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Acquired Thrombocytopenia |  |
| Acquired thrombocytopenias are reported frequently in dogs and cats, less often in horses, and rarely in other species. Numerous causes have been identified, most involving immunologic or direct destruction of platelets. |
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Ehrlichial diseases, caused by
Ehrlichia
platys
and
E
canis
, cause mild to severe thrombocytopenia in dogs.
Ehrlichia
platys
infection (see
ehrlichiosis and related infections,
Ehrlichiosis and Related Infections) usually is characterized by mild, often cyclic thrombocytopenia in the acute stages of the disease. Chronic infections often have constant mild to moderate thrombocytopenia. Morula (single to multiple, round to oval basophilic inclusions) can sometimes be identified in platelets of infected dogs. The thrombocytopenia is seldom severe enough to result in clinical bleeding tendencies. Ticks are the
likely vectors.
E
canis
infections (
Ehrlichiosis and Related Infections) are characterized by variable alterations in total WBC count, PCV, and platelet count. In acute infections, there is usually thrombocytopenia and possibly anemia or leukopenia. In chronic infections, there may or may not be thrombocytopenia or anemia; however, there is often leukocytosis and sometimes hyperglobulinemia (monoclonal or polyclonal). Infected dogs may have epistaxis, melena, gingival bleeding, retinal hemorrhage,
hematoma formation, and prolonged bleeding after venipuncture or surgery. |
| Neoplasms like hemangiosarcoma may be associated with consumptive thrombocytopenia. Immunologic and inflammatory mechanisms cause increased platelet consumption and decreased platelet survival. However, bleeding tendencies without thrombocytopenia occasionally exist. Altered platelet function due to an acquired membrane defect has been associated with hyperglobulinemia. Vasculitis also may contribute to the hemostatic disorder. Bovine viral diarrhea virus may cause thrombocytopenia
in cattle. |
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Primary immune-mediated thrombocytopenia (also called
idiopathic thrombocytopenia or
idiopathic thrombocytopenic purpura) is characterized by immune-mediated destruction of either circulating platelets or, less commonly, marrow megakaryocytes. It has been seen in dogs and horses. Clinical signs include petechiae of the gingivae or skin and ecchymosis, melena, or epistaxis. Platelets are usually <100,000/µL. Low platelet concentration and low mean platelet volume have been noted in the early
stages but not in the later stages. Evaluation of megakaryocytes (by bone marrow aspiration) helps determine if circulating platelets or marrow megakaryocytes are targeted by antibody. A test for platelet factor 3 released from damaged platelets has been unreliable or not readily available commercially. A megakaryocyte immunofluorescence assay that detects antibodies on megakaryocytes has been done, but an adequate bone marrow aspiration sample must be obtained. A direct test for the
presence of antiplatelet antibodies—an ELISA that detects platelet-bound antibodies—has been reported to have good sensitivity (94%) but is not highly specific for primary immune-mediated thrombocytopenia. A negative test result likely rules out primary immune-mediated thrombocytopenia as the cause of thrombocytopenia; however, a positive test result could indicate either primary immune-mediated thrombocytopenia or secondary immune-mediated thrombocytopenia (eg,
thrombocytopenia associated with autoimmune hemolytic anemia, lymphoproliferative diseases, systemic lupus erythematosus). Administration of corticosteroids, starting at a fairly high dose and then tapering (as in the treatment of immune-mediated hemolytic anemia,
Hemolytic Anemia) is recommended. Other treatments reported are administration of danazol and ascorbate. Splenectomy should be reserved as a treatment for animals that have recurrent episodes
of thrombocytopenia. Vincristine has been used to enhance the release of platelets from marrow megakaryocytes, but its usefulness to decrease immune destruction of platelets is questionable. |
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Vaccine-induced thrombocytopenia has been reported in dogs vaccinated repeatedly with modified live adenovirus and paramyxovirus vaccines. The thrombocytopenia occurs 3-10 days after repeat vaccination, is usually transient, and may be sufficiently mild that a bleeding tendency will not be evident unless superimposed on another platelet or coagulation disorder. The thrombocytopenia may develop due to antibody production against viral antigens attached to platelet
surfaces or to nonspecific binding of antigen-antibody complexes to platelet surfaces. |
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Drug-induced thrombocytopenia has been reported in dogs, cats, and horses. One mechanism is marrow suppression of megakaryocytes or generalized marrow stem cell suppression (after administration of estrogen, chloramphenicol, phenylbutazone, diphenylhydantoin, and sulfonamides). Another mechanism is increased platelet destruction and consumption (after administration of sulfisoxazole, aspirin, diphenylhydantoin, acetaminophen, ristocetin, levamisole, methicillin, and
penicillin). Drug reactions are idiosyncratic and therefore unpredictable. Platelets usually return to normal shortly after the drug is discontinued. Drug-induced bone marrow suppression may be prolonged. |
