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Primary Pulmonary Tuberculosis

  • Primary Pulmonary Tuberculosis describes the pulmonary pathology and clinical consequences which result following initial infection with M. tuberculosis . For a discussion of the microbiology, host defense, treatment, and detection of this organism please refer to the Mycobacterium tuberculosis page.
Clinical Consequences
  • Overview
    • The clinical consequences of primary pulmonary disease depend on the strength of host cell-mediated immunity. In most healthy adults, the natural progression of disease is described in "Limited Primary Disease" below. However, in those with impaired cell-mediated immunity such as immunocompromised patients, AIDS patients, children, or the elderly, severe disease may result as described in "Primary Progressive Disease" below.
  • Limited Primary Disease
    • Limited Primary Disease often does not display any symptomology. As described in the "Immune Response" section of the Mycobacterium tuberculosis page, successful cell-mediated immunity either kills infected macrophages or induces them to kill internalized organisms. Cell-mediated Immunity also orchestrates development of granulomas which physically isolate infected foci from normal tissue. The central area of tuberculous granulomas undergo caseous necrosis while the surrounding host cells include macrophages, lymphocytes, and giant cells. Over time these areas of granulomatous inflammation can scar over and calcify, which can be observed on chest radiography as radio-dense nodules. When a radio-dense nodule in the lung parenchyma is accompanied by another in the hilar or paratracheal lymph nodes, this is termed a "Ghon Complex".
  • Primary Progressive Disease
    • In those with deficient cell-mediated immunity serious pulmonary disease may result following initial infection. Infected pulmonary foci continue to enlarge and are characterized by expanding areas of caseous necrosis. These growing lesions can erode bronchi or their branches, thus draining their contents and leaving empty cavities, leading to "Cavitations" which can be observed as radiolucent circles on chest radiography. Erosion of pulmonary vasculature can lead to hemorrhage within the respiratory parenchyma that is manifested by hemoptysis. Alternatively, erosions into the pleura can lead to pleural effusions or empyema. Finally, spread of organisms to regional lymph nodes can appear as hilar or mediastinal lymphadenopathy. In those with severely reduced cell-medaited immunity lympho-hematogenous dissemination of organisms can seed nearly any tissue in the body resulting in signs and symptoms of extrapulmonary tuberculosis.
  • The initial foci of infection in primary pulmonary tuberculosis are the lower and middle lung lobes since infective respiratory droplets tend to deposit in these loci due to their greater levels of ventilation as discussed in pulmonary ventilation distribution.