The principal portal of entry of the tubercle bacilli as well as the major organ of disease is the lung. Inhaled tubercle bacilli are deposited in the basal segments of the lower lobe, middle lobe, lingula, or anterior segments of the upper lobe, the so-called primary infection segments. Alveolar macrophages that are nonspecifically activated (natural immunity) engulf the inhaled bacilli and are transported to regional lymph nodes. Infected macrophages produce chemokines that result in recruitment of additional macrophages and circulating monocytes, which in turn secrete significant amounts of proteolytic enzymes, generating an exudative lesion (11). Activated mono-nuclear phagocytes (MP) also secrete tumor necrosis factor, which incite granuloma formation. Eventually, T cells activated by chemokines in the draining lymph nodes as well as natural killer (NK) cells are attracted to the site of inflammation with subsequent production of interferon-gamma, which in turn activates tuberculostatic macrophage functions. At this stage (acquired immunity), the onset of cell-mediated immunity and delayed type hypersensitivity responses, which occur after approximately
3 wk of initial infection, are associated with a positive dermal reactivity to standarddose tuberculin antigen. The characteristic tubercle granuloma or the Ghon complex ultimately develops consisting of organized collections of epithelioid cells, lymphocytes, and capillaries; tubercle bacilli are confined and their growth restrained within lesions showing caseous necrosis, surrounding fibrosis, and ultimate healing (12). Reactivation (secondary or postprimary) TB is associated with uncontrolled cell destruction by cytolytic T cells, NK cells, and activated MP cells, which promote granuloma liquefaction and rupture into the bronchoalveolar and vascular systems promoting widespread microbial dissemination.
Containment of the TB infection results in an asymptomatic and noninfectious state with a positive tuberculin skin test reaction (TB infection); the viable tubercle bacilli remain dormant indefinitely with intact host immune integrity. Factors that compromise host immunity, e.g., HIV infection, aging, illicit drug use, alcoholism, poor nutrition, and certain chronic diseases, may result in reactivation of latent TB infection (TB disease). The increased frequency of TB seen in aging may be explained in large part by the impairment of cell-mediated immunity, which results from senescence (demonstrated in murine models) as well as age-associated diseases (diabetes mellitus, malignancy), renal impairment, malnutrition, and immunosuppressive agents (13).
Approximately 90% of TB disease cases in the elderly are due to reactivation of primary infection (9). TB infection without disease may occur in 30%-50% of individuals in elderly nursing facility residents as demonstrated by positive tuberculin skin tests. Rarely, previously infected older persons may eventually eliminate the viable tubercle bacilli and revert to a tuberculin negative state; nevertheless, these persons are at risk for new infection (reinfection) with Mtb. Thus older persons potentially at risk for TB consist of individuals never exposed to Mtb, those with latent and dormant primary infection that may reactivate, and others who are no longer infected and consequently at risk for reinfection.
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