2011
DOI: 10.1016/j.rvsc.2010.11.018
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Relationship between splenic sequestration and thrombocytopenia in Trypanosoma evansi infection in rats

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Cited by 4 publications
(2 citation statements)
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“…There is an array of possible reasons for a decrease in platelet numbers associated with T . evansi infection, including reduction of the platelet life span, splenic and hepatic sequestration, self-immune response and/or disseminated intravascular coagulation, characterized by systemic activation of blood coagulation, due to constant contact with trypomastigote forms and the vascular endothelium [ 12 , 69 , 70 ].…”
Section: Discussionmentioning
confidence: 99%
“…There is an array of possible reasons for a decrease in platelet numbers associated with T . evansi infection, including reduction of the platelet life span, splenic and hepatic sequestration, self-immune response and/or disseminated intravascular coagulation, characterized by systemic activation of blood coagulation, due to constant contact with trypomastigote forms and the vascular endothelium [ 12 , 69 , 70 ].…”
Section: Discussionmentioning
confidence: 99%
“…Many pathologic, nutritional or environmental factors were found to play a role in activating or inhibiting of specific elements in clotting system by their effects on platelet, and/or endothelial function (Taylor et al, 2000). Findings of present study were revealed on significant decreases in platelet count of T. evansi infected camels, which caused either by splenic sequestration (Da Silva et al, 2010) or extravascular destruction of circulating platelets by the mononuclear phagocytic system (Kipper et al, 2011). Also, it suggested that thrombocytopenia occurs where the surface proteins of Trypanosoma adhere to blood cells as platelets being more susceptible to phagocytosis in spleen and liver (Naessens, 2006;Bezie et al, 2014).…”
Section: Discussionmentioning
confidence: 50%