In the aftermath of an acute cardiovascular event such as stroke, patients and families frequently ask whether preceding circumstances such as viral illnesses, stress, and other medical or surgical events brought on the disease. Although it seems intuitive to patients and families that acute precipitants or disease triggers play a substantial role, the evidence to support this concept has accumulated slowly.(1,2) Support for acute systemic infection as a trigger of stroke, a particularly interesting hypothesis, continues to grow.(3) The potential mechanisms underlying such a relationship include systemic inflammation, endothelial dysfunction, and activation of the clotting system by infectious organisms or the systemic response to them.(4,5).