Complicated Acute Pericarditis and Peripheral Venous Catheter-Related Bloodstream Infection Caused by Methicillin-Resistant Staphylococcus aureus after Influenza B Virus Infection: A Case Report

Acute pericarditis is inflammation of the pericardium with or without effusion and is rare in children, though it can progress to significant effusion or cardiac tamponade. Etiology is often idiopathic and presumed viral/postviral; however, identifiable pediatric causes are frequently bacterial and often associated with bacteremia. Management depends on severity and cause: many presumed viral cases respond to nonsteroidal anti-inflammatory drugs and colchicine, while bacterial pericarditis and purulent effusions require antibiotics and pericardial drainage. This report describes a 14-month-old girl with acute pericarditis complicated by sepsis and MRSA PVC-related bloodstream infection following recent influenza B infection, successfully treated without pericardial drainage.

The discussion references literature indicating that influenza-associated pericarditis is generally uncommon in children but can be severe, occasionally resulting in large effusions and tamponade (including reports with influenza A and B). MRSA pericarditis, though rare, often presents with bacteremia, sepsis, and a high likelihood of requiring surgical intervention. Secondary bacterial infections after influenza commonly occur about one week post-infection and worsen outcomes. Mechanistic studies suggest influenza can impair host antibacterial defenses by attenuating IL-1β production and increasing IL-10 via regulatory T cells, which deactivates macrophages and reduces protective cytokines, thereby predisposing to bacterial superinfection. Bedside ultrasound is emphasized in prior reports as critical for rapid assessment of pericardial effusion and tamponade to guide timely interventions.

Case report methodology: A previously healthy 14-month-old female presented nine days after illness onset with persistent high fever, cough, and worsening dyspnea after a positive rapid antigen test for influenza B without antiviral therapy. At a prior hospital on day 7, a peripheral venous catheter (PVC) had been inserted and prednisolone 1 mg/kg/day administered; she deteriorated and was transferred. Initial assessment included vital signs, cardiopulmonary examination (muffled heart sounds, decreased breath sounds left base, wet rales), and inspection of the PVC site (redness, swelling, slight purulent discharge). Laboratory tests showed leukocytosis (WBC 34,200/μL; 85% neutrophils), anemia (Hb 8.9 g/dL), elevated inflammatory markers (CRP 29.75 mg/dL, procalcitonin 1.10 ng/mL), elevated BNP (235 pg/mL), normal troponin-I (<10 pg/mL), and elevated LDH (453 U/L). Imaging included chest X-ray (cardiomegaly; cardiothoracic ratio 0.60), transthoracic echocardiography (pericardial effusion; thickness 8.6 mm; no respiratory variation, biventricular dysfunction, or global hypokinesia), ECG (sinus tachycardia, PR depression and concave ST elevation in II, III, aVF, V2–V6; PR elevation and ST depression in aVR and V1), and contrast-enhanced chest CT (pericardial effusion and left pleural effusion with atelectasis). Microbiology: Two consecutive peripheral blood cultures were obtained and the PVC removed; empiric cefotaxime 150 mg/kg/day plus vancomycin 45 mg/kg/day was started. Aerobic blood culture flagged gram-positive cocci within one day; mass spectrometry identified MRSA. Antimicrobial susceptibility showed resistance to beta-lactams and susceptibility to vancomycin (MIC ≤1 μg/mL) and daptomycin (0.5 μg/mL). The same MRSA grew from the PVC tip (>15 CFU) and a skin swab from the insertion site. Therapy was de-escalated to vancomycin. Anti-inflammatory therapy for pericarditis included aspirin 30 mg/kg/day and colchicine 0.02 mg/kg/day; diuretics were added. Serial bedside transthoracic echocardiography was performed to monitor effusion and cardiac function. No pericardiocentesis was performed given absence of tamponade physiology or ventricular dysfunction. Dosing of anti-inflammatory agents was tapered as symptoms improved. Duration: Two weeks of intravenous antimicrobial therapy inpatient; aspirin discontinued at 99 days and colchicine at 188 days in outpatient follow-up.

