Two Pediatric Cases of Left-sided, Native-valve Streptococcus pneumoniae Endocarditis

To the Editors: Endocarditis remains a rare but serious manifestation of invasive pneumococcal disease. We highlight 2 pediatric cases that underscore the potential for morbidity and substantial complications associated with pneumococcal infective endocarditis (IE). A 12-year-old previously healthy, vaccinated male presented with 6 days of fever, cough, headache and abdominal pain. He had undergone dental cleaning with tooth extraction 3 weeks prior and tested positive for influenza A 1 week before admission. Further details of his clinical presentation, course and management are outlined in Table 1. Imaging demonstrated left lower lobe pneumonia and a large, mobile echodensity on the anterior mitral valve (MV) leaflet, moderate mitral regurgitation and mitral stenosis. Preantibiotic blood culture grew a pan-susceptible Streptococcus pneumoniae isolate identified as serotype 6 unable to distinguish serogroup (6A/B/C/D). TABLE 1. - Clinical Features and Hospital Courses of 2 Pediatric Cases of Pneumococcal Endocarditis at a United States Tertiary Care Hospital in Winter 2022 Case Presenting Symptoms Admission Labs Antimicrobial Therapy Echo Findings Surgical Intervention Complications Hospital Disposition 1 6 days fever to max 105°F, productive cough, diarrhea, headache WBC 23000/L,ANC 16000/L, Hgb 12 g/dL, PLT 77000/uL, BUN 28, Cr 1.0 mg/dL, albumin 3.0 g/dL, PCT 91 ng/mL, CRP 15 mg/dL, ESR 30 mm/hour - 6 weeks of antibiotics after mitral valve replacement- Ceftriaxone ANC, absolute neutrophil count; BUN, blood urea nitrogen; Cr, creatinine; CPR, cardiopulmonary resuscitation; CRP, C-reactive protein (normal 0 – 0.9 mg/dL); CSF, cerebrospinal fluid; ESR, erythrocyte sedimentation rate (normal 0 – 20 mm/hour); Hgb, hemoglobin; MCA, middle cerebral artery; PCT, procalcitonin (normal < 0.25 ng/mL); PEA, pulseless electrical activity; PLT, platelets; RBC, red blood cell; WBC, white blood count. Due to the risk of embolization, he underwent MV vegetation resection and valvuloplasty. The culture of the MV grew S. pneumoniae. His course was complicated by anterior MV leaflet perforation, severe mitral regurgitation, cardiogenic shock and new atrial arrhythmias ultimately requiring MV replacement. In addition to several septic emboli, he suffered a right-sided cardioembolic middle cerebral artery stroke and underwent an emergent thrombectomy with significant improvement in neurologic deficits. A 15-year-old vaccinated female with complex, single-ventricle congenital heart disease (double outlet right ventricle with d-malposed great arteries, complex inlet ventricular septal defect with straddling MV and pulmonary stenosis) presented with 1 week of cough, fever and fatigue. She also reported 2 days of severe headache and influenza A infection 3 weeks before admission. She had undergone multiple palliative surgeries with Fontan completion at age 2 and subsequently developed progressive aortic valve regurgitation (AR) requiring aortic valvuloplasty and subaortic conal tissue resection 1 year before admission. Details of her presentation and hospital course are outlined in Table 1. Brain magnetic resonance imaging revealed sinusitis, ventriculitis and small frontal and parietal infarcts. Blood and cerebrospinal fluid cultures grew pan-susceptible S. pneumoniae (serotype 19A). Admission echocardiogram revealed stable, moderate AR without vegetations, while a subsequent echocardiogram 13 days later revealed aortic valve (AV) IE with moderate to severe AR. Ventricular dysfunction and acute worsening of AR required emergent AV replacement, which was complicated by cardiac arrest requiring cardiopulmonary resuscitation. After AV replacement, brain magnetic resonance imaging demonstrated diffuse cerebral microhemorrhages without evidence of stroke. Despite overall clinical recovery, she experienced persistent right sensorineural hearing loss and neurocognitive deficits. We report 2 pediatric cases of pneumococcal IE ultimately requiring valvular replacement, in whom septic emboli and valvular destruction developed weeks after initial diagnosis and initiation of treatment for IE. Both cases occurred following a recent influenza infection, consistent with studies that have suggested that viral infections, including influenza, may increase the risk of invasive pneumococcal disease. These cases highlight the potential for pneumococcal IE to result in severe, progressive valvular destruction despite prior pneumococcal vaccination, drug-susceptible isolates, and prompt bacteremia resolution and further highlight the importance of coordinated, multidisciplinary care to reduce the morbidity of these infections.1–3