**3. Pathogenesis of tuberculous pericarditis**

Tubercle bacilli access the pericardium via three mechanisms: (1) retrograde lymphatic spread from mediastinal, paratracheal, and peribronchial lymph nodes [3], (2) hematogenous spread (dominant in immunocompromised hosts) [4], and (3) direct contiguous spread from adjacent structures such as the lungs, pleura, and spine (infrequent) [3]. When the guest is immunocompetent, tuberculous pericardial disease is localized to the pericardial space. Usually in a paucibacillary condition, tubercle proteins trigger an important cell-mediated hypersensitivity response with T-helper cell (subtype 1) predominant cytokine release, leading to an inflammatory exudative effusion and its hemodynamic sequelae [5, 6]. The immune response to the viable acid-fast bacilli penetrating the pericardium is responsible for the morbidity associated with tuberculous pericarditis. In patients with dysfunctional immunity as occurred in HIV/AIDS, there is evidence that mycobacterial replication is active, bacillary loads are high, and the clinical manifestations of tuberculous pericarditis are related to the impact of the infectious and virulent nature of the Mtb itself in addition to the hemodynamic sequelae [4–7].

There are four pathological stages of tuberculous pericarditis: (1) fibrinous exudation, initial polymorphonuclear leukocytosis, abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells; (2) serosanguineous effusion with a predominantly lymphocytic exudate with monocytes and foam cells; (3) absorption of effusion with organization of granulomatous caseation and pericardial thickening caused by fibrin, collagenosis, and, ultimately, fibrosis; and (4) constrictive scarring. The fibrosis generated between the visceral pericardium and the parietal pericardium can calcify and adhere to the myocardium, generating a cuirass around the heart, preventing the correct diastolic filling, and generating the clinical syndrome of constrictive pericarditis [8].

Tuberculous pericarditis presents clinically in three forms: pericardial effusion, constrictive pericarditis, and a combination of effusion and constriction.
