Introduction

Platelet–bacterial interactions contribute to the pathogenesis of hematological infections. Interactions may occur directly with platelets, resulting in bacterial invasion or induction of platelet aggregation. Bacterial invasion of platelets is a key feature of Rickettsial and Ehrlichial infections. Induction of platelet aggregation in vivo, resulting in formation of mural thrombi on heart valves in infective endocarditis, appears to be a response to certain infecting bacteria. During bacteremia or sepsis, platelet microaggregates form and thrombocytopenia is observed. The propensity for bacterial cells to trigger platelet aggregation and thrombosis in vivo suggests concomitant procoagulant activation. Procoagulant activity can also be up-regulated by bacterial products, such as lipopolysaccharides (LPS) and expression of thrombin-like enzymes, resulting in the incorporation of platelets into aggregates or thrombi. Conversely, certain bacteria express toxins and other proteases that will inhibit platelet function or cause platelet lysis and contribute to coagulopathy. More than 30 species of bacteria show platelet activating or inhibitory functions, many of which have been documented to occur during naturally occuring infection in mammals or in experimental animal or human models. This chapter will present examples of platelet dysfunction that results from clinical infections, followed by an examination of partnered bacterial ligands and platelet receptor or targets, and will conclude with a survey of key mechanistic models of platelet–bacterial interactions.

That bacteria in the blood interact with circulating platelets has been recognized since early in the last century (see review by Clawson).