Pathology may vary slightly with species, but in general it is very similar. Thus we will use white-tailed deer as a model.

Clinical pathology: Leukopenia and lymphopenia, often severe, are consistent findings during the first week of infection. Hematocrits and total plasma protein concentrations typically decrease during this time period. Activation of the coagulation and fibrinolytic systems occurs. Platelet counts may be decreased. As seen in these graphs, based on experimental BTV infections in white-tailed deer, activated partial thromboplastin time (APTT) is often severely prolonged and there is a progressive decrease in Factors VIII and XII activities during the first week following infection. Prothrombin time (PT) may be prolonged late in the acute phase. Factor 5 activity and fibrinogen concentration may be increased as they are acute phase reactants. Fibrin/fibrinogen degradation products (FDP’s) may be detected.

Summary of common clinical pathologic findings:

Lesions progress with increasing duration of disease from edema, to hemorrhagic diathesis, to ulceration, but animals typically have a combination of these lesions.

Early in the disease, as we see here, there may be swelling of mucosal surfaces, tongue, lips and head and neck

Hydrothorax, hydropericardium and pulmonary edema may be observed

Serous fluid may be seen along fascial planes in skeletal muscle (left). The spleen is often enlarged and congested and the lymph nodes swollen, edematous, and hemorrhagic (right).

As the disease progresses endothelial damage and the development of disseminated intravascular coagulation lead to the development of hemorrhages. Petechial and ecchymotic (left) to suffusive hemorrhages (right) may be seen on serosal surfaces.

Hemorrhages are seen throughout the heart.

Typical lesions are hemorrhages on the serosal surface of the pylorus (left) and at the base of the pulmonary artery (right).

Severe hyperemia to hemorrhage is seen in the forestomachs. Occasionally severe hemorrhagic enteritis will be seen mimicking clostridial type enteritis.

With time, vascular lesions will lead to necrosis and ulceration. Typical findings will be ulceration of the tongue and palate.

Changes in the buccal papillae will progress from congestion to hemorrhage to necrosis and ulceration. This change can be subtle but should always be looked for.

Severe ulceration of the forestomachs may occur.

In chronically affected animals or animals that recover there may have atrophy and/or scarring of rumen and sloughing hooves. Malnutrtional may lead to death.

Histopathology: Microscopic changes are very mild and are relatively nonspecific. This is a systemic disease so a variety of tissues have lesions, but the best tissues to examine are tongue, buccal papillae, forestomachs, abomasum (particularly at the pylorus), intestinal tract, and heart. In these tissues, as seen in this photomicrograph of lip, there is endothelial cell swelling and mild perivascular infiltration, especially involving the microvasculature.

Hemorrhage and thrombosis may also be seen, again involving smaller vessels. Note the hemorrhage in the lamina propria of the tips of the buccal papillae in the left photomicrograph and the hemorrhage and thrombosis in the tip of a ruminal papillae in the right photomicrograph.

Myonecrosis of the tongue, tunica muscularis of the gastrointestinal tract, and myocardium is often seen in conjunction with the hemorrhage. Note the congestion, hemorrhage and myonecrosis in the tunica muscularis of this abomasum (left) and in the myocardium (right).

Ulceration of mucosal surfaces occurs subsequent to hemorrhage and necrosis in the underlying tissues as seen in the photomicrograph of a buccal papillae.

Electron Microscopy: BTV and EHDV infect endothelium where virus replication results in the formation of viral associated macrotubues (35 nm in diameter) (VT), viral matrices (VM), and ~65 nm viral particles (P) in the endothelial cell cytoplasm.

Pathogenesis

Following transmission by Culicoides, initial replication occurs in macrophages in local lymph nodes. A low titer viremia carries virus to secondary sites of replication, principally the spleen. This is followed by a high titer viremia and virus infection of endothelium. Viral replication in the microvasculature endothelium results in endothelial cell necrosis. Endothelial denudation exposes the vessel basement membrane which activates platelets and the clotting cascade. This results in thrombosis which triggers the fibrinolytic system. Vascular damage and disseminated intravascular coagulation result in hemorrhage and tissue necrosis. Tissue necrosis leads to ulceration of mucosal surfaces.

In this electron micrograph of a capillary, there has been loss of the lining endothelium. This triggered coagulation resulting in the formation of a thrombus composed of fibrin and degranulated platelets (T). A neutrophil is escaping through a rupture in the basement membrane. As this is occurs throughout the body, a consumptive coagulopathy develops. The formation of disseminated thrombi triggers the fibrinolytic system. The combination of consumptive coagulopathy and fibrinolysis results in DIC.

Immunosuppression may also occur altering the outcome of disease. Animals will often have concurrent bacterial bronchopneumonia, as seen in this white-tailed deer, possibly a result of immunosuppression.

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