The role of hypervirulent Staphylococcus aureus infections in the development of deep vein thrombosis.

Patients with sepsis frequently have activated coagulation pathways triggered by tissue factor, reduced levels of anticoagulation factors, reduced fibrinolysis, activated endothelial surfaces, and activated platelets. These processes result in disseminated intravascular coagulation and microthrombus formation and contribute to multi-organ system failure. S aureus surface proteins and exotoxins can contribute to thrombus formation through effects on the coagulation pathway and on anticoagulation factors. In addition, S aureus can activate endothelial surfaces and platelets. Some exotoxins such as the Panton-Valentine leukocidin can cause leukocyte lysis and additional injury to endothelial surfaces. These events can cause microthrombosis and deep venous thrombosis. Several case series have described an association between acute hematogenous osteomyelitis secondary to S aureus and the development of deep venous thrombosis in extremities. In addition, a recent clinical case review of staphylococcal community-acquired pneumonia demonstrated that patients who died secondary to these infections frequently had deep venous thrombosis. These observations support the idea that S aureus can contribute to thrombus formation. We recently cared for a patient who developed splanchnic vein thrombosis during an episode of staphylococcal cellulitis associated with bacteremia and multi-organ system failure. The pathogenesis of splenic vein thrombosis differs from the pathogenesis of deep venous thrombosis in the extremities in some, but not all, respects. Clearly the presence of circulating staphylococci and associated proteins could contribute to the formation of thrombi in the splanchnic circulation. Patients with hypervirulent staphylococcal infections require evaluation for deep venous thrombosis in extremities and in unusual sites. The development of these clots has a potentially significant impact on management and outcome. This review considers the pathogenesis of deep vein thrombosis in patients with sepsis, the potential contributions of Staphylococcus aureus in this process, and clot formation in unusual locations which greatly increases the complexity of patient care.