactivation occurs to create active disease.About 10% of infected persons will develop active tuberculosis, with the highest risk of developing active disease in the first 2 years after infection. Certain host factors are associated with an increased risk of developing active disease. Patients with the man immunodeficiency virus (HIV) have a greatly increased risk of developing active tuberculosis and may progress from latent disease to active disease at a rate of 10% per year.*59/348/5*
