Brief report: Chronic murine schistosomiasis causes aberrant hemostasis

Schistosomiasis afflicts >250 million people worldwide, leading to an annual loss of >3 million disability-adjusted life years. Schistosoma mansoni causes intestinal schistosomiasis with parasite eggs either transversing intestinal tissue or lodging within the liver and other organs, causing intestinal hemorrhage and liver pathology. Large (∼1 cm) adult worms survive for years within blood vessels, but we lack a clear understanding of their impact on hemostasis. We used a chronic mouse model of schistosomiasis to determine the impact on platelet numbers, phenotype and function. Hemostatic function was assessed by platelet phenotyping (flow cytometry and proteomics), whole blood aggregometry, and longitudinal coagulometry. Although platelets from schistosome-infected mice lack elevated surface P-selectin and activated αIIbβ3, unbiased proteomic analysis reveals infection-induced increases in MHC-I, IgM and IgG antibodies, and complement components. Whole blood from schistosome-infected mice spontaneously aggregates in the absence of exogenous agonists. Conversely, prothrombin and activated partial thromboplastin times are prolonged at the chronic stage of infection (10–12 weeks). A mouse model of S. mansoni infection shows wide-ranging changes in hemostatic function which may have clinically relevant implications for populations in endemic regions. •Schistosomiasis causes thrombocytopenia and spontaneous whole blood aggregation.•Platelet proteomics reveals marked changes in protein expression without increased P-selectin or integrin activation.•Longitudinal analysis shows prolonged coagulation (prothrombin time and activated partial thromboplastin time) during chronic infection.