Abstract: African horse sickness (AHS), caused by the vector-borne African horse sickness virus (AHSV), is endemic to sub-Saharan Africa and infection results in high mortality in naïve equine populations. Clinical signs include submucosal petechiae and prolonged bleeding post venepuncture indicative of hypocoagulation. Pathological activation of haemostasis may result from tissue factor expression as a result of vascular endothelial damage or dysfunction, the proposed pathologic mechanism in AHS, potentially resulting in disseminated intravascular coagulation (DIC). Objective: To describe haemostatic changes during experimental AHSV infection and to characterise DIC using plasma-based and viscoelastic assays. Methods: In vivo experiments. Methods: Four horses were experimentally infected with AHSV. Blood samples were obtained before infection, then every 24 h until humane euthanasia. Haematology and thromboelastography (TEG) were performed and prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen and D-dimer concentrations, as well as activities of antithrombin (AT) and coagulation factors II, VII, VIII, X, and XII were measured. Results: Over the disease course, TEG variables showed increased clot initiation time (R) and decreased α-angle, maximum amplitude (MA), and clot strength (G). The velocity curve showed decreased maximum rate of thrombus generation (MRTG) and thrombus generation (TG), and increased time to maximum rate of thrombus generation (TMRTG). Prothrombin time, aPTT and D-dimer concentration increased while AT activity decreased. All horses developed severe thrombocytopenia. Conclusions: Horses experimentally infected with AHSV developed a consumptive coagulopathy with a bleeding phenotype. These findings fulfil the criteria of overt DIC characterised by procoagulant activation, inhibitor consumption and increased fibrinolytic activity.
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Overview
The study investigated blood clotting changes in horses experimentally infected with African horse sickness virus (AHSV).
It demonstrated that infection leads to overt disseminated intravascular coagulation (DIC), a severe disorder of blood clotting and bleeding.
Background
African horse sickness (AHS) is a viral disease transmitted by insects, primarily affecting horses in sub-Saharan Africa.
The causative agent is the African horse sickness virus (AHSV), which causes high death rates in horses with no prior immunity.
Clinical signs include bleeding under mucous membranes (petechiae) and prolonged bleeding after venepuncture, indicating problems with blood clotting (hypocoagulation).
The underlying pathology likely involves vascular damage leading to abnormal activation of the blood clotting cascade.
This pathological clotting activation can result in disseminated intravascular coagulation (DIC), where widespread clotting and bleeding occur simultaneously.
Objective
To describe changes in the blood clotting system during experimental AHSV infection in horses.
To characterize the features of DIC using detailed laboratory tests including plasma-based coagulation assays and viscoelastic testing (thromboelastography, TEG).
Methods
Four horses were experimentally infected with AHSV under controlled conditions.
Blood samples were collected prior to infection and then every 24 hours until humane euthanasia was necessary.
Laboratory tests performed on the blood samples included:
Haematology to monitor blood cell counts.
Thromboelastography (TEG) to evaluate the dynamics of clot formation and breakdown in whole blood.
Coagulation assays measuring prothrombin time (PT) and activated partial thromboplastin time (aPTT), which assess function of the clotting pathways.
Measurement of fibrinogen and D-dimer concentrations, markers of clot formation and breakdown.
Activity levels of key anticoagulant and clotting factors including antithrombin (AT) and coagulation factors II, VII, VIII, X, and XII.
Results
TEG revealed a progression toward impaired clotting:
Increased clot initiation time (R), meaning it took longer to start forming clots.
Decreased α-angle and maximum amplitude (MA), indicating slower and weaker clot formation.
The velocity curve parameters showed a reduction in the rate and amount of thrombus (clot) formation and a delay in reaching maximum thrombus generation.
Traditional coagulation tests showed prolonged PT and aPTT, consistent with impaired clotting ability.
Plasma D-dimer levels increased, indicating enhanced breakdown of fibrin clots and thus active fibrinolysis.
Antithrombin activity decreased, showing consumption of natural anticoagulants.
All horses developed severe thrombocytopenia (low platelet counts), contributing to bleeding risk.
Conclusions
Infection with AHSV in horses causes consumptive coagulopathy — a condition where clotting factors and platelets are used up extensively, impairing normal clotting.
The bleeding symptoms observed are due to this consumptive coagulopathy combined with active breakdown of clots (fibrinolysis).
The laboratory features meet criteria for overt disseminated intravascular coagulation (DIC), involving three main characteristics:
Activation of procoagulant pathways.
Consumption of clotting inhibitors like antithrombin.
Increased fibrinolytic activity leading to clot breakdown.
This research provides valuable insight into the pathophysiology of AHS in horses and offers potential targets for monitoring and treatment of coagulopathy during the disease.
Cite This Article
APA
Schliewert EC, Hooijberg EH, Goddard A.
(2026).
Experimental infection of horses with African horse sickness virus results in overt disseminated intravascular coagulation.
Equine Vet J, 58(2), 619-629.
https://doi.org/10.1002/evj.70134
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