B49-43 Recurrent Purulent Pericarditis and Cardiac Tamponade Due to Methicillin-Sensitive Staphylococcus Aureus Following Recent Covid-19-Associated Pericarditis

Abstract Background Purulent pericarditis is now rare in the antibiotic era but carries high mortality without prompt drainage and targeted therapy. Recent reports suggest that viral pericardial inflammation, particularly after COVID-19 infection, may predispose to secondary bacterial seeding by Staphylococcus aureus. Case A 67-year-old man with coronary artery disease, diabetes, obesity, and poor dentition presented with pleuritic chest pain shortly after recovering from COVID-19 infection. Initial work-up revealed acute pericarditis with a small circumferential effusion and non-obstructive coronary disease on angiography. He improved on corticosteroids, colchicine, and non-steroidal anti-inflammatory therapy and was discharged. Within days, he re-presented with recurrent positional chest pain and dyspnea. Echocardiography demonstrated a moderate effusion that rapidly progressed to a large, with tamponade physiology. Pericardiocentesis evacuated approximately 900 mL of straw-colored fluid with symptomatic relief. Despite transient improvement, the patient again developed chest discomfort and dyspnea. Repeat imaging revealed re-accumulation of a large pericardial effusion with pericardial enhancement and a concurrent left pleural effusion. A second pericardiocentesis drained nearly 1 L of purulent fluid. Cultures of both pericardial and pleural samples grew methicillin-sensitive Staphylococcus aureus. Owing to early recurrence despite drainage and anti-inflammatory therapy, cardiothoracic surgery performed a subxiphoid pericardial window with pleural drainage. He completed six weeks of intravenous cefazolin with continued colchicine and gradual taper of corticosteroids. Serial echocardiograms over subsequent weeks showed a small residual fibrinous effusion without tamponade physiology. Discussion This case highlights the potential for S. aureus superinfection of a recently inflamed pericardium following viral pericarditis. The rapid transformation from serous to purulent effusion underscores the need for close early follow-up after discharge and low threshold for repeat imaging when symptoms recur. The presence of both pericardial and pleural MSSA infection suggests contiguous thoracic spread rather than hematogenous dissemination. Early escalation from needle drainage to surgical window achieved durable source control and prevented constrictive physiology. Conclusion MSSA purulent pericarditis may complicate recent COVID-19 pericarditis even in immunocompetent patients. Clinicians should maintain high suspicion for secondary bacterial infection when effusions enlarge rapidly or recur soon after initial drainage. Prompt recognition, combined medical-surgical management, and structured imaging follow-up are essential to optimize outcomes. This abstract is funded by: none