A case report of fulminant primary purulent pericarditis due to Streptococcus pyogenes presenting with cardiac tamponade in a seemingly immunocompetent adult

Abstract

Background

Primary purulent pericarditis due to Streptococcus pyogenes is exceedingly rare in adults, with fewer than 10 cases reported in the literature to date. Most reported cases have occurred in the setting of an immunocompromised state, thoracic procedures, or identifiable infectious foci.

Case summary

A 63-year-old immunocompetent man experiencing homelessness with a past medical history of alcohol-use disorder and plaque psoriasis presented in acute hypoxemic respiratory failure. Transthoracic echocardiography revealed a large fibrinous pericardial effusion with tamponade physiology. Emergent pericardiocentesis yielded 600 ml of purulent fluid, and cultures grew S. pyogenes. Despite appropriate antimicrobial therapy, recurrent pericardial effusion developed, necessitating creation of a pericardial window. Extensive infectious and immunologic evaluation did not identify an underlying immunodeficiency or primary source. The hospital course was complicated by secondary infections, progressive multi-organ failure, septic shock, and death on hospital Day 61.

Discussion

Purulent pericarditis secondary to S. pyogenes remains an extremely rare diagnosis with a high mortality rate. This aggressive case is striking, given the absence of a clear infectious nidus and the need for early recognition and definitive source control. This case report emphasizes multiple aetiologies of purulent pericarditis, regardless of perceived source, especially those of undomiciled status or facing ongoing social inequities.

Learning points.

• Purulent pericarditis is a rare pathology, but associated with high mortality, highlighting the need for prompt evaluation and treatment.

• There are multiple aetiologies of bacterial purulent pericarditis, and acute bacterial infection is even possible without evidence of a systemic infection.

• Group A Strep, while rare, exists as a possible infectious aetiology for purulent pericarditis for patients who are seemingly immunocompetent.

• This case highlights the need to consider exposure-related vulnerability and functional immune impairment in patients experiencing homelessness or severe social disadvantage.

Introduction

There is limited literature regarding the diagnosis of primary purulent pericarditis from Streptococcus pyogenes. In this report, we describe a case of group A Streptococcus–related purulent pericarditis in an otherwise seemingly immunocompetent 63-year-old undomiciled male, resulting in cardiac tamponade requiring emergent pericardiocentesis and subsequent pericardial window.

Purulent pericarditis is an infectious and pro-inflammatory condition of the pericardium associated with a multitude of bacterial and viral organisms. Seeding of the pericardium is most often due to transit of bacteria from blood-borne, respiratory, or post-surgical infectious sources. Commonly implicated agents include Staphylococcus aureus, Streptococcus pneumoniae, and Mycobacterium tuberculosis.¹ In comparison, purulent pericarditis secondary to S. pyogenes is rare and has been previously reported in limited case reports of post-surgical complications, immunocompromised individuals, and paediatric patients.^2–5 This case presentation elucidates the aggressive pathology of purulent pericarditis and the importance of early recognition of alternative aetiologies, in particular those cases of unhoused and resource-limited individuals.

Summary figure

Case presentation

A 63-year-old man experiencing homelessness with a history of alcohol-use disorder and plaque psoriasis presented to the emergency department (ED) with acute hypoxemic respiratory failure. His initial vitals were: Blood pressure 121/78 mmHg, heart rate 126 bpm, respiratory rate 44 breaths/min. His exam was notable for significant tachycardia with reported regular rhythm and no murmurs, rubs, or additional heart sounds appreciated. He was tachypneic, rhonchorous, and in appreciable respiratory distress with intercostal retractions evident. Due to increased work of breathing, he was immediately escalated to bi-level positive airway pressure in the ED with subsequent oxygen saturation of 98%.

Notable labs upon admission demonstrated a leukocytosis of 19.85 ×10³/µl (Ref 3.40–11.20 10³/µl), bicarbonate of 9 mmol/l (Ref 21.0–26.0 mmol/l), lactic acid of 2.9 mmol/l (Ref 0.5–2.2 mmol/l), BUN 131 mg/dl (Ref 8–23 mg/dl), creatinine of 15 mg/dl (Ref 0.67–1.17 mg/dl), alkaline phosphatase 456 U/l (Ref 40–129 U/l), troponin-T HS of 79 ng/l (Ref ≤22 ng/l), and N-terminal pro-beta natriuretic peptide of >70 000 pg/ml (Ref ≤124 pg/ml). Chest x-ray demonstrated a small left pleural effusion with adjacent atelectasis or consolidation. Electrocardiogram (Figure 1) demonstrated sinus tachycardia with occasional premature ventricular complexes and non-specific repolarization abnormalities, along with subtle electrical alternans appreciated.

