Pleural tuberculosis

Abstract

Tuberculous pleural effusions occur in up to 30% of patients with tuberculosis. It appears that the percentage of patients with pleural effusion is comparable in human immunodeficiency virus (HIV)-positive and HIV-negative individuals, although there is some evidence that HIV-positive patients with CD4+ counts <200 cells x mL(-1) are less likely to have a tuberculous pleural effusion. There has recently been a considerable amount of research dealing with the immunology of tuberculous pleurisy. At present, we have more evidence that activated cells produce cytokines in a complex pleural response to mycobacteria. Intramacrophage elimination of mycobacterial antigens, granuloma formation, direct neutralization of mycobacteria and fibrosis are the main facets of this reaction. With respect to diagnosis, adenosine deaminase and interferon gamma in pleural fluid have proved to be useful tests. Detection of mycobacterial deoxyribonucleic acid (DNA) by the polymerase chain reaction is an interesting test, but its usefulness in the diagnosis of tuberculous pleurisy needs further confirmation. The recommended treatment for tuberculous pleurisy is a 6 month regimen of isoniazid and rifampicin, with the addition of pyrazinamide in the first 2 months. HIV patients may require a longer treatment. The general use of corticosteroids is not recommended at this time, but they can be used in individuals who are markedly symptomatic.

Cystatin F Depletion in Mycobacterium tuberculosis-Infected Macrophages Improves Cathepsin C/Granzyme B-driven Cytotoxic Effects on HIV-Infected Cells during Coinfection.

“…Additionally, high levels of NK recruitment have been observed in tuberculous pleural effusions and in early innate granulomas [57]. Pleurisy is a common manifestation of TB, often observed during the primo-infection [41]. It is also frequently observed in HIV-coinfected patients, where high levels of virus particles are present at the sites of Mtb infection [40,41].…”

“…Pleurisy is a common manifestation of TB, often observed during the primo-infection [41]. It is also frequently observed in HIV-coinfected patients, where high levels of virus particles are present at the sites of Mtb infection [40,41]. Coincidently, higher levels of CstF were found in pleural effusion of TB patients than in other inflammatory conditions [42].…”

“…One of the most frequent manifestations of TB during HIV coinfection is pleurisy [39]. Both the pleural milieu and the granuloma structure provide the appropriate contact between Mtb-infected cells and HIV-infected lymphocytes in a particular environment of cytokines and other factors that, all together, help viral replication and spread [40,41]. Surprisingly, CstF levels were found to be significantly increased in the pleural fluids of TB patients compared to other inflammatory conditions [42].…”

Approach to Empyema Necessitatis

“…Since the advent of antituberculous chemotherapy and preventive medicine, tuberculous empyema has become an uncommon disease, and thus empyema necessitatis has become extremely rare. Empyema necessitatis occurs when an encapsulated empyema erodes through the parietal pleura and discharges its contents outside the pleural cavity [1, 8]. Tuberculosis is more likely to give rise to empyema necessitatis than abscesses produced by other pyogenic organisms because of the chronicity of tuberculous empyema.…”

The immunosuppressive Tuberculosis-associated microenvironment inhibits viral replication and promotes HIV-1 latency in CD4+ T cells

“…Pleural effusion is an excess of fluid recovered from the pleural space of the human respiratory compartment and is found in approximately 30% of TB patients (27). This excess of fluid is caused by the spread of Mtb into the pleural space, leading to subsequent local inflammation and leukocyte infiltration (28). Importantly, in HIV-1/TB coinfected persons, the formation of PE is more common and contains high HIV-1 titers, compared to serum from the same individual (29–31).…”