Aerococcus Urinae Infective Endocarditis-related Stroke: A Case Report

Aerococcus urinae is a Gram-positive, catalase-negative coccus that was first defined in 1992. A. urinae is responsible for up to 0.8% of all cases of urinary tract infection. Typical predisposing factors include male sex, age >65 years and pre-existing urinary pathology. A. urinae is a rare cause of endocarditis but has a high associated morbidity and mortality. Sepsis or septic shock is the primary clinical presentation but there have been several reports of cerebral ischemic events in the setting of A. urinae endocarditis. These case descriptions are very limited and do not include brain imaging. We describe the clinical course of a 75 year-old man who, in the setting of A. urinae mitral valve endocarditis, presented with symptoms and imaging findings consistent with embolic cerebral infarction. Importantly, mitral valve vegetation was detected only after transesophageal echocardiography. Given the risk of morbidity without treatment, these data support pursuing a transesophageal approach even when transthoracic echo is negative. Journal of Cardiovascular Diseases & Diagnosis J o u r n a l o f C ar dio vas cular Dases & ia g n o s i s


Introduction
Aerococcus urinae is a Gram-positive, catalase-negative coccus. Occurring rarely, the few reports of cerebral ischemic events in the setting of A. urinae-mediated infective endocarditis (IE) are limited. We provide details of the case of a patient with stroke due to presumed cardiogenic embolism that was subsequently found to be caused by A. urinae-mediated IE.

Case Report
The patient was a 75 year old African-American man with a history of hypertension, hyperlipidemia, diabetes and chronic kidney disease who presented with a low grade fever and leukocytosis. His blood pressure was 167/76 mmHg, heart rate 102 BPM, and temperature 100.4⁰F. A II/VI diastolic murmur was present. He was somnolent but easily arousable on presentation to the hospital. Neurological examination was otherwise notable for global aphasia, left gaze preference, right nasolabial fold flattening, and right lower extremity drift. Laboratory testing included a normal basic metabolic panel except for an elevated creatinine (2.3 mg/dL), BUN (24 mg/dL) and glucose (277 mg/dL). There was a neutrophil-predominant leukocytosis (WBC 16.5×10 9 /L) and normocytic anemia (Hg 13.4 g/dL, MCV 91fL) with a normal platelet count. Urinalysis, urine culture and toxicology screening were unremarkable. Magnetic resonance imaging of the brain ( Figure 1A-F) showed multiple areas of restricted diffusion in the left hemisphere within multiple vascular territories. Magnetic resonance angiography of the head and neck did not demonstrate any extraor intracranial steno-occlusive disease (images not shown). Further evaluation included a transthoracic echocardiogram which showed trivial valvular regurgitation and no evidence of an intra-cardiac shunt (images not shown). Consistent with the patient's II/VI diastolic murmur, subsequent transesophageal ultrasonography demonstrated a 1.0×0.4 cm mobile echodensity on the anterior mitral valve leaflet ( Figure 1G). There were no clinical stigmata of endocarditis.
Although our patient had several cerebrovascular risk factors, the distribution of acute ischemic injury on MRI brain was compatible with a thromboembolic source associated with native mitral valve IE. He was started on vancomycin which was continued for four days until cultures finalized without evidence of staphylococcus. Additionally, Sunnerhagen et al. describe the association between A. urinae mediated IE and "an occlusion of the medial cerebral artery" [6].
Although the incidence of IE ranges between 1.5 and 11.6 cases per 100,000 people, the risk of IE-mediated stroke is only 0.158 ± 0.091 per 100,000 [7] and extremely rare when the causative organism is A. urinae. Suspicion of IE-related stroke should nonetheless remain high when the radiographic pattern of ischemic injury suggests a cardioembolic source and the patient has a fever, heart murmur, evidence of valvular disease on echocardiography or positive blood cultures. Importantly, although TTE in our patient did not show valvular disease, the TEE demonstrated a mitral valve vegetation providing a source of embolism to explain the distribution of abnormalities found on MR imaging.
It is suggested that a normal TTE effectively excludes infective endocarditis and that TEE is therefore unnecessary [8]. However, the rate of detection of valvular vegetations with TTE is less than 50-percent compared to TEE, suggesting that a transthoracic approach has limited detection capacity [9]. Given the risk of morbidity without treatment, these data support pursuing a transesophageal approach even when TTE is negative.