Schematic representation of arthropod salivary proteins acting on primary and secondary haemostasis. Haematophagous arthropods (HA) induce injuries to vascular endothelium when probing for a blood meal. The initial event of this vascular damage is vasoconstriction (1), which retards extravascular blood loss and enhances the adhesion of platelets to exposed subendothelial collagen. This adhesion activates platelets (2) and causes the release of platelet activation agonists (Adenosine diphosphate (ADP), Thrombin, Thromboxane A2 (TXA2), serotonin (5-HT)) as well as platelet membrane integrin receptor αIIbβ3. Fibrinogen binds to this receptor and crosslinks platelets to form a platelet plug. The blood coagulation cascade (3) is then initiated to strengthen the platelet plug with fibrin at the site of injury. The coagulation cascade is separated into two pathways converging into a common pathway. The contact activation pathway (intrinsic) involves high-molecular weight kininogen (HMWK), prekallikrein (PK), factor XII, factor XI and factor IX (3a), and the tissue factor pathway (extrinsic) involves the tissue factor and factor VII complex (3b). Both pathways lead to the activation of factor X. The common pathway leads to the generation of thrombin from prothrombin and the ultimate production of insoluble fibrin from fibrinogen. HA have evolved anti-haemostatic salivary proteins that inhibit specific agonists and factors of platelet aggregation and the blood coagulation cascade. The known actions of some HA salivary proteins listed in Additional file 1 are indicated. (Salivary protein affiliation to HA families is indicated by colour as represented on the bottom right corner legend).