RESUMO
Canine babesiosis is a tick-borne parasitic disease caused by the intraerythrocytic parasites, Babesia canis and Babesia gibsoni. A lethargic, weak, American Staffordshire Terrier (pit bull) dog, which had regenerative, normocytic, normochromic anemia, was shown by polymerase chain reaction analysis to be infected with B. gibsoni. Transmission electron microscopy of ethylenediamine tetraacetic acid-treated blood disclosed many well-preserved, intraerythrocytic babesia trophozoites. Four morphologic forms of babesia trophozoites are described (small spheres, small rods, irregular forms lacking pseudoinclusions, and large spheres having pseudoinclusions) and are compared with intraerythrocytic forms of B. canis and B. gibsoni described in other light and electron microscopic studies of in vivo and in vitro Babesia infections. This is the first detailed transmission electron microscopic study of canine B. gibsoni-infected red blood cells in North America.
Assuntos
Babesia/crescimento & desenvolvimento , Babesiose/veterinária , Doenças do Cão/parasitologia , Anemia/sangue , Anemia/parasitologia , Anemia/patologia , Anemia/veterinária , Animais , Babesia/genética , Babesia/ultraestrutura , Babesiose/sangue , Babesiose/parasitologia , Babesiose/patologia , DNA de Protozoário/química , DNA de Protozoário/genética , Doenças do Cão/sangue , Doenças do Cão/patologia , Cães , Eritrócitos/parasitologia , Eritrócitos/ultraestrutura , Feminino , Microscopia Eletrônica/veterinária , Reação em Cadeia da Polimerase/veterináriaRESUMO
Ten cases of thymic hematoma in young dogs (9-24 weeks of age) were reviewed. Anticoagulant rodenticide toxicosis was confirmed in 5 cases. Histologically, hemorrhage caused variable expansion of thymic lobules and interlobular septa. The medulla appeared to be the primary site of hemorrhage. In areas of severe hemorrhage, normal lobular architecture was lost and lymphocytes were admixed in the hemorrhagic exudate. Vasculitis, necrosis of capillaries, and degeneration of the capsule were observed in infarcted areas. In 2 cases, angiofibroplasia indicated a longer interval between onset of thymic hemorrhage and death. The lesions are similar to those in 5 cases of idiopathic thymic hemorrhage. Appropriate samples were not available for anticoagulant rodenticide analysis in 3 of these 5 idiopathic cases. Lesions in confirmed cases of anticoagulant rodenticide toxicosis also are compatible with published descriptions of idiopathic and spontaneous thymic hemorrhage, but are inconsistent with normal thymic involution. Analysis for anticoagulant rodenticides is indicated in cases of thymic hematoma when an obvious cause is not detected at necropsy.