TYPE-I GLANZMANNS-THROMBASTHENIA IN A GREAT PYRENEES DOG

An X-month-old female Great Pyrenees dog with chronic epistaxis and a history of gingival bleeding during shedding of deciduous teeth was ev aluated for platelet function. Platelet morphology was normal at both the light and electron microscopic level. Platelet number and mean pla telet volume were also normal. Platelet aggregation responses to adeno sine diphosphate, collagen, platelet activating factor, and thrombin w ere markedly reduced, although shape change responses were normal. Clo t retraction was markedly impaired. Monoclonal antibody (MoAb) Y2/51, a murine anti-human platelet beta(3), antibody that cross-reacts with canine platelet beta(3), and MoAb 5G11, a murine anti-dog platelet a(I Ib)beta(3) antibody, bound minimally to affected dog platelets, as dem onstrated by flow cytometry. Binding of MoAb Y2/51 was not detectable by immunoblot. MoAb CAP1, a murine anti-dog fibrinogen receptor-induce d binding site antibody, failed to bind to affected dog platelets, as demonstrated by flow cytometry. A reduction in glycoproteins alpha(IIb ) and beta(3), was demonstrated by two-dimensional protein electrophor esis. This is the first reported case of type I Glanzmann's thrombasth enia in the dog that closely resembles the clinical syndrome and the p latelet morphology described in type I Glanzmann's thrombasthenia of h uman beings.