However, the recent vaccination against H. influenzae may also affect the frequency of pericarditis secondary to H. influenzae . Pneumococcal, streptococcal, and meningococcal pericarditis have diminished in frequency since the introduction of penicillin. The clinical course is generally milder than that observed with other purulent pericarditis. Occasionally, other organisms may cause acute purulent pericarditis, including pseudomonas, salmonella, enteric bacilli, listeria, N. gonorrhea. The incidence of anaerobic infection may be underestimated because of the improper handling of specimens for cultures and these infections should be suspected when pericarditis develops in association with lung abscesses, intra-abdominal infection, or a penetrating wound.
Mycobacterium tuberculosis is more responsible for chronic pericardial disease.
Normally, the pericardium places no significant limit on the amount of venous return that can be accommodated within the heart at rest and exercise. When there is pericardial effusion, the available space to handle venous return is reduced and if there is excessive pericardial fluid, there may be severe limitation of venous return, and therefore of cardiac output. The capacity of the pericardium is limited by its natural stiffness. Rapid accumulation of fluid is tolerated less well than slow accumulation, which may allow large amounts of pericardial fluids to collect without producing symptoms. The stiffness of the pericardium is influenced by the disease process, and if there is thickening, as in bacterial infection, the ability of the pericardium to dilate may be less than normal.