Medical education
Lessons from practice
Volume 206 - Issue 3
Streptococcus pyogenes pericarditis in a healthy adult: a common organism in an uncommon site
Authors: Lauren C Giudicatti, Gar-Hing Lee, Claire Italiano and Nik Stoyanov
Med J Aust 2017; 206 (3): 113-114. || doi: 10.5694/mja16.00421
Published online: 20 February 2017
Published online: 20 February 2017
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Clinical record
A 64-year-old man presented with progressive dyspnoea, chest pain and rigors 5 days after returning from the United States. This was preceded by a 3-week history of sore throat, left submandibular lymphadenopathy and non-productive cough and fevers, which began while he was overseas.
The patient’s overseas travel was limited to major cities. His past medical history was unremarkable. He did not smoke, consume excessive alcohol or use illicit drugs. The patient did report a dental root infection in the week before travel, which completely resolved following drainage.
On presentation to our hospital, the patient was alert and afebrile but hypotensive with blood pressure of 80/60 mmHg on a peripheral vasopressor infusion. Vital signs included a heart rate of 106 beats/min, respiratory rate of 36 breaths/min and oxygen saturation of 99% on supplemental oxygen (4 L/min). Heart sounds were muffled with no pericardial rub heard. Jugular venous pressure was elevated and his electrocardiogram showed low voltage QRS complexes and saddle-shaped ST elevation laterally (Figure 1).
Inflammatory markers revealed a white cell count of 26.7 × 109/L (reference interval [RI], 4–11 × 109/L) with predominant neutrophilia and a C-reactive protein level of 207 mg/L (RI, < 5 mg/L).
Chest x-ray showed left lower lobe consolidation with an ipsilateral effusion. Computed tomography pulmonary angiogram (CTPA) was performed to rule out pulmonary embolism and unexpectedly revealed a 1.5 cm circumferential pericardial effusion (Figure 2). A transthoracic echocardiogram then confirmed tamponade physiology (Figure 3) and was used to guide emergency pericardiocentesis and pigtail catheter placement. About 350 mL of purulent straw-coloured fluid was drained, resulting in immediate haemodynamic improvement.
Biochemistry of the pericardial fluid showed an exudate with a glucose level of < 0.5 mmol/L (RI, 5.9–8.8 mmol/L), a lactate dehydrogenase level of 1270 U/L (RI, 276–517) and a protein level of 56 g/L (RI, 28–38 g/L), with a fluid–serum ratio of 0.875 (RIs based on the methods of Ben-Horin and colleagues).1 Microscopy yielded moderate numbers of gram-positive cocci with subsequent culture of Streptococcus pyogenes. Sequencing of the bacterial genome revealed this to be emm-1, sequence type 28. The pericardial drain was left in situ for 48 hours and drained a total of 975 mL. Analysis of pleural fluid showed a reactive, culture-negative transudate.
Serial echocardiograms during admission demonstrated increasing fibrinous organisation of the residual effusion. Despite this, the patient recovered completely after 4 weeks of intravenous benzylpenicillin and 2 weeks of oral amoxicillin. A transthoracic echocardiogram at 2 months showed complete resolution of the pericardial effusion without constriction.
Bacterial causes represent only 5% of infectious pericarditis cases in developed countries, with the vast majority attributed to viral infection or autoreactivity.2,3 Among bacterial pericarditis cases, Staphylococcus aureus is most frequently implicated (22–31%), while Streptococcus pyogenes is exceedingly uncommon.3 In the post-antibiotic era, there is an increasing trend towards haematogenous spread as the primary mechanism of pericardial infection, as opposed to direct extension from respiratory sources.2,3
Advances in molecular techniques have facilitated the identification of over 250 types of S. pyogenes based on sequencing of the emm gene, which encodes the M protein, an important determinant of organism virulence.4 Emm-1 is the most common isolate causing invasive disease in Australia.3 Sequence type 28 in particular is highly virulent and may account for the rare invasive syndrome described here.
Untreated, purulent pericarditis is invariably fatal and, even with appropriate therapy, mortality approaches 40%.3 In a review of eight cases of S. pyogenes pericardial effusion in children aged under 15 years, all progressed to tamponade and one to death.5 Any evidence of tamponade with a history of fever should prompt immediate echocardiography.2 Our patient was initially presumed to be in septic shock, and the diagnosis may have been missed or delayed if not for the incidental finding on CTPA.
Drainage of a pericardial effusion is recommended in the following settings: suspicion of neoplastic or bacterial aetiology; symptomatic effusion refractory to medical therapy; and any case of tamponade.2 Guidelines regarding duration of pericardial drainage are currently lacking, although it is acceptable to remove catheters when less than 30 mL is drained in 24 hours.2 In one case series of 1108 patients, 71% of patients with large effusions undergoing pericardiocentesis eventually required pericardiectomy owing to inadequate drainage.6 Bacterial effusions are particularly prone to rapid re-accumulation and loculation.2 Although pericardiocentesis is often the quickest and simplest method of drainage, a surgical approach via a subxiphoid window remains the gold standard.2
Purulent pericarditis is a rare but potentially fatal condition, which may present in otherwise healthy adults. Attention to early clinical signs of tamponade followed by prompt echocardiography may be lifesaving.Lessons from practice
Streptococcus pyogenes pericarditis can rapidly progress to tamponade and death if left untreated.
Purulent pericarditis may be initially misdiagnosed as septic shock, potentially delaying pericardiocentesis.
Targeted antimicrobial therapy and adequate drainage of purulent pericardial effusions are key in allowing full clinical recovery.
Figure 1 – Electrocardiogram showing low voltage QRS complexes and saddle-shaped ST elevation laterally.
Competing interests
No relevant disclosures.
References
- Ben-Horin S, Shinfield A, Kachel E, et al. The composition of normal pericardial fluid and its implications for diagnosing pericardial effusions. Am J Med 2005; 118: 636-640.
- European Society of Cardiology. 2015 Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J 2015; 36: 2921-2964.
- Punkuweit S, Ristic A, Serefovic P, Maisch B. Bacterial pericarditis: diagnosis and management. Am J Cardiovasc Drugs 2005; 5: 103-112.
- O’Grady K, Kelpie L, Andrews R, et al. The epidemiology of invasive group A streptococcal disease in Victoria, Australia. Med J Aust 2007; 186: 565-569.
- Permira A, Tolan R. Invasive group A Streptococcus infection presenting as purulent pericarditis with multiple splenic abscesses: case report and literature review. Clin Pediatr 2012; 51: 436-441.
- Sagrista-Sauleda J, Angel J, Permanyer-Miralda G, Soler-Soler J. Long-term follow up of idiopathic chronic pericardial effusion. N Engl J Med 1999; 341: 2054.