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( Mycobacterium tuberculosis)
Mycobacterium tuberculosis (MTB) is a pathogenic bacterial species in the genus Mycobacterium and the causative agent of most cases of tuberculosis.[1] First discovered in 1882 by Robert Koch, M. tuberculosis has an unusual, waxy coating on the cell surface (primarily mycolic acid), which makes the cells impervious to Gram staining; acid-fast techniques are used instead. The physiology of M. tuberculosis is highly aerobic and requires high levels of oxygen. Primarily a pathogen of the mammalian respiratory system, MTB infects the lungs, causing pneumonia.[1] The M. tuberculosis genome was sequenced in 1998.[2][3] When in the lungs, M. tuberculosis is taken up by alveolar macrophages, but they are unable to digest the bacterium. Its cell wall prevents the fusion of the phagosome with a lysosome. Specifically, M. tuberculosis blocks the bridging molecule, early endosomal autoantigen 1 (EEA1); however, this blockade does not prevent fusion of vesicles filled with nutrients. Consequently, the bacteria multiply unchecked within the macrophage. The bacteria also carried the UreC gene, which prevents acidification of the phagosome.[5] The bacteria also evade macrophage killing by neutralizing reactive nitrogen intermediates. The ability to construct M. tuberculosis mutants and test individual gene products for specific functions has significantly advanced our understanding of the pathogenesis and virulence factors of M. tuberculosis. Many secreted and exported proteins are known to be important in pathogenesis.[6]
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