Acute infectious pericarditis refers to inflammation of the pericardium caused by direct or indirect colonization by infectious agents. The most common form is viral pericarditis, followed by bacterial, tuberculous, fungal, and parasitic forms.
Patients often report a recent infection of the respiratory or gastrointestinal tract, or a systemic infection. The symptomatology includes both typical signs of pericarditis and systemic infectious symptoms:
Specific symptoms of pericarditis:
Pleuritic chest pain: acute, located in the left retrosternal area, radiating to the back and shoulders. Worsens in the supine position and improves with the trunk leaning forward.
Pericardial friction rub: superficial, harsh, discontinuous sound, audible on chest auscultation, indicative of pericardial inflammation.
Dyspnea: more pronounced in cases with abundant pericardial effusion.
Signs of cardiac tamponade: hypotension, jugular venous distension, pulsus paradoxus in more severe cases.
Systemic symptoms of infection:
Fever: higher in bacterial and tuberculous forms.
General malaise, asthenia and diffuse muscle pain.
Elevated inflammatory markers: ESR, CRP, leukocytosis, high ferritin in the most severe cases.
Viral Pericarditis
Viral pericarditis is the most frequent cause of infectious pericarditis and is often self-limiting, with a tendency to recur. Viral transmission occurs via hematogenous spread, direct extension from upper respiratory tract infections, or immunomediated reaction.
Most common viral agents:
Enteroviruses (Coxsackie B, Echovirus) → responsible for the majority of cases.
Influenza and Parainfluenza viruses → associated with seasonal outbreaks.
Herpesviruses (CMV, EBV, VZV) → more frequent in immunocompromised patients.
HIV → direct pericarditis or secondary to opportunistic infections (Mycobacterium avium, Cryptococcus).
Diagnosis:
ECG: typical four-stage changes with diffuse ST-segment elevation.
Viral biomarkers: PCR for specific viruses on blood and pericardial fluid.
Echocardiography: mild to moderate pericardial effusion, rarely tamponade.
Treatment: rest, NSAIDs as first-line and colchicine to reduce the risk of recurrences. Corticosteroids are reserved for selected cases with post-viral autoimmune pericarditis.
Bacterial Pericarditis
Bacterial pericarditis is less frequent but much more severe, often with an unfavorable prognosis in the absence of prompt treatment. Spread can occur via:
Direct extension from pulmonary, mediastinal or endocardial infections.
Hematogenous spread from bacteremia (e.g. Staphylococcus aureus, Streptococcus pneumoniae).
Penetrating injuries or cardiac surgery.
The pericardial effusion is typically serofibrinous or purulent, with severe symptoms such as high fever, tachycardia and signs of systemic toxicity.
Diagnosis:
Blood cultures to identify the pathogen.
Pericardial fluid analysis: bacterial culture, Gram stain and PCR.
Echocardiography: presence of purulent effusion and possible signs of cardiac tamponade.
Treatment: initial broad-spectrum antibiotic therapy with vancomycin + ceftriaxone, to be tailored based on culture results. Evacuative pericardiocentesis is often required.
Tuberculous Pericarditis
Tuberculous pericarditis is caused by Mycobacterium tuberculosis and develops through hematogenous spread or rupture of an infected mediastinal lymph node.
Clinical features:
Abundant and slowly progressive effusion.
Presence of caseous nodules and lymphocytic infiltration in the pericardium.
Subacute symptomatology with evening fever, night sweats and weight loss.
Diagnosis:
Detection of tubercle bacilli (Ziehl-Neelsen stain, PCR on pericardial fluid).
Quantiferon-TB test and pericardial biopsy in doubtful cases.
Treatment: antitubercular therapy (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) for at least 6-9 months. Pericardiocentesis is indicated in massive effusions.
Fungal and Parasitic Pericarditis
Fungal and parasitic pericarditis are rare and more frequent in immunocompromised patients. They are characterized by an insidious course and slow progression to constrictive pericarditis.
Treatment: antifungals (Amphotericin B, Fluconazole) or antiparasitic agents (Albendazole, Benznidazole for Chagas). In cases of advanced fibrosis, pericardiectomy may be required.
General Management
In addition to etiological therapy, the following are used:
NSAIDs as first-line for viral forms.
Corticosteroids only in post-infectious autoimmune forms.
Pericardiocentesis for abundant effusions or risk of tamponade.
Pericardiectomy in chronic or refractory cases.
References
Imazio M, et al. Management of pericardial diseases. Nat Rev Cardiol. 2020;17(11):693-706.
Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964.
Ristic AD, et al. Pericardial disease: an update on etiology, pathophysiology, diagnosis, and treatment. J Am Coll Cardiol. 2021;78(18):1920-1935.
LeWinter MM. Clinical practice: pericarditis. N Engl J Med. 2014;371(25):2410-2416.
Maisch B, et al. Pericardial diseases: new insights and unresolved issues. Heart Fail Rev. 2018;23(1):3-14.
Spodick DH. Acute pericarditis: current concepts and practice. JAMA. 2003;289(9):1150-1153.
Tsang TS, et al. Diagnosis and management of pericardial effusion. Mayo Clin Proc. 2002;77(4):406-413.
Troughton RW, et al. Medical therapy in pericardial disease: an update. Circulation. 2018;137(7):743-754.
Caforio ALP, et al. Myocarditis and pericarditis: pathogenesis, diagnosis, and treatment. Nat Rev Cardiol. 2023;20(5):297-312.
Brucato A, et al. Recurrent pericarditis: current perspectives. Clin Cardiol. 2022;45(3):249-258.
Bottcher H, et al. Bacterial pericarditis: etiology, clinical manifestations, and treatment. J Infect. 2021;82(1):35-43.
Haque A, et al. Tuberculous pericarditis: diagnostic challenges and management. Chest. 2020;158(6):2402-2411.