Native Valve Emphysematous Endocarditis Caused by Finegoldia magna in a Novel Pathogenic Role Margot Cohen, MD,* Elizabeth H. Stephens, MD, PhD,† Michael Garshick, MD,‡ Shih-Hsiu Wang, MD,§ Shalom Z. Frager, MD,* Lauren Mautner, MD,* Fabrizio Remotti, MD,§ and Jai Radhakrishnan, MD|| Abstract: Endocarditis presenting with invasion of the myocardium by gas-forming organisms is rare, previously limited to Escherichia coli and Clostridia species. We describe a case of native valve emphysematous en- docarditis presenting with stroke and ultimately leading to left ventricular rupture and the patient's untimely death. Premortem blood cultures and postmortem pathologic and histologic examination yielded Finegoldia magna (formerly Peptostreptococcus magnus) in a novel pathogenic role. As detection methods continue to improve for Finegoldia magna, it is im- portant to increase awareness of the pathogenic role of this organism. Key Words: endocarditis, emphysematous endocarditis, finegoldia magna, peptostreptococcus, magnus (Infect Dis Clin Pract 2016;24: 57–59) CASE REPORT An 86-year-old woman presented to the emergency depart- ment of a New York City hospital after being found collapsed on the floor in her home, responsive but unable to rise. The pa- tient had a medical history of poorly controlled type 2 diabetes mellitus, a remote stroke with no residual deficits, and peripheral vascular disease status post remote right below the knee amputa- tion and left transtarsal amputation 2 years previously. At baseline, the patient was independent in all activities of daily living, using a wheel chair for mobility and intermittently ambulating with pros- theses. According to the patient's neighbor, the patient had a 1-day history of general malaise, anorexia, hyperglycemia, and dark urine. There was no history of antecedent fevers, night sweats, or chills. However, over the past 9 months the patient had been un- dergoing treatment for poorly healing ulcerations on her left transtarsal amputation site, complicated by chronic osteomyelitis of the underlying femoral head. She intermittently took oral anti- biotics, and the amputation site was casted with cast changes per- formed every 3 weeks. She had no previous history of cardiac disease or cardiac surgery, and a previous echocardiogram demon- strated an ejection fraction of 55% with no valvular pathology. On presentation to the hospital, the patient was found to have atrial fibrillation with rapid ventricular response. She had a tem- perature of 37.2°C, heart rate of 135 beats per minute, blood pres- sure of 135/95 mm Hg, and respiration rate of 24 breaths per minute, saturating 100% on room air. She was agitated and unable to state her location, age, or the date. Her physical examination was notable for clear lungs, a 3/6 apical systolic murmur, new left-sided hemiparesis, and 2 areas of chronic ulceration on the transtarsal amputation site, the posterior of which had an eschar and underlying bogginess from which purulent material was expressed on deep palpation. Laboratory testing revealed hyperglycemia with a blood glu- cose of 475 mg/dL, acute kidney injury (creatinine of 2.68 mg/dL from a baseline of 0.9 mg/dL), leukocytosis with a white blood cell count of 23 Â 10(9)/L and 94% neutrophil predominance, lactic acidosis with a venous lactate of 3.9 mmol/L, and an ele- vated troponin of 6.33 ng/mL without ST segment changes or Q waves noted on electrocardiogram. Initial noncontrast computed tomography (CT) scan of the head revealed a punctate focus of low density, Hounsfield units consistent with air, within the right anterior frontal lobe. The pa- tient was diagnosed with an acute stroke, but tissue plasminogen activator was held due to elevated international normalized ratio (1.7). The patient was admitted to the intensive care unit and a do- butamine infusion was initiated. The patient remained afebrile, but repeat labs demonstrated a further rise in her white blood cell count to 35 Â 10(9)/L. Although initial blood cultures were pend- ing, empiric antibiotics including vancomycin, levofloxacin, az- treonam, and metronidazole were started. On hospital day 2, a noncontrast CT scan of the chest demon- strated air within the posterior mitral annulus, the left ventricular wall and surrounding the ascending aorta. A moderate pericardial effusion was also present (Fig. 1A, B). A transthoracic echocar- diogram on 2.5 μg/min dobutamine showed an ejection fraction of 60%, severe hypokinesis of the mid-to-apical anterior septum, dyskinesis of a thinned, calcified basal inferolateral wall, a small pericardial effusion, and echodense mobile material on the mi- tral valve with moderate mitral regurgitation (Fig. 1C). Antibi- otics were switched to meropenem, vancomycin, rifampin, and gentamycin for presumed endocarditis with septic emboli. On hospital day 3, the patient suddenly became unresponsive and underwent cardiac arrest. The health care proxy decided to hold resuscitative efforts and the patient expired. An autopsy was performed. Blood cultures from admission later speciated to Finegoldia magna with a 99.9% identification using the RapID ANA II System (Remel, Lenexa, KS). Postmortem examination displayed 600 mL of blood in the pericardial sac and rupture (1.6 Â 0.9 cm defect) of the posterior lateral wall of the left ventricle. A 2.8 Â 1.7 cm vegetation was found on the posterior leaflet of the mitral valve. Hematoxylin and eosin staining of the mitral valve revealed severe inflamma- tion and necrosis with inflammation extending into the adjacent myocardium and pericardium surrounding the rupture site, lead- ing to massive myocardial necrosis (Fig. 1D). Numerous gas bubbles and clusters of gram-positive cocci were seen in the area of myocardial necrosis (Fig. 1D, E), consis- tent with an infection caused by gas-forming bacteria and corre- sponding to premortem imaging demonstrating air within the posterior mitral annulus and left ventricular wall (Fig. 1A, B). Microscopic examination of the transtarsal amputation site ulcer also showed clusters of gram-positive cocci on histology (Fig. 1F). From the Departments of *Medicine, and †Cardiothoracic Surgery, Columbia University Medical Center, New York, NY; ‡Department of Cardiology, NYU Langone Medical Center, New York, NY; and Departments of §Pathology, and ||Nephrology, Columbia University Medical Center, New York, NY. Correspondence to: Margot Cohen, MD, 129,Milstein Hospital, 177 Fort Washington Avenue, 6th floor 6C-12, New York, NY 10032. E-mail: mec2136@columbia.edu. The authors have no funding or conflicts of interest to disclose. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 1056-9103 CASE REPORT Infectious Diseases in Clinical Practice • Volume 24, Number 1, January 2016 www.infectdis.com 57 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.