Mitral valve endocarditis-induced thromboembolic and hypercoagulable disease in a rhesus macaque, with a literature review.

A 23-y-old female rhesus macaque (Macaca mulatta) from a long-term research colony developed progressive clinical decline, with lethargy, nasal discharge, and hematologic abnormalities, including persistent leukocytosis, neutrophilia, thrombocytopenia, and anemia. Despite treatment with enrofloxacin, deterioration led to euthanasia. Autopsy revealed severe vegetative endocarditis of the left atrioventricular (mitral) valve with intralesional gram-positive cocci, confirmed immunohistochemically as Staphylococcus aureus. Histologically, disseminated thromboembolic arterial disease was present in the lungs, tracheobronchial lymph node, kidneys, and spleen, with concurrent hepatic central vein thrombosis and coagulative necrosis of hepatocytes, supporting a concurrent hypercoagulable state. A PCR assay of the mitral valve tissue targeting the bacterial 16S ribosomal RNA gene was negative for S. aureus (interpreted as a false-negative result), acknowledging the limitation of PCR testing of formalin-fixed tissues caused by DNA damage and fragmentation. The absence of heart-failure cells and pulmonary edema made primary congestive heart failure unlikely and instead supported systemic inflammatory response syndrome with secondary multi-organ ischemic injury as the cause of death. In infective endocarditis, sustained bacteremia and inflammatory mediator release drive endothelial dysfunction, a hypercoagulable state, and widespread microvascular thrombosis, resulting in impaired tissue perfusion and organ failure.8,22 Accordingly, the dominant life-threatening process in our case was not mechanical cardiac failure, but disseminated thromboembolic disease and ischemic injury to downstream organs. This pattern is well recognized in both human and veterinary literature; morbidity and mortality in infective endocarditis are frequently driven by septic embolization and systemic complications, rather than intrinsic cardiac dysfunction.