During the course of a routine physical examination two months prior to admission, this 57-year-old white male was noted to have a lesion in the upper lobe of the right lung. Initially, he was treated for two weeks with ampicillin. He was then admitted to an outside hospital for further study. All studies including sputum studies for tubercle bacilli, bronchial washings, and bronchoscopy were negative and he was discharged. Review of systems revealed the presence of mild dyspnea on exertion, accompanied by a slightly productive cough. Of interest was the fact that the patient had been PPD positiveMycobateria grow very slowly on culture plates, with cultures requiring up to 6 weeks for a positive finding. In lieu of cultures, a more rapid diagnostic test is the PPD--purified protein derivative of tuberculosis--test. PPD is injected under the skin of an individual and then the area is reexamined in 48-72 hours for signs of an inflammatory reaction. A positive test indicates previous exposure to M. tuberculosis. for the past 4 to 5 years, but this had never been evaluated. On this hospital admission, physical and laboratory examinations were negative. Radiographic examination of the chest revealed a 2 x 2-cm density in the right lower lung field. Several small cavities were identified in this area on CT scan.
The patient underwent a thoracotomyA thoracotomy is a surgical procedure in which an opening is made in the chest wall., at which time a portion of the upper lobe of the right lung was removed. Examination of the cut surface revealed small white nodules measuring up to 0.2 cm in diameter.
Lung: TB H&E
Lung: TB AFGT
In primary pulmonary TB you get (1) parenchymal subpleural lesions, often just above or just below the interlobar fissure, and (2) enlarged caseousCaseous means cheesy. lymph nodes draining the parenchymal focus (usually the hilar lymph nodes).
M. tuberculosis has no known exotoxins, endotoxins or histolytic factors. Its pathogenicity is due to the fact that it resists phagocytic killing and sets up a delayed hypersensitivity reaction. Virulent M. tuberculosis organisms have cord factor, sulfatides, LAM, heat shock protein and they activate complement.
The initial infection with M. tuberculosis leads to a T cell-mediated immune response that controls 95% of infections. Alveolar macrophages phagocytose the organisms and then transport them to the hilar lymph nodes. Macrophages cannot kill the mycobacteria so the organisms multiply, lyse the host cell, infect other macrophages, and sometimes disseminate via the blood to other parts of the lung and elsewhere in the body.
After a few weeks, T cell-mediated immunity develops and leads to activation of macrophages so they can kill intracellular mycobacteria via reactive nitrogen intermediates. This process leads to formation of epithelioid cell granulomas and clearance of the mycobacteria. Also, CD8+ suppresser T cells kill macrophages that are infected with mycobacteria, resulting in the formation of caseating granulomas. These processes during the primary infection with M. tuberculosis result in a calcified scar in the lung parenchyma and in the hilar lymph node. This combination is called the Ghon complex.
- Rodrigues DS, Medeiros EA, Weckx LY, Bonnez W, Salomão R, Kallas EG. Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease. Clin Exp Immunol 2002 Apr;128(1):149-54A normal PaCO2 is 35 to 45 mmHg..