Mycobacterium tuberculosis is a slow-growing aerobic rod that has a unique, multilayered cell wall that contains a variety of lipids that account for its acid-fast property. Transmission occurs through inhalation of droplet nuclei into the lungs. Persons with active tuberculosis who excrete stainable mycobacteria in saliva or sputum are the most infectious.4
Once the organisms reach the lungs, host defenses are activated.5 In immunocompetent persons, such defenses may kill off the inhaled mycobacteria and prevent infection. Some organisms may survive, however, and be transported to the regional lymph nodes, where the host's cell-mediated immunity is further activated to contain the infection. Granulomas, known as tubercles, may form as a result of this process, which involves activated macrophages. Tubercles are a sign of primary infection and may progress to caseation necrosis and calcification leading to the Ghon complex. 4 In most cases, the bacteria are contained in the tubercles, but some organisms enter the thoracic duct and spread throughout the body, where they may remain dormant for many years. This is referred to as latent infection and is manifested by a positive tuberculin skin test.5 In most cases of dissemination in immunocompetent hosts, the organisms do not find a suitable area to proliferate. Survival is favored in areas of high oxygen content or blood flow, such as the apical and posterior segments of the upper lobe and the superior segment of the lower lobe of the lung, the renal cortex, the meninges, the epiphyses of long bones, and the vertebrae. 4 In immunocompromised hosts, hematogenous spread occurs early, as normal host defenses are unable to contain the organisms, and disseminated disease occurs.4
The latent infection may reactivate when a host's immune system is no longer capable of containing the foci of previous hematogenous spread. The young, the elderly, or patients with other chronic debilitating diseases are at higher risk for such reactivation disease. For immunocompetent hosts with latent infection, there is a 5 to 10 percent chance of developing reactivation tuberculosis over a lifetime. 5 The population at risk for HIV infection is also at risk for tuberculosis. As the host defense system weakens, latent infection may progress to reactivation tuberculosis. The incidence of reactivation tuberculosis in HIV patients is reported at 7 percent per year.5
Current research centers around the basic science involved in the host response to mycobacteria. The key cells are the alveolar macrophages and T lymphocytes, especially the T-helper cells, and the various cytokines and interleukins that are released into circulation. One of the key cytokines released by macrophages is interferon 8 (IFN-8) which seems to correlate with clinical findings.6 For patients with active tuberculosis, but whose sputum smear is negative and whose chest radiograph is without cavitation, IFN-8 levels are high and there is a lymphocytic cell predominance in the bronchoalveolar lavage fluid. IFN-8 increases in patients who are improving with treatment for tuberculosis. As information on the role of cytokines is revealed by research, more specific new therapies may be developed to enhance or block important mediators.
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