Pathophysiology of Tuberculosis
نویسنده
چکیده
When many infectious units of 1-3 bacilli are inhaled, a phenotypically hardy bacillus is likely to be among them. In addition, the alveolar macrophages apparently vary in their capacity to destroy bacilli [1]. Staining for acid-fast bacilli is very useful for demonstrating M. tuberculo‐ sis (A). Fig. 1 reveals histologic manifestation of tuberculosis over the time course. Histologi‐ cally, tuberculosis displays exudative inflammation (B), proliferative inflammation (D) and productive inflammation (C) depending on the time course. Using animal experiments and an inhalation exposure system, the pathologic condition of the infected animals was followed up for one year. Exudative inflammation was observed for the first 10 days. Thereafter, granulo‐ mas, which corresponded to foci of proliferative inflammation, were formed. Cavity formation was not recognized in animal tuberculosis, except for rabbits. Using rabbit models, Dr. Arthur Dannenberg described the pathology of tuberculosis in detail [2, 3]. There are five stages: onset, symbiosis, early stages of caseous necrosis, interplay of cell-mediated immunity and tissue damaging delayed-type hypersensitivity, and liquefaction and cavity formation. In stage 1, tubercle bacilli are usually destroyed or inhibited by the mature resident alveolar macrophages that ingest them. If bacilli are not destroyed, they grow and eventually destroy the alveolar macrophages. In stage 2, bacilli grow logarithmically within the immature nonactivated macrophages. These macrophages enter a tubercle from the bloodstream. This stage is termed symbiosis because bacilli multiply locally without apparent damage to the host, and macro‐ phages accumulate and divide. In stage 3, the stage at which caseous necrosis first occurs, the number of viable bacilli becomes stationary because their growth is inhibited by the immune response to tuberculin-like antigens released from bacilli. Stage 4 is the stage that usually determines whether the disease becomes clinically apparent. Cell-mediated immunity plays a major role in this situation. The cytotoxic delayedtype hypersensitivity immune response
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