(1787) Hidden Claws: Bartonella Endocarditis as a Mimicker and a Cause of Lethal PR3 ANCA Vasculitis

Introduction: Bartonella spp. accounts for ~3-4% of all blood culture-negative endocarditis (BCNE). The incubation period is usually 2-4 weeks via a facultative intraerythrocytic infection, although a subacute bacteremia can last for months. Patients’ symptoms can mimic vasculitis with few going on to develop a true infection-induced vasculitis, thereby obscuring a clear treatment. We detail a case of Bartonella endocarditis that went undiagnosed for months as physicians struggled to explain multi-organ failure in a previously healthy male, ultimately leading to his death.

Description: A 56 year-old male presented to the clinic for 5 months of weight loss with labs notable for pancytopenia, normal kidney and liver function, and an anti-nuclear antigen of 1:640. Work up revealed hepatosplenomegaly, a negative bone marrow biopsy, a liver biopsy showing porto-sinusoidal vascular disease, and a transthoracic echocardiogram with mitral (MV) and aortic (AV) valve thickening.

Nine months later, he was admitted to the hospital for abdominal pain. Labs showed pancytopenia, acute kidney failure and an elevated PR3. The patient underwent splenic artery embolization. His course was complicated by acute respiratory failure followed by a seizure and cardiac arrest. Bronchoscopy revealed diffuse alveolar hemorrhage while a CT head showed subarachnoid hemorrhage. Given concern for autoimmune vasculitis (AiV), he was started on plasmapheresis with initial improvement.

Transesophageal echocardiogram showed mobile masses on both the MV and AV. Bartonella henselae PCR was positive so plasmapheresis was stopped and antibiotics were initiated. The patient then sustained a large frontal intraparenchymal hemorrhage with a 6 mm midline shift. CT angiogram showed short segment beaded morphology in the superior left M2 middle cerebral artery (MCA). Patient’s family opted for comfort care.

Discussion: This case highlights the unique overlap in the presentation and pathophysiology of Bartonella spp. BCNE sequelae and AiV. This case is a reminder that BCNE can also induce a true AiV, as evidenced by the patient’s MCA beading; thus, patients may benefit from treatment of both. Particularly for patients with no other rheumatological involvement, BCNE should be ruled out as a possible cause when investigating AiV.