- A 14-month-old girl developed acute pericarditis with pericardial effusion following influenza B infection, complicated by sepsis and MRSA PVC-related bloodstream infection. - Initial vitals: T 39.1°C, BP 92/65 mmHg, HR 158 bpm, RR 65/min, SpO2 99% on 5 L/min O2. Exam: muffled heart sounds; decreased left basal breath sounds; inflamed PVC site with purulence. - Labs: WBC 34,200/μL (85% neutrophils), Hb 8.9 g/dL, Hct 27.0%, platelets 359,000/μL, CRP 29.75 mg/dL, procalcitonin 1.10 ng/mL, BNP 235 pg/mL, troponin-I <10 pg/mL, LDH 453 U/L. - Imaging: CXR cardiothoracic ratio 0.60; echocardiogram pericardial effusion 8.6 mm without ventricular dysfunction; ECG with diffuse ST elevations and PR depression; CT with pericardial effusion and left pleural effusion/atelectasis. - Microbiology: MRSA isolated from blood culture, PVC tip (>15 CFU), and skin swab at PVC site; vancomycin MIC ≤1 μg/mL; daptomycin MIC 0.5 μg/mL. - Management: Immediate removal of PVC; empiric cefotaxime + vancomycin, then de-escalated to vancomycin; anti-inflammatory therapy with aspirin and colchicine; diuretics; frequent bedside echocardiography; no pericardiocentesis. - Clinical course: Fever and dyspnea improved the next day; pericardial effusion decreased and returned to baseline in following days; discharged after 2 weeks of IV antibiotics; aspirin stopped at day 99 and colchicine at day 188; no recurrence or complications over 4-year follow-up.

This case highlights acute pericarditis in a child in the setting of recent influenza B infection, complicated by MRSA PVC-related bloodstream infection leading to sepsis. The temporal sequence suggests initial influenza-related pericardial inflammation followed by secondary MRSA bacteremia from the PVC site, a known window of vulnerability approximately one week after influenza when host antibacterial defenses are impaired. Literature indicates that influenza-associated pericarditis, while uncommon, can progress to large effusions and tamponade; MRSA pericarditis often presents severely with sepsis and commonly requires surgical drainage. Immunologic studies suggest influenza can attenuate IL-1β responses and increase IL-10 via regulatory T cells, contributing to susceptibility to bacterial superinfection. In this patient, targeted therapy (vancomycin) with prompt source control (PVC removal) and anti-inflammatory therapy, accompanied by close hemodynamic and echocardiographic monitoring, resulted in rapid improvement without the need for pericardiocentesis. Frequent bedside ultrasound was pivotal to assess for tamponade physiology and to guide continued conservative management. The findings reinforce the need in pediatric pericarditis to aggressively search for bacterial causes—especially in the presence of sepsis or skin/soft tissue infection—and to tailor therapy accordingly while vigilantly monitoring for progression to tamponade.

In pediatric acute pericarditis, especially with signs of sepsis or recent viral illness, early identification of the causative organism and initiation of targeted antimicrobial therapy are critical to prevent deterioration and mortality. Bedside echocardiography should be used frequently to monitor for progression to cardiac tamponade and to evaluate treatment response, potentially obviating the need for invasive drainage when hemodynamics are stable. When etiology is uncertain, prioritize cause elucidation with cultures and imaging if stable; if unstable, treat urgently for suppurative pericarditis with antibiotics and consider pericardial drainage. Ongoing vigilance for complications of MRSA bacteremia (e.g., endocarditis, osteomyelitis, abscess) is necessary to determine treatment duration. Future work may further clarify immunologic mechanisms of post-influenza bacterial superinfection and optimal management pathways in pediatric pericarditis.

As no pericardiocentesis or pericardial fluid analysis was performed due to clinical stability and absence of tamponade, the direct etiologic contribution of influenza B versus MRSA to the pericardial effusion cannot be definitively determined. This is a single-patient case report, limiting generalizability. Prednisolone exposure prior to transfer may have influenced the clinical course and immune response.