{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T17:06:30Z","timestamp":1773335190158,"version":"3.50.1"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T00:00:00Z","timestamp":1773273600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Vet. Sci."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Babesia rossi<\/jats:italic>\n                      infection in dogs is associated with severe hemostatic dysregulation and systemic inflammation. The close interplay between innate immunity and coagulation in pathological states, including acute infections, may lead to thrombus formation, termed thromboinflammation, and has been proposed to underlie disease severity and poor outcomes. The objectives of this study were to investigate the presence of thromboinflammation in dogs with\n                      <jats:italic>B. rossi<\/jats:italic>\n                      infection by characterizing the overall hemostatic state, using thromboelastography (TEG) and plasma-based assays, and the systemic inflammatory response using acute phase reactants as markers, and further to determine whether, if present, thromboinflammation was associated with disease severity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Ninety-seven dogs naturally infected with\n                      <jats:italic>B. rossi<\/jats:italic>\n                      and 15 healthy control dogs were included. Diagnosis of babesiosis was confirmed by reverse line blot polymerase chain reaction. Blood samples were collected at presentation, prior to any treatment. Hemostatic function was assessed using TEG, routine coagulation assays, coagulation factor activity, and fibrinolysis markers. C-reactive protein (CRP) and serum amyloid A (SAA) were measured as markers of systemic inflammation. Twelve of the Babesia-infected dogs died (12%).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Babesia<\/jats:italic>\n                      -infected dogs demonstrated hemostatic abnormalities marked by severe thrombocytopenia and a procoagulant state, including platelet activation, preserved clot strength, and elevated fibrinogen concentrations. Thromboelastography further revealed delayed clot initiation and propagation with maintained clot firmness, whereas conventional assays showed prolonged prothrombin time and activated partial thromboplastin time, along with markedly reduced coagulation factor activities in non-survivors. Minimal fibrinolysis was observed on TEG and was associated with elevated \u03b12-antiplasmin activity and the presence of fibrin microthrombi in multiple organs. Markedly elevated CRP and SAA concentrations confirmed the simultaneous presence of systemic inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>B. rossi<\/jats:italic>\n                      infection in dogs induced thromboinflammation characterized by thrombocytopenia, platelet activation, coagulation factor consumption, fibrinolytic shutdown and systemic inflammation. Thromboinflammation may drive endothelial injury, microthrombosis, and an increased risk of organ failure and death. Future therapeutic interventions targeting thromboinflammation may improve patient outcomes.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fvets.2026.1712262","type":"journal-article","created":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T05:28:58Z","timestamp":1773293338000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Thromboinflammation in dogs with virulent babesiosis"],"prefix":"10.3389","volume":"13","author":[{"given":"Amelia","family":"Goddard","sequence":"first","affiliation":[{"name":"Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria","place":["Onderstepoort, South Africa"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johan P.","family":"Schoeman","sequence":"additional","affiliation":[{"name":"Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria","place":["Onderstepoort, South Africa"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew L.","family":"Leisewitz","sequence":"additional","affiliation":[{"name":"Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria","place":["Onderstepoort, South Africa"]},{"name":"Department of Clinical Sciences, Auburn University College of Veterinary Medicine","place":["Auburn, AL, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter N.","family":"Thompson","sequence":"additional","affiliation":[{"name":"Department of Production Animal Studies, Faculty of Veterinary Science, University of Pretoria","place":["Onderstepoort, South Africa"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annemarie T.","family":"Kristensen","sequence":"additional","affiliation":[{"name":"Department of Veterinary Clinical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen","place":["Copenhagen, Denmark"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,12]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"34","DOI":"10.1038\/nri3345","article-title":"Thrombosis as an intravascular effector of innate immunity","volume":"13","author":"Engelmann","year":"2013","journal-title":"Nat Rev Immunol"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"7","DOI":"10.1016\/j.jtha.2023.07.020","article-title":"Thromboinflammation in acute injury: infections, heatstroke, and trauma","volume":"22","author":"Iba","year":"2024","journal-title":"Thromb Haemost"},{"key":"ref3","doi-asserted-by":"publisher","first-page":"666","DOI":"10.1038\/s41569-021-00552-1","article-title":"Interplay between inflammation and thrombosis in cardiovascular pathology","volume":"18","author":"Stark","year":"2021","journal-title":"Nat Rev Cardiol"},{"key":"ref4","doi-asserted-by":"publisher","first-page":"958","DOI":"10.1055\/s-0037-1615947","article-title":"A cell-based model of hemostasis","volume":"85","author":"Hoffman","year":"2001","journal-title":"Thromb Haemost"},{"key":"ref5","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1111\/j.1476-4431.2008.00380.x","article-title":"The role of tissue factor and tissue factor pathway inhibitor in health and disease states","volume":"19","author":"DelGiudice","year":"2009","journal-title":"J Vet Emerg Crit Care (San Antonio)"},{"key":"ref6","doi-asserted-by":"publisher","first-page":"451","DOI":"10.1097\/MBC.0b013e328346ef3f","article-title":"The role of tissue factor in systemic inflammatory response syndrome","volume":"22","author":"Egorina","year":"2011","journal-title":"Blood Coagul Fibrinolysis"},{"key":"ref7","doi-asserted-by":"publisher","first-page":"1399","DOI":"10.3390\/jcm12041399","article-title":"Immunothrombosis: molecular aspects and new therapeutic perspectives","volume":"12","author":"Marcos-Jubilar","year":"2023","journal-title":"J Clin Med"},{"key":"ref8","doi-asserted-by":"publisher","first-page":"231","DOI":"10.1111\/jth.13911","article-title":"Inflammation and thrombosis: roles of neutrophils, platelets and endothelial cells and their interactions in thrombus formation during sepsis","volume":"16","author":"Iba","year":"2018","journal-title":"Thromb Haemost"},{"key":"ref9","doi-asserted-by":"publisher","first-page":"1599639","DOI":"10.3389\/fimmu.2025.1599639","article-title":"Thromboinflammation vs. immunothrombosis: strategies for overcoming anticoagulant resistance in COVID-19 and other hyperinflammatory diseases. 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