Vancomycin-resistant enterococcal (VRE)
bacteremia is associated with higher mortality rates and longer hospitalizations than
vancomycin-sensitive enterococcal (VSE)
bacteremia. A 67-year-old man with a right
psoas abscess and pacemaker-associated tricuspid valve
endocarditis in September 2020 grew VSE Enterococcus faecium from blood cultures that cleared after administration of intravenous
vancomycin and
gentamicin. Subsequently, he underwent tricuspid valve repair, pacemaker removal, and partial lead extraction. Valve and postoperative blood cultures grew VRE E. faecium, which cleared after administration of intravenous
daptomycin. One VSE and two VRE isolates were collected and sequenced. All isolates belonged to E. faecium multilocus sequence type ST17 and were closely related, having <20 mutations in pairwise genome comparisons. Vancomycin resistance was due to the acquisition of a plasmid-encoded VanA operon. None of the isolates encoded the
virulence factors asa1, gelE, cylA, or hyl; all encoded a homologue of efaAfm. VSE E. faecium, but not VRE E. faecium isolates, encoded a
glucose transporter gene mutation. Two VRE E. faecium isolates formed more robust biofilms than the VSE E. faecium isolate (p < 0.001). The VRE E. faecium isolates, which generated larger biofilms than the VSE E. faecium isolate, could have remained protected in the heart valve and only caused
bacteremia when disrupted during cardiac surgery. This study demonstrates that bacteria detected in the bloodstream of patients with
endocarditis may not fully represent the organisms adherent to the cardiac valves or indwelling devices.