Intravenous ceftriaxone for 4 weeks resulted in complete clinical recovery in an 80-year-old man with Streptococcus mitis bacteremia and severe calcific aortic stenosis.
Case Report (n=1)
Severe calcific valvular disease can obscure endocardial infection on echocardiography, necessitating reliance on clinical and microbiologic evidence for the management of infective endocarditis.
Abstract Background Viridans group streptococci, particularly Streptococcus mitis, are well-established causes of native valve infective endocarditis. Severe calcific aortic stenosis may hinder visualization of vegetations and reduce the sensitivity of transesophageal echocardiography. We describe a case of Streptococcus mitis bacteremia in a patient with severe calcific aortic stenosis and nondiagnostic echocardiography, managed as probable infective endocarditis based on clinical and microbiologic evidence. Case Discussion An eighty-year-old man with atrial fibrillation, coronary artery disease, alcoholic cirrhosis, an atonic bladder requiring intermittent catheterization, and recurrent exudative pleural effusions presented with urinary retention and inability to self-catheterize after Foley catheter removal. He appeared septic on arrival. Laboratory evaluation showed leukocytosis of 18,000 per microliter with 87 percent neutrophils, thrombocytosis of 527,000 per microliter, and a lactate concentration of 4.2 millimoles per liter. Blood cultures yielded gram-positive cocci in chains in all four bottles; Streptococcus mitis was identified after forty-eight hours of incubation, consistent with the slower growth pattern characteristic of viridans streptococci. Computed tomography of the chest and abdomen demonstrated a moderate left pleural effusion without a drainable collection. A pleural tap demonstrated an exudative effusion by Light’s criteria. Transthoracic and transesophageal echocardiography revealed severe calcific aortic stenosis and posterior mitral annular calcification, without vegetations, abscess, or new regurgitation. No peripheral stigmata of infective endocarditis or alternative infectious source were identified. The patient met Modified Duke Criteria for possible infective endocarditis and received four weeks of intravenous ceftriaxone from the first negative blood culture, resulting in complete clinical recovery. Discussion Severe calcific valvular disease may obscure endocardial infection and result in false-negative echocardiography. Although infection with Streptococcus mitis in individuals with calcific valve disease is recognized, specific descriptions of nondiagnostic echocardiography in this setting remain limited. In selected cases, cardiac computed tomography may assist in evaluating heavily calcified valve structures, and positron-emission tomography may identify extracardiac infectious foci. False negative transesophageal echocardiography results occur in an estimated ten to fifteen percent of infective endocarditis cases, particularly in the presence of significant calcification or small vegetations. In patients with severe calcific aortic stenosis and viridans streptococcal bacteremia, when imaging does not align with clinical suspicion, management should incorporate microbiologic findings, clinical judgment, and guideline-supported decision-making. References: 1. Habib G, et al. 2015 ESC Guidelines for the management of infectiveendocarditis. Eur Heart J. 2015;36(44):3075-3128. 2. Baddour LM, et al. Infective endocarditis in adults: diagnosis, antimicrobialtherapy, and management. Circulation.2015;132:e1-e75. 3. Ren Z, et al. Preoperative false-negative echocardiography in native-valveinfective endocarditis. Cardiovasc Ultrasound. 2021;19(1):2. This abstract is funded by: None
Zoarob et al. (Fri,) conducted a case report in Streptococcus mitis bacteremia and severe calcific aortic stenosis (n=1). Intravenous ceftriaxone was evaluated on Clinical recovery. Intravenous ceftriaxone for 4 weeks resulted in complete clinical recovery in an 80-year-old man with Streptococcus mitis bacteremia and severe calcific aortic stenosis.