Catastrophic antiphospholipid syndrome in a community-acquired methicillin-resistant Staphylococcus aureus infection: a review of pathogenesis with a case for molecular mimicry.

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has remarkable pathogenicity and can cause severe infections, such as necrotizing pneumonia, necrotizing fasciitis, and sepsis. To our knowledge, no case of CA-MRSA resulting in catastrophic antiphospholipid syndrome (CAPS) has been reported. Furthermore, no specific pathogenic link between these two disorders has been described. Staphylococcal sequence homologies and binding capabilities to plasma protein β2-glycoprotein I (β2-GPI) may result in anti-β2-GPI antibody production. These antibodies represent the critical prothrombotic factor in pathogenesis of antiphospholipid syndrome and CAPS. However, the development of CAPS requires additional prothrombotic activities. In our case, sepsis and CA-MRSA-induced leukocytolysis likely represent the activity required to transform a hypercoagulable state into the life threatening, diffusely thrombotic CAPS. The presence of anti-β2GPI-antibodies and diffuse microvascular occlusion are characteristic of CAPS. However, other life threatening syndromes cause microvascular thrombi and multiorgan failure, and more studies are needed to determine the frequency of antiphospholipid antibodies and clinical syndromes consistent with CAPS in patients with staphylococcal infections.