Figure 1.

Subtle electrical alternans on ECG suggestive of pericardial effusion.

He was empirically treated for community-acquired pneumonia with ceftriaxone and doxycycline. Due to worsening hypoxia, he was transferred to the intensive care unit (ICU), with escalation of non-invasive positive pressure support and broadening of his antibiotics to vancomycin and piperacillin-tazobactam.

Transthoracic echocardiography (TTE) views are shown in Figure 2, involving parasternal short axis (A), parasternal axes via 90° X-plane (B), apical four-chamber (C) and parasternal long axis (D), and revealed a large fibrinous pericardial effusion measuring 1.2 cm adjacent to the right ventricle, 1.3 cm inferior to the left ventricle, and 1.6 cm around the left ventricular apex, with notable diastolic right atrial invagination and marked respiratory variability of trans-mitral and trans-tricuspid diastolic velocities, consistent with cardiac tamponade (Figure S1).

Figure 2.

Parasternal short axis (A), parasternal axes using X-plane (B), apical four-chamber (C), and parasternal long axis (D), revealed a large fibrinous pericardial effusion with features consistent with cardiac tamponade.

Emergent pericardiocentesis with pericardial drain placement was performed in the ICU and yielded approximately 600 cc of purulent fluid (Figure 3). His post-procedural TTE identified a now trace pericardial effusion with normal IVC size and normal respiratory variability consistent with RA pressures of 5–10 mmHg. Pericardial fluid cultures grew gram-positive cocci, which speciated as Group A Streptococcus, and subsequent antibiotic therapy was narrowed to penicillin. Moreover, he was initiated on continuous veno-venous hemofiltration for renal failure in the setting of purulent infection.

Figure 3.

Post-pericardiocentesis fluid collection, showing purulent contents.

Admission blood cultures were negative for S. pyogenes but subsequently grew Cryptococcus neoformans, prompting initiation of systemic antifungal therapy with liposomal amphotericin B and fluconazole. Lumbar puncture was also performed and excluded central nervous system involvement. Despite appropriate intravenous penicillin therapy and initial pericardial drainage, serial transthoracic echocardiography demonstrated re-accumulation of pericardial fluid, and the patient required surgical pericardial window on hospital Day 13. Fluid obtained from the second pericardial procedure resulted in negative cultures, but concurrent bronchoalveolar lavage (BAL) performed additionally grew Aspergillus fumigatus in BAL culture. Given the occurrence of multiple infectious processes, a comprehensive immunologic and rheumatologic evaluation—including HIV testing, autoimmune screen for vasculitis, and advanced testing for rare immunodeficiency syndromes at the National Institutes of Health (Table 1)—was undertaken but did not identify an underlying condition.

Table 1.

The National Institutes of Health immunologic marker evaluation

Sample/analyte	IL-17A	IFN-γ	GM-CSF	IFN-α	IL-23
Blank	43	67	32	20	39
Normal Control	469	406	358	540	138
Positive Control	10 493	10 891	12 496	6287	16 719
Patient sample	142	164	120	156	67

GM-CSF, granulocyte-macrophage colony-stimulating factor; IFN, interferon; IL, interleukin.

His subsequent hospital course included acute melena, hypotension, and vancomycin-resistant Enterococcus bacteraemia, with CT scans confirming recurrent moderate pleural effusions and recurrent pericardial effusion with increased ascites requiring paracentesis (3L of straw-coloured fluid removed).

The patient ultimately progressed to septic shock, was emergently intubated, and expired on Day 61 of hospitalization after cardiac arrest.

