Pericarditis is inflammation of the cardiac pericardium, and it has a broad variety of etiologies, ranging from infectious to noninfectious causes. Among infectious pericarditis, viral causes usually predominate, and bacterial pericarditis is less commonly reported. Clinical presentations of bacterial pericarditis are usually subtle and overlooked until significant pericardial effusion and cardiac tamponade develop. Untreated bacterial pericarditis is universally fatal. Purulent bacterial pericarditis, including tuberculous (TB) pericarditis, are discussed here.

Etiology
Staphylococcus aureus and Streptococcus pneumoniae are the two most common pathogens causing bacterial pericarditis, although gram-negative bacilli and anaerobes are gaining more attention recently. Neisseria meningitidis, Neisseria gonorrhoeae, Mycoplasma pneumoniae, and Legionella pneumophila are rarely reported as the causes of bacterial pericarditis. Pericarditis due to Borrelia burgdorferi is less common than myocarditis. Oropharyngeal anaerobes (particularly Actinomyces, Prevotella, Peptostreptococcus, Propionibacterium, and Fusobacterium) play an important role in bacterial pericarditis in patients with complicated head and neck infections, either as a direct result of or seeding from the bloodstream to the pericardium.

In children, S. aureus and N. meningitidis are the most common causes of bacterial pericarditis, whereas the incidence of pericarditis due to Haemophilus influenzae has been significantly reduced since the introduction of childhood immunization with the H. influenzae type B conjugate vaccine.

In patients with HIV infection, Mycobacterium tuberculosis, Mycobacterium avium-intracellulare (MAI), and Mycobacterium kansasii are responsible for up to 50% of the cases of pericarditis/pericardial effusion. On the other hand, 1%-5% of pericarditis in non-HIV-infected patients is caused by M. tuberculosis.

Pathogenesis
The major mechanisms of seeding of bacteria to the pericardium are:

• Contiguous spread from the infectious focus in the chest; S. pneumoniae is the most common organism in association with pneumonia and pleural empyema. Oral anaerobes are predominant organisms in esophageal perforation into the pericardium.
• Extension of a perivalvular abscess from endocarditis into the pericardium; S. aureus and Salmonella spp. account for the majority of cases of bacterial pericarditis in this category.
• Hematogenous seeding; S. aureus and other non-pneumococcal streptococci are the most common.
• Direct introduction from penetrating trauma or cardiothoracic surgery. Clostridial pericarditis is common in gunshot wounds to the chest, but polymicrobial infections are mostly encountered in these situations.

Each of the described mechanisms is responsible for approximately 25% of cases of bacterial pericarditis, though the actual incidence is variably reported in the literature.

Tuberculous pericarditis has several distinct pathogenetic mechanisms. It may result from a hematogenous spread from the primary infection, lymphatic spread from intrathoracic lymph nodes, or a contiguous spread from pulmonary TB. Nonetheless, it is not uncommon to locate the primary focus of infection because most tuberculous pericarditis cases are secondary to reactivation tuberculosis.

Clinical features
Patients with bacterial pericarditis usually present with acute illness from a severe systemic infection. Fever and dyspnea are the two most commonly presenting symptoms. Chest pain and pathognomonic pericardial friction rub are reported in only about one-third to half of patients with pericarditis. Pericardial rub could be absent when there is significant effusion, which dampens friction between the two pericardial surfaces. Consequently, the diagnosis of pericarditis is frequently delayed until the patient develops hemodynamic instability due to a large pericardial effusion or cardiac tamponade.

On the other hand, tuberculous pericarditis usually presents as an insidious process with nonspecific symptoms. Night sweats, cough, dyspnea, and weight loss are the most commonly presenting symptoms, and chest pain is more common than other causes of bacterial pericarditis. Symptoms of pericarditis in HIV-infected individuals could be masked by those of other opportunistic infections and usually overlooked. A high index of clinical suspicion is required in this patient population. Constrictive pericarditis, effusive pericarditis, myopericarditis, and cardiac tamponade are recognized complications of tuberculous pericarditis.

Regardless of the etiology of bacterial pericarditis:

• Constrictive pericarditis – Broadbent sign (11th and 12th rib retraction due to pericardial adhesions to the diaphragm), Friedreich's sign (rapid y descent of the jugular venous wave), and Kussmaul's sign (a paradoxical rise in jugular venous pressure on inspiration) are observed;
• Pericardial effusion – Ewart's sign (a triangular area of dullness at the tip of the left scapula along with tubular breath sounds and egophony at the same location) is noted;
• Cardiac tamponade – Pulsus paradoxus (a fall of systolic blood pressure of >10 mm Hg during the inspiratory phase) and Beck's triad (hypotension, muffled heart sounds, and distended neck veins) are present.

Recognition of these physical signs requires astute clinical experience and skills.