Neonatal Marfan syndrome (MFS) is a severe form of classic MFS caused by mutations in a specific region of the fibrillin 1 gene (FBN1). We report a case of an infant with neonatal MFS who presented with flexion contractures in utero and severe skeletal and cardiovascular manifestations at birth. A novel de novo missense mutation in exon 26 of FBN1 was demonstrated. Because of potential new therapies, it is increasingly important to recognize neonatal MFS in utero as well as shortly after birth to initiate the appropriate diagnostic work-up and management.

Intentional scheduling of clerkship students to enhance preceptor continuity resulted in significant positive outcomes echoing the relationship-based educational benefits of longitudinal clerkships, particularly in regards to student assessment and feedback. Clerkship directors and other medical educators should consider implementing small changes within block clerkships to maximize student-preceptor continuity.

Key Clinical MessageAlthough the role of ANCA in infective endocarditis is unclear, Bartonella henselae has been implicated as the culprit in cases of PR3‐ANCA positive subacute bacterial endocarditis (SBE) with glomerulonephritis. In this case, a Coombs‐positive autoimmune hemolytic anemia and glomerulonephritis accompanied a PR3‐ANCA positive SBE caused by Bartonella henselae.

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