An Unusual Case of Seizure: S. Lugdunensis Associated AICD Lead Endocarditis
Author: Gillian Belnavis, MD, Additional Authors**
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Introduction
Infective endocarditis (IE) involving a cardiac implantable electronic device (CIED) has a high mortality. While IE can precipitate neuro-embolic events, rarely does it present as a seizure. We describe a case of Staphylococcus lugdunensis IE involving an automatic implantable cardioverter defibrillator (AICD) presenting as focal seizures.
Case Presentation
A 21-year-old male with a history of hypertension, type 2 diabetes mellitus, and idiopathic dilated cardiomyopathy with an ejection fraction of 32% status post single-chamber AICD implantation, on home inotropes, presented with a history of shaking of his left face and arm. The patient self-discontinued his milrinone prior to admission due to perceived side-effects. On physical examination, the patient had a right peripherally inserted central catheter. He was afebrile and hemodynamically stable with bibasilar crackles, lower extremity edema and shifting abdominal dullness. There were no focal neurological deficits. Initial labs revealed normal troponin levels, elevated pro-BNP of 5050 pg/mL and a normal white blood cell count. Blood cultures were drawn and the patient was restarted on milrinone infusion in addition to his prescribed medications: aspirin, carvedilol, metolazone and furosemide. Four out of four blood cultures then resulted positive for Staphylococcus lugdunensis. Vancomycin was started and later de-escalated to oxacillin according to susceptibilities. Dedicated MRI with contrast, seizure protocol, was recommended by the neurology team for further assessment. It showed an acute-on-subacute right middle cerebral artery infarction that was deemed by the neurology team to be the likely source of his historical focal seizures. A transesophageal echocardiogram demonstrated several filamentous masses attached to his AICD lead, the largest measuring 1.3 x 0.9 cm. The AICD was explanted and subsequently replaced once blood cultures were negative for 72 hours. The patient was discharged home in stable condition to complete six weeks of oxacillin. Unfortunately, he was readmitted two weeks later with mixed septic and cardiogenic shock and subsequently expired.
Discussion
Neurologic manifestations are among the most common extra-cardiac complications of IE, occurring in up to 20-55% of patients. These complications can include stroke, transient ischemic attack, purulent or aseptic meningitis, intracranial hemorrhage, headache, seizure or encephalopathy and can be a major determinant of poor prognosis. Staphylococcus lugdunensis is a coagulase negative staphylococcus that is an uncommon cause of IE with an aggressive clinical course and a high rate of complications. The organism produces a biofilm by binding to von Willebrand factor through Fbl, a fibrinogen-binding protein unique to Staphylococcus lugdunensis. This enables it to tightly adhere to vessel walls, bioprosthetic material and native tissues. Although most Staphylococcus lugdunensis isolates are susceptible to oxacillin, as was with our case, the formation of biofilm plays a major role in its pathogenesis and impairs the efficacy of antibiotics.
Conclusion
Staphylococcus lugdunensis is a uncommon cause of IE. Due to proclivity to form biofilms patients with CIEDs are particularly susceptible. A high index of suspicion for IE is crucial when the only initial presenting sign is a neurologic manifestation.
**Additional Authors:
Gillian Belnavis, MD, Division of Cardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, OH
Jordan Gavin, MD, Division of Cardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, OH
Rosario Colombo, MD, Division of Cardiovascular Medicine, Jackson Health System, Miami, FL
