A 1-Year-Old with Mycobacterium tuberculosis Endocarditis with Mass Spectrometry Analysis of Cardiac Vegetation Composition.

In this study, we report the first case of Mycobacterium tuberculosis endocarditis in an immunocompetent child born in the United States. Mass spectrometry of the vegetation identified coagulation, humoral immune proteins, neutrophil granule proteins, and histones. Few neutrophils on histopathology suggest that neutrophil extracellular traps may contribute to tuberculous endocardiac mass formation.

Right atrial tuberculoma: a diagnosis too late.

Solitary intra-cardiac cavity tuberculoma is extremely rare and often only diagnosed during a post-mortem. We report a case of right atrial tuberculoma causing right atrial outflow tract obstruction in an immune-compromised man. The diagnosis of cardiac tuberculoma was made through the detection of mycobacterium tuberculosis DNA by tuberculosis-polymerase chain reaction in the pericardial fluid. The patient succumbed five days after admission but an autopsy was refused by his family.

Memory lymphocytes from tuberculous effusions: purified protein derivative (PPD) stimulates accelerated activation marker expression and cell cycle progression.

Accelerated PPD-specific proliferation and generation of CD4+ cytotoxic effectors by mononuclear leucocytes (MNL) from tuberculous effusions (EMNL) has been previously reported by our laboratory. In order to explore the contribution of the state of activation of MNL to accelerated reactivity, EMNL and peripheral blood (PB)MNL from seven patients with tuberculosis were assessed both ex vivo and after PPD stimulation. Flow cytometry revealed no difference in the activation state (IL-2 receptor and HLA-DR expression) or cell cycle progression ex vivo. However, CD4+ CD29+ memory T cells were accumulated in EMNL compared with PBMNL. In vitro stimulation of EMNL with PPD resulted in accelerated expression of activation markers and progression through the cell cycle (peak after 4 days), whilst PBMNL exhibited normal activation kinetics (peak after 7 days). Accelerated reactivity could not be accounted for by quantitative differences in effusion CD4+ CD29+ memory T cells compared with blood, but may be due to a qualitative difference in effusion memory T cells, which are shown to be in a postactivation state of differentiation. T cells entering S and G2/M phases of the cell cycle were largely of the activated memory phenotype. Activation marker expression occurred in association with up-regulation of CD4 antigen expression on the surface of EMNL. Thus accelerated expression of activation markers and cell cycle progression by CD4+ CD29+ memory T cells may in part account for accelerated PPD reactivity in tuberculous effusions.

Humoral response to mycobacterial heat shock proteins in patients with constrictive pericarditis caused by tuberculosis and its implications for pathogenesis.

Tuberculous pericarditis is one of the commonest causes of cardiac failure in Transkei and the surrounding regions in southeast Africa. About 20% of patients with clinically diagnosed tuberculous pericardial effusion go on to develop pericardial fibrosis (i.e., construction), a complication which is associated with significant mortality and morbidity. The pathological mechanisms underlying this aberrant inflammatory response are poorly understood, and there is a lack of reliable pointers (clinical or laboratory) in predicting the likelihood of development of constriction. We studied the humoral response to mycobacterial heat shock proteins (65 and 71 kDa) in 25 patients with culture-positive tuberculous pericardial effusion and found a significant correlation between high anti-mycobacterial hsp60 antibody titers (before treatment) and subsequent development of fibrosis (P = 0.035 by logistic regression), which is independent of the effect of the use of prednisolone as adjuvant therapy. Possible mechanisms underlying the pathogenesis of pericardial constriction in tuberculosis are postulated.

Immune reactions in tuberculous and chronic constrictive pericarditis. Clinical data and diagnostic significance of antimyocardial antibodies.

Humoral immune reactions were analyzed in 12 patients with exudative tuberculous pericarditis, 10 patients with constrictive pericarditis due to former tuberculosis, 10 patients with viral pericarditis, 20 patients with pulmonary tuberculosis, and 98 healthy donors. Pericarditis occurred in 12.5% of the patients with tuberculosis, whereas the incidence of tuberculosis in the 149 patients with pericarditis was 8%. Repeated pericardial puncture and pericardial effusions of greater than 500 ml with impending cardiac tamponade had to be performed in 4 patients. Clinical data indicated probable myocardial involvement in 4 of 12 patients. Antimyolemmal antibodies, which are a muscle-specific subtype of antisarcolemmal antibodies, were found in all patients with exudative tuberculous pericarditis and viral perimyocarditis, in only 1 of 12 patients with constrictive pericarditis, and in no patients with pulmonary tuberculosis. Antifibrillary antibodies--primarily of the antimyosin type--were missed in patients with viral heart disease but were demonstrated in 75% of patients with tuberculous pericarditis. Only sera with complement-fixing antimyolemmal antibodies of the IgG type in titers greater than 1:40 induced cytolysis of vital adult heterologous cardiocytes isolated and enriched by silica sol gradient centrifugation. These findings suggest not only that antimyolemmal antibodies are diagnostic indicators of perimyocardial involvement in tuberculous pericarditis, but also that they may play a significant role in its pathogenesis.