Biofilm-Forming ST-45 Staphylococcus aureus Causing Late Pulmonary Homograft Endocarditis Post-Ross Procedure

Abstract

Pulmonary homografts are typically resistant to infection and are favored in valve replacement for endocarditis, including in Ross procedures. We report a rare case of late-onset, aggressive pulmonary valve endocarditis occurring seven years post-Ross in a 40-year-old man with no identifiable risk factors. The patient presented with fever, dyspnea, and oliguria, complicated by immune complex glomerulonephritis and septic pulmonary emboli. Blood cultures prior to antibiotic treatment yielded an oxacillin-susceptible Staphylococcus aureus (OSSA) isolate. Genotypic and phenotypic characterization revealed an ST-45, agr group IV strain, positive for the ica operon and exhibiting robust biofilm formation. Although lacking major virulence toxins (PVL, SEA, ETA, TST), the strain encoded a wide array of MSCRAMMs (fnbA, sdrE, spa, atl, can, clfA/B), facilitating adherence to fibronectin, fibrinogen, and collagen. This adhesive profile supports early colonization, biofilm maturation, and vegetation development—key mechanisms in persistent endovascular infection and evasion of host immunity. The strain was resistant only to penicillin, remaining susceptible to all other antibiotics tested. The patient was treated with targeted antimicrobial therapy, corticosteroids, and haemodialysis, followed by urgent homograft explantation and reimplantation using peripheral cardiopulmonary bypass on a fibrillating heart to avoid aortic manipulation. Postoperative recovery was uneventful, and homograft function remained stable at 18 years. This case highlights the rare but severe potential for homograft infection in Ross patients and underscores the value of comprehensive microbiological evaluation in guiding timely surgical and medical management.