Primary tuberculosis Sample Clauses

Primary tuberculosis. Once inhaled, most M. tuberculosis organisms will settle in the upper respiratory epithelium, where they are likely to be expelled by the mucociliary escalator (Nardell, 1993). The few bacteria reaching the deep lung are phagocytosed by alveolar macrophages and either killed or else survive to initiate an infection (▇▇▇▇▇▇▇▇▇▇, 1993; ▇▇▇▇▇▇▇▇▇▇▇, 1996). The fate of the bacillus within the infected cell depends on the type and activation state of cell found. It is believed that a bacillus is able to survive within a macrophage if the phenotype of the phagocytic cell interacting with M. tuberculosis displays an anti-inflammatory phenotype also known as “alternative activation state”. These cells have increased expression of pattern recognition receptors such as the mannose and scavenger receptors facilitating cell and bacillus interaction but they also have a reduced oxidative burst and they are unable to eliminate the bacillus (▇▇▇▇▇▇▇▇▇▇▇, 1996). Once inside the phagocyte, the mycobacteria modulate the behaviour of its phagosome by preventing its fusion with acidic, hydrolytically-active lysosomes (▇▇▇▇▇ et al., 2007; ▇▇▇▇▇▇▇▇-▇▇▇▇▇▇▇▇ et al., 1994). Over the next 2 to 3 weeks, surviving organisms multiply, kill their host macrophages and release more bacilli infecting additional host cells. Pulmonary inflammation due to interaction of bacillus with macrophages and other cells results in recruitment of monocytes, neutrophils, and primed T cells and B cells to lungs, culminating in formation of granulomatous lesions (Figure 1.2). Granuloma formation is the classic pathologic feature of TB, and serves as an effective means for containing pathogens, preventing their continued growth and dissemination. In its early stage, the granuloma has a core of infected macrophages enclosed by foamy macrophages and other mononuclear phagocytes, surrounded by lymphocytes. This tissue response contains the infection and spells the end of the period of rapid replication for the mycobacteria. As the granuloma matures it develops an extensive fibrous capsule that encases the macrophage core and excludes the majority of lymphocytes from the centre of the structure. Concomitant with this transition is a marked reduction in the number of blood vessels penetrating the granuloma. At this stage there is a noticeable increase in the number of foamy macrophages responsible for the accumulation of caseous debris in the centre of the granuloma, which portends progression to active disea...