M. tuberculosis is an aerobic, nonmotile, non-spore-forming rod that is highly resistant to drying, acid, and alcohol. It is transmitted from person to person via droplet nuclei containing the organism and is spread mainly by coughing. A person with active but untreated TB infects approximately 10–15 other people per year. The probability of transmission from one person to another depends on the number of infectious droplets expelled by a carrier, the duration of exposure, and the virulence of the M. tuberculosis. The risk of developing active TB is greatest in patients with altered host cellular immunity, including extremes of age, malnutrition, cancer, immunosuppressive therapy, HIV infection, end-stage renal disease, and diabetes.
TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade and replicate within alveolar macrophages. Inhaled mycobacteria are phagocytized by alveolar macrophages, which interact with T lymphocytes, resulting in differentiation of macrophages into epithelioid histiocytes [7]. Epithelioid histiocytes and lymphocytes aggregate into small clusters, resulting in granulomas. In the granuloma, CD4 T lymphocytes (effector T cell) secrete cytokines, such as interferon-γ, which activate macrophages to destroy the bacteria with which they are infected. CD8 T lymphocytes (cytotoxic T cell) can also directly kill infected cells [8]. Importantly, bacteria are not always eliminated from the granuloma, but can become dormant, resulting in a latent infection. Another feature of human TB granulomas is the development of necrosis in the center of the tubercles.
The primary site of infection in the lungs is called the Ghon focus [9]. It either enlarges as disease progresses or, much more commonly, undergoes healing. Healing may result in a visible scar that may be dense and contain foci of calcification. During the early stage of infection, organisms commonly spread via lymphatic channels to regional hilar and mediastinal lymph nodes and via the bloodstream to more distant sites in the body. The combination of the Ghon focus and affected lymph nodes is known as the Ranke complex. The initial infection is usually clinically silent. In approximately 5% of infected individuals, immunity is inadequate and clinically active disease develops within 1 year of infection, a condition known as progressive primary infection [10]. For most infected individuals, however, TB remains clinically and microbiologically latent for many years.
In approximately 5% of the infected population, endogenous reactivation of latent infection develops many years after the initial infection (this has also been called “postprimary TB”) [10]. The reactivation TB tends to involve predominantly the apical and posterior segments of the upper lobes and the superior segments of the lower lobes. This location is likely due to a combination of relatively higher oxygen tension and impaired lymphatic drainage in these regions [11]. As distinct from primary infection site, in which healing is the rule, reactivation TB tends to progress. The main abnormalities are progressive extension of inflammation and necrosis, frequently with development of communication with the airways and cavity formation. The endobronchial spread of necrotic material from a cavity may result in TB infection in the same or in other lobes. Hematogenous dissemination may result in miliary TB.
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