Discussion

The aetiology of pericarditis is notoriously difficult to identify, with approximately 80%–90% of cases believed to be idiopathic in nature, generally with presumption of a viral aetiology. Those most commonly identified in the inpatient setting are viral such as Coxsackievirus, Epstein–Barr virus, Cytomegalovirus and Parvovirus, or idiopathic in nature.^6,7 Purulent pericarditis is a rare infectious complication encompassing less than 1% of cases of pericarditis, but with an associated mortality of up to 30% and risk of constrictive pericarditis, highlighting the need for prompt identification and treatment of this condition.^8,9

The most common causes of purulent pericarditis involve seeding from bacterial pathogens by haematogenous routes, respiratory and direct inoculation from a surgical site, or procedure-associated infections. These infectious organisms include S. aureus and S. pneumoniae, with M. tuberculosis predominantly documented in developing countries, along with occasional atypical bacteria.^8,10 Rarer sources such as fungi and anaerobic bacteria have been implicated predominantly in the literature of immunocompromised hosts, such as individuals living with HIV.^4,5 Other non-infectious causes of pericarditis and accumulation of pericardial fluid expansion involve malignancy—predominantly lung and breast cancer—and various inflammatory and autoimmune conditions, including but not limited to lupus and rheumatoid arthritis.¹⁰

In cases such as this, where clinical tamponade develops, immediate pericardiocentesis and eventual pericardial window may be required for haemodynamic stabilization and adequate infectious source control. Recurrent pericarditis with pericardial effusions has a reported incidence of up to 30% in these cases.¹¹ In these cases, current ESC 2025 guidelines recommend consideration of early surgical intervention for prevention of pericardial constriction. Although not performed in this case, there may also be a role in intrapericardial fibrinolysis to reduce complications in more loculated or fibrinous effusions.⁶

While not seen in this case report, typical changes of widespread ST elevations along with PR depressions on EKG, and a pericardial friction rub, can be observed in approximately 25%–50% of cases.¹² Electrical alternans and ‘swinging heart’ were noted on review of telemetry and transthoracic echocardiography data during this patient’s hospitalization.

Purulent pericarditis secondary to S. pyogenes remains an extremely rare complication. To our knowledge, there have been fewer than ten reported adult cases of group A Streptococcus–related purulent pericarditis. This case report documents the eighth known case to date.^2–5,13,14 This case is particularly striking given the lack of evidence for haematologic seeding, no prior procedure, and no known respiratory or oropharyngeal infection leading to pericardial spread. The aetiology of this patient’s presentation remains an enigma. Although no identifiable autoimmune or immune-deficient cause was found, his concurrent fungal and bacterial infections lend support to the hypothesis that his undomiciled status, resource inequality, and alcohol use disorder led to a state of increased exposure risk for this particular microbe of S. pyogenes. It is known that excessive alcohol usage has deleterious effects on both innate and adaptive immune systems, and could have increased his risk for purulent pericarditis.⁷ Prior works have also cited observational data of an increased risk of invasive streptococcal infections (including S. pyogenes) in undomiciled individuals.^15,16 This report aims to provide evidence of a primary S. pyogenes infection without a clearly identifiable source.

Lead author biography

Kyle LaPenna, MD, PhD, is an internal medicine resident physician at New York Presbyterian—Weill Cornell Medical Center.

Supplementary material

Supplementary material is available at European Heart Journal – Case Reports online.

Author contributions

Kyle LaPenna (Conceptualization, Investigation, Methodology, Writing—original draft, Writing—review & editing [lead]), Jonathon Mitchell (Conceptualization, Investigation, Methodology, Writing—original draft, Writing—review & editing [supporting]), John Mancini (Conceptualization, Investigation, Methodology, Visualization, Writing—original draft, Writing—review & editing [supporting]), Khanh Pham (Conceptualization, Data curation, Investigation, Visualization, Writing—original draft, Writing—review & editing [supporting]), and Pritha Subramanyam (Conceptualization, Investigation, Methodology, Project administration, Resources, Validation, Visualization, Writing—original draft, Writing—review & editing [supporting])

Consent: The patient reported in this case is deceased. Despite the best efforts of the authors, they have been unable to contact the patient's next-of-kin to obtain consent for publication. Every effort has been made to anonymise the case. This situation has been discussed with the editors.

Funding

The authors received no private or public funding support for the purposes of this manuscript.

Data availability

All data presented in this article shall be shared upon reasonable request by corresponding author.