# Thromboinflammation in dogs with virulent babesiosis

## TL;DR

This study shows that dogs infected with Babesia rossi experience dangerous blood clotting and inflammation, which can lead to organ failure and death.

## Contribution

The study identifies thromboinflammation as a key mechanism in severe canine babesiosis caused by B. rossi.

## Key findings

- Babesia-infected dogs showed severe thrombocytopenia and a procoagulant state with platelet activation.
- Systemic inflammation markers CRP and SAA were significantly elevated in infected dogs.
- Thromboinflammation was linked to microthrombi in organs and increased risk of death.

## Abstract

Babesia rossi 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 B. rossi 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.

Ninety-seven dogs naturally infected with B. rossi 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%).

Babesia-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 α2-antiplasmin activity and the presence of fibrin microthrombi in multiple organs. Markedly elevated CRP and SAA concentrations confirmed the simultaneous presence of systemic inflammation.

B. rossi 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.