The mucosal bleeding time is almost always prolonged. Von Willebrand disease is suspected in animals with clinical blood clotting disorders in which blood tests show normal platelet values and in which tests for coagulation factors of the plasmatic coagulation cascade are normal. Animals affected by type 3 rarely reach old age. With this type, there is often extreme bleeding in the mucous membranes, muscles and joints, which can lead to bleeding to death. Type 3 is the most severe form of Von Willebrand disease, as no Von Willebrand factor can be formed. Depending on the extent of this defect, the symptoms can be mild to very severe. With type 2 a normal amount of the factor is formed, but the factor itself is defective. The symptoms are often less pronounced and depend on the race and the situation. Type 1 summarizes cases with a partial deficiency in the Von Willebrand factor necessary for blood clotting. Von Willebrand disease in animals is divided into three types, analogous to Willebrand-Jürgens syndrome in humans. However, many of the affected animals only show an increased tendency to bleed after injections, blood samples or surgical interventions. Symptoms of Von Willebrand disease include bleeding gums, nosebleeds, and hematuria. The age of diagnosis varies widely depending on the severity of the disease and can range from newborns to old individuals, with severe cases usually diagnosed in younger animals.
It occurs particularly frequently ( prevalence between 10 and 70%) in Dobermann, Kromfohrlander, German Shepherd, Golden Retriever, Miniature Schnauzer, Welsh Corgi Pembroke, Shetland Sheepdog, Basset Hound, Scottish Terrier, Standard Poodle and Manchester Terrier. The disease has been described in more than fifty different breeds of dogs. Depending on the severity of the deficiency, this leads to an increased bleeding time in the case of injuries and thus to a higher blood loss, which can be fatal due to shock or anemia.
As a result, if there is an injury, there is no adhesion and aggregation of the platelets, and blood clotting remains limited to the plasmatic component of hemostasis. If the formation of the Von Willebrand factor is disturbed by a mutation of the associated gene, the animal cannot produce any or insufficiently functioning Von Willebrand factor. If an injury occurs, the factor binds to the collagens that are exposed and binds the blood platelets to itself, which triggers cellular hemostasis and the platelets begin to close the wound ( platelet aggregation ). In healthy animals, the factor is located on the inner wall of the blood vessels and in the platelets.
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