INFECTIOUS PERICARDITIS

Acute infectious pericarditis is an inflammation of the pericardium caused by direct or indirect colonization of infectious agents. The most common form is viral pericarditis, followed by bacterial, tuberculous, fungal, and parasitic pericarditis.

Patients often report a recent infection involving the respiratory or gastrointestinal tract or a systemic infection. The clinical presentation includes both typical pericarditis symptoms and systemic infectious symptoms:

Specific symptoms of pericarditis:

• Pleuritic chest pain: acute, localized in the left retrosternal area, radiating to the back and shoulders. It worsens in the supine position and improves when sitting up and leaning forward.
• Pericardial friction rub: a superficial, rough, and discontinuous sound, best heard on auscultation when the patient is leaning forward.
• Dyspnea: more pronounced in cases with significant pericardial effusion.
• Signs of cardiac tamponade: hypotension, jugular vein distension, and pulsus paradoxus in severe cases.

Systemic infectious symptoms:

• Fever: higher in bacterial and tuberculous pericarditis.
• General malaise, fatigue, and diffuse muscle pain.
• Elevated inflammatory markers: ESR, CRP, leukocytosis, and high ferritin in severe cases.

VIRAL PERICARDITIS

Viral pericarditis is the most common cause of infectious pericarditis and is often self-limiting but prone to recurrence. Viral transmission occurs through the bloodstream, direct extension from upper respiratory infections, or an immune-mediated response.

Most common viral agents:

• Enteroviruses (Coxsackie B, Echovirus) → responsible for most cases.
• Influenza and Parainfluenza viruses → associated with seasonal outbreaks.
• Herpesviruses (CMV, EBV, VZV) → more common in immunocompromised patients.
• HIV → direct pericardial infection or secondary to opportunistic infections (Mycobacterium avium, Cryptococcus).

Diagnosis:

• ECG: characteristic four-stage evolution with diffuse ST-segment elevation.
• Viral biomarkers: PCR for specific viruses in blood and pericardial fluid.
• Echocardiography: mild to moderate pericardial effusion, rarely leading to tamponade.

Treatment: rest, NSAIDs as first-line therapy, and colchicine to reduce recurrence risk. Corticosteroids are reserved for selected cases of post-viral autoimmune pericarditis.

BACTERIAL PERICARDITIS

Bacterial pericarditis is less common but significantly more severe, often with a poor prognosis if not treated promptly. The infection can spread via:

• Direct extension from pulmonary, mediastinal, or endocardial infections.
• Hematogenous dissemination from bacteremia (e.g., Staphylococcus aureus, Streptococcus pneumoniae).
• Penetrating wounds or post-cardiac surgery infections.

Pericardial effusion is typically serofibrinous or purulent, with severe systemic symptoms, including high fever, tachycardia, and signs of systemic toxicity.

Diagnosis:

• Blood cultures to identify the causative pathogen.
• Pericardial fluid analysis: bacterial culture, Gram stain, and PCR.
• Echocardiography: purulent effusion with potential cardiac tamponade.

Treatment: broad-spectrum antibiotic therapy (vancomycin + ceftriaxone), later adjusted based on culture results. Pericardiocentesis is often required for drainage.

TUBERCULOUS PERICARDITIS

Tuberculous pericarditis is caused by Mycobacterium tuberculosis and typically results from hematogenous spread or rupture of an infected mediastinal lymph node.

Clinical characteristics:

• Large, slowly progressive pericardial effusion.
• Presence of caseous granulomas and lymphocytic infiltration in the pericardium.
• Subacute symptoms, including evening fever, night sweats, and weight loss.

Diagnosis:

• Detection of tuberculosis bacilli (Ziehl-Neelsen stain, PCR on pericardial fluid).
• Quantiferon-TB test and pericardial biopsy in doubtful cases.

Treatment: anti-tuberculosis therapy (Rifampin, Isoniazid, Pyrazinamide, Ethambutol) for at least 6–9 months. Pericardiocentesis is indicated for massive effusions.

FUNGAL AND PARASITIC PERICARDITIS

Fungal and parasitic pericarditis are rare and occur primarily in immunocompromised patients. They are characterized by an insidious course and slow progression toward constrictive pericarditis.

Main causes:

• Fungal: Histoplasma capsulatum, Candida spp., Aspergillus spp.
• Parasitic: Trypanosoma cruzi (Chagas disease), Echinococcus granulosus.

Diagnosis:

• Blood and pericardial fluid cultures.
• Serological tests for systemic infections.

Treatment: antifungals (Amphotericin B, Fluconazole) or antiparasitic drugs (Albendazole, Benznidazole for Chagas disease). In advanced fibrosis, pericardiectomy may be required.

GENERAL MANAGEMENT

Beyond the etiological therapy, management includes:

• NSAIDs as first-line treatment for viral and inflammatory pericarditis.
• Corticosteroids only in post-infectious autoimmune cases.
• Pericardiocentesis for large effusions or suspected tamponade.
• Pericardiectomy in chronic or refractory cases.