Progression of the tuberculosis granuloma
The cycle of TB infection begins with dispersion of infectious aerosols or droplet nuclei, which contain active tubercle bacilli exhaled into the air during coughing, sneezing, and so on. A dose of 1-10 bacilli are dispersed throughout the air, making the risk of transmission likely. In the patient’s lung, the bacilli are phagocytized by alveolar macrophage cells, which then invade the underlying epithelium. Here, monocytes from nearby blood vessels form the beginning of a granuloma, as the immune system attempts to ward off the disease. This is a hallmark characteristic of tuberculosis.
Within the granuloma, a core of infected macrophages is surrounded by foamy macrophages, mononuclear phagocytes, and lymphocytes. The result is a fibrous capsule with increased foamy macrophages, presumed to create the typical caseous debris (necrotic tissue resembling cheese) in the center of the granuloma. Although it appears contained immunologically, the caseous center tends to liquefy and cavitate as it empties thousands of M. tuberculosis bacilli into the airway. The cycle is complete as the damaged lungs produce a cough that, once again, contains the highly transmissible infectious droplet nuclei.
Infected macrophages may be carried by the lymphatic system or hematogenously (eg, in the blood of the compromised host, like those with HIV/AIDS) to lymph nodes, kidneys, epiphyses of the long bones, vertebral bodies, and son on, as well as to the lungs. After three to eight weeks, despite widespread infection, there are no immediate symptoms or signs other than a positive TB skin test (TST). In children, the elderly, non-white races, and AIDS patients, the disease progresses quickly to pneumonia from hilar or mediastinal lymph nodes to cavitation in the bronchi. It is here that the distribution of caseous material occurs, such as in acute miliary TB (disseminated disease) or TB meningitis, particularly in children. Patients infected at ages over 30 years and less than 65 years have a better prognosis compared to children, adolescents, young adults, and the elderly, because they have a lower risk of tissue necrosis.
In general, hypersensitivity develops during the 3 to 8 week period after infection, signaling the action of cellular immunity and control of the infection. At this time, a skin test reaction will be positive indicating latent infection exists. However, as previously stated, in high risk groups, progression of disease to cavitation in the lung and hematogenous dissemination are likely to occur.