An inherited platelet function defect in a Simmental crossbred herd.

Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph.
Canadian journal of veterinary research = Revue canadienne de recherche vétérinaire (Impact Factor: 0.85). 05/1997; 61(2):128-33.
Source: PubMed

ABSTRACT An inherited bleeding disorder, resembling Simmental hereditary thrombopathy (SHT), has been identified in a Simmental crossbred herd. In an affected bull calf, initially evaluated because of excessive bleeding from a vaccination site, the platelet aggregation response to the agonist, adenosine-diphosphate (ADP) was essentially absent and the aggregation response to platelet activating factor (PAF16) was reduced by at least 70%. The initial laboratory assessment of platelet function in the dam and sire yielded results which were within normal limits. The sire was not available for further testing. The dam, also a daughter of this sire, was subsequently shown to have a partially reduced aggregation response to ADP. Of 18 other offspring of the sire evaluated, 6 were also identified as having a partially impaired aggregation response. The maximum aggregation response to ADP and PAF16 in these 6 calves was approximately 50% of the level exhibited by unaffected animals. In contrast, the coagulation profiles were normal for all animals except for a heifer calf which also exhibited a partially impaired aggregation response. The plasma level of the coagulation protein, factor XI, was reduced in this heifer calf which suffered a fatal hemorrhage following dehorning. This report appears to be the 1st to have identified animals putatively heterozygous for SHT on the basis of the in vitro platelet aggregation response to ADP.

  • [Show abstract] [Hide abstract]
    ABSTRACT: The morphological alterations induced by the activation of bovine platelet rich plasma suspensions with the inflammatory mediator, platelet activating factor (PAF), and following the activation of washed bovine platelet suspensions with thrombin are described. The unstimulated bovine platelet exhibits a smooth oval or discoid shape and granules are randomly dispersed throughout the cytoplasm. The initial activation response to PAF is the development of irregularly shaped cells, the migration of granules to the periphery of the cell and the appearance of large pseudopodia devoid of membrane organelles. As activation continues and large platelet aggregates form, two zones of irregularly shaped, discrete platelets are evident within each large aggregate: an outer zone in which the cells are devoid of granules and an inner zone in which many of the platelets exhibit the typical ultrastructural features of a non-activated cell. In washed platelet preparations activated with thrombin, virtually all platelets undergo shape change and yet many cells retain their alpha granules. In addition, discrete irregularly shaped agranular platelets are also found. The distinctive morphological alterations observed in activated bovine platelets are likely associated with the absence of an open canalicular system, characteristic of many other types of mammalian platelets, and with the ability of the cytoplasmic microtubule coil to reorganise into a linear array following thrombin activation. It is postulated that the bovine platelet has evolved as a cell that can respond to various stimuli, for example inflammatory mediators, by releasing active metabolites from its granular stores without forming platelet-platelet bridges that can serve as a foci for thrombus formation. In this manner the bovine platelet can effectively function as an inflammatory cell without acting as a potent thrombogenic agent.
    Comparative Haematology International 05/1997; 7(2):88-94. DOI:10.1007/BF02652573
  • [Show abstract] [Hide abstract]
    ABSTRACT: To present the latest information on inherited platelet disorders in domestic animals. Research articles and reviews spanning 40 years available on PubMed. Information regarding inherited platelet disorders in people is plentiful and often descriptions of human conditions have led to the identification of similar disorders in veterinary species. There are exceptions, however, in which specific inherited platelet disorders were first described in animals with subsequent identification in people. Many inherited platelet disorders have been documented in animals at the functional and molecular level and that information is presented in this review. Much progress has been made in the past 20 years in the characterization of inherited platelet disorders in animals at the functional, biochemical, and molecular level. The study of inherited platelet disorders has greatly enhanced the understanding of platelet physiology and has led in some instances to the development of platelet inhibitory medications. Characterization of inherited disorders at the molecular level greatly facilitates diagnosis and identification of affected and heterozygous animals thus avoiding propagation of the defect by breeders. When used with available functional and biochemical diagnostic tests, it significantly enhances the quality of care and case management.
    01/2012; 22(1):30-41. DOI:10.1111/j.1476-4431.2011.00702.x
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tests that evaluate many aspects of platelet function have been applied in both human and veterinary medicine for the monitoring of treatment with platelet function inhibitors and for detection of platelet function abnormalities (inherited or acquired). Interspecies variation in the response to various platelet agonists is an important consideration when methods that have been developed for people are applied in other species. At the present time, many of these assays are not readily available in standard veterinary practice. Advanced platelet function testing for veterinary patients is offered at select academic institutions. Discussion with a specialist is recommended when considering the use of these tests, and the relative strengths and limitations of each assay should be considered in the interpretation of test results.
    Veterinary Clinics of North America Small Animal Practice 01/2012; 42(1):173-88. DOI:10.1016/j.cvsm.2011.09.013 · 1.04 Impact Factor


1 Download
Available from