A Unique Presentation of Bacterial Group G Streptococcus Myopericarditis

Abstract

Perimyocarditis and myopericarditis are inflammatory conditions of the pericardium and myocardium, often of idiopathic or infectious etiology, with viral infections being the most common. Nonrheumatic streptococcal myopericarditis (NSM) is a rare condition that can mimic acute myocardial infarction. This case report presents a 22-year-old male with no prior medical history who developed NSM following a streptococcal pharyngitis infection. The patient presented with pleuritic chest pain, tightness, and decreased exercise tolerance. Laboratory studies revealed elevated troponin levels and positive Streptococcus G antigen. Treatment included ampicillin-sulbactam, colchicine, ibuprofen, and dexamethasone. The patient’s symptoms resolved, and he was discharged with amoxicillin-clavulanate, colchicine, and ibuprofen.

Introduction

Inflammation of the pericardium and myocardium is known as pericarditis and myocarditis, respectively. When the inflammation of the pericardium spreads to the myocardium, it becomes perimyocarditis. Myopericarditis is similar to pericarditis but with evidence of myocardium involvement, such as elevated cardiac biomarkers or imaging studies revealing normal wall motion. ¹ Although the cause of myopericarditis is often idiopathic, other common causes include infectious agents. Viral infections are more commonly implicated. However, other bacterial, fungal, and parasitic infections have also been noted. ¹ Nonrheumatic streptococcal myopericarditis (NSM) can appear days after upper respiratory infection symptoms. The NSM can mimic more insidious diseases such as acute myocardial infarction and therefore should be promptly evaluated and treated. ² Although the incidence of myopericarditis has not been established, we present a rarity of streptococcal G infection causing myopericarditis in a young, otherwise healthy male. Upon literature review, only 7 case reports mentioned NSM, making this case unique in its nature.

Case Presentation

A 22-year-old male with no prior medical diagnoses presented with a 2-day period of positional pleuritic chest pain and tightness. The patient endorsed that 1 week before presentation, current symptoms were preceded by pharyngitis with concomitant odynophagia, a subjective fever, and chills, all of which lasted a week and were self-resolved. The pain was initially intermittent and became constant and progressively more intense, prompting his emergency room visit. The patient endorsed a decrease in exercise tolerance after walking 2 blocks. The patient reported never having similar symptoms. He denied exposure to sick contacts or recent travel. He denied any family history of cardiac issues. The patient admitted to smoking marijuana once a day. On arrival, vitals revealed a blood pressure of 123/81 mm Hg and a heart rate of 53 beats per minute, and saturating at 99% on room air. A physical exam revealed the pharynx was erythematous with exudates without any cervical lymphadenopathy. Laboratory studies were remarkable for elevated levels of Troponin-I at 6311 ng/mL (normal level: 3-23) and a C reactive protein (CRP) of 22.3 mg/L (normal level: <9.9). Complete blood count was not remarkable for leukocytosis. Serology was positive for Strep G Antigen. The electrocardiogram (EKG) revealed sinus bradycardia without PR prolongation or ischemic changes. Blood cultures were negative. Throat culture revealed Group G beta hemolytic streptococci. The patient was administered ampicillin-sulbactam, colchicine, ibuprofen, and dexamethasone. The patient underwent a transthoracic echocardiogram (TTE), which revealed a left ventricular (LV) ejection fraction mildly decreased at 50% to 55%, no LV hypertrophy, and a normal filling pattern with no wall motion abnormalities. On the second day of hospitalization, the patient endorsed the complete resolution of chest pain and shortness of breath. He was discharged on amoxicillin-clavulanate, colchicine, and ibuprofen and reported resolution of symptoms on outpatient follow-up.

Discussion

Nonrheumatic streptococcal myopericarditis was first described by Gore and Saphir ³ in 1947 in a large autopsy series showing 35 fatal myocarditis cases in the setting of acute tonsillitis. Since then, the incidence of NSM has been rising, yet it is still underreported. It is imperative to rule out acute rheumatic fever in patients with streptococcal tonsillitis with cardiac involvement. Acute rheumatic fever is a known sequela of streptococcal tonsillitis, which is significant for cardiac involvement. Rarely, nonrheumatic streptococcal tonsillitis can cause acute myopericarditis, which presents similarly to acute viral myocarditis. Clinical symptoms include positional chest pain, ECG changes, and elevated cardiac enzymes. The underlying mechanism of NSM is still yet to be understood. Suspected underlying mechanisms consist of autoimmunity triggered by cross-reactivity between streptococcal antigen and myocardium or direct effects of streptococcal toxins on the myocardium.^4,5

Nonrheumatic streptococcal myopericarditis can present with symptoms mimicking acute STEMI. Mokabberi et al described a case series involving 8 young adults (ages 20-35) who developed streptococcal pharyngitis–associated myocarditis, presenting with chest pain, ST-segment elevation on ECG, and elevated cardiac biomarkers. Despite these STEMI-like symptoms, coronary angiography showed normal arteries, and cardiac magnetic resonance (CMR) imaging revealed myocarditis with subepicardial late gadolinium enhancement. All patients had recent streptococcal infections and recovered with antibiotics and supportive care. ⁶

Similarly, Upadhyay et al reported 9 cases of acute nonrheumatic streptococcal myocarditis in young adults, primarily males, who also presented with chest pain and ST-segment elevation on ECG. The average latency from sore throat to chest pain was 3 days, with Group A streptococcus confirmed in 56% of cases and Group G streptococcus in 22%. Coronary angiography showed no obstructive lesions, and CMR confirmed myocarditis in some patients. All patients fully recovered with antibiotic therapy. ⁷ In both series, none of the patients met the Jones criteria for acute rheumatic fever. The patients were predominantly young males, with Group A streptococcus being more common than Group G streptococcus.

According to the revised Jones criteria, the major criteria for acute rheumatic fever in low-risk populations are carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules, and the minor criteria include polyarthralgia, hyperpyrexia (≥38.5°C), Erythrocyte Sedimentation Rate (ESR) ≥60 mm/h, and/or CRP ≥ 3.0 mg/dL, and prolonged PR interval. The diagnosis of acute rheumatic fever is made with the presence of 2 major criteria or 1 major and 2 minor criteria, which the first episode of the disease, in our patient’s case, did not meet. ⁸ Classically, chest pain occurs within 7 days from the initiation of a sore throat; however, in acute rheumatic fever, signs and symptoms develop within 2 to 3 weeks from the onset of streptococcal pharyngitis. Antistreptolysin elevation, positive serum streptococcal antigen, and positive throat culture with elevated ESR and CRP, in the absence of Jones criteria, can guide the diagnosis of NSM. Along with the myocardial involvement, cardiac enzyme levels can be elevated, and ECG changes such as ST-segment elevation may be observed. Cardiac imaging modalities such as transthoracic echocardiography or transesophageal echocardiography can be used to rule out valvular pathologies and help differentiate it from acute rheumatic fever. Cardiac magnetic resonance imaging may be helpful in detecting cardiac involvement. The NSM has a good prognosis and can be completely cured with adequate antibiotic treatment. The treatment of choice is oral penicillin. After full recovery, prophylaxis is not recommended due to the lack of recurrence. Distinguishing NSM from acute rheumatic fever is crucial to decrease morbidity and mortality.