Pathogenesis of tuberculosis
Medikoe Wellness Expert
80 feet road indira nagar, Bengaluru Aug 5, 2021
The cycle of tuberculosis infection begins with the dispersion of M. TB aerosols. A dose of 1-10 bacilli is spread throughout the air, making the risk of transmission more probable. In the patient's lung, the bacilli are phagocytosed by alveolar macrophage cells, which invade the underlying epithelium. Here, monocytes from the blood vessels nearby form the beginning of a granuloma, as the immune system tries to ward off the infection. This is a hallmark characteristic of TB.
A centre of infected macrophages is enclosed with foamy macrophages, lymphocytes and mononuclear phagocytes within the granuloma. The result is a fibrous capsule with increased foamy macrophages, considered to produce the typical caseous debris (necrotic tissue resembling cheese) in the centre of the granuloma. Although it appears contained immunologically, the caseous centre tends to liquefy and cavitate as it empties thousands of M. TB bacilli into the airway. The cycle is concluded as the infected lungs give out a cough that, once again, contains the extremely transmissible infectious droplet nuclei.
The lymphatic system may carry infected macrophages to the lungs, lymph nodes, kidneys, epiphyses of the long bones, and other body areas. Infected macrophages might as well be carried in the blood of an immunocompromised host (e.g., AIDS patient). After three to eight weeks, there are no immediate symptoms or signs other than a positive tuberculosis skin test (TST) despite widespread infection. In kids, the elderly, AIDS patients and the non-white races, the disease can progress quickly to pneumonia from hilar or mediastinal lymph nodes to cavitation in the bronchi. This is when the distribution of caseous material happens, such as in acute miliary tuberculosis (disseminated disease) or tuberculosis meningitis, especially in children. Infected patients of ages over 30 years and less than 65 years have a more favourable prognosis than children, adolescents, young adults, and the elderly because they have a lower risk of tissue necrosis.
Generally, hypersensitivity develops during the three-to-eight week period after infection, signalling the action of cellular immunity as well as the control of the infection. At this time, a skin test response will be positive, suggesting that the latent infection exists. However, as previously stated, in high-risk groups, progression of the disease to cavitation in the lung and hematogenous dissemination are likely to occur.
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