Hematologic and bone marrow changes in dogs experimentally infected with Rangelia vitalii
Version of Record online: 4 MAR 2013
© 2013 American Society for Veterinary Clinical Pathology
Veterinary Clinical Pathology
Volume 42, Issue 1, pages 31–39, March 2013
How to Cite
França, R. T., Da Silva, A. S., Costa, M. M., Paim, F. C., Soares, J. F., Labruna, M. B., Mazzanti, C. M. and Lopes, S. T.A. (2013), Hematologic and bone marrow changes in dogs experimentally infected with Rangelia vitalii. Veterinary Clinical Pathology, 42: 31–39. doi: 10.1111/vcp.12023
- Issue online: 4 MAR 2013
- Version of Record online: 4 MAR 2013
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- myeloid:erythroid ratio;
Rangelia vitalii is a tick-transmitted piroplasm that causes both hemolytic and hemorrhagic disease in dogs in Brazil.
The aim of this study was to evaluate the response of the bone marrow in dogs experimentally infected with R vitalii during the acute stage of the disease.
For this study, 2 groups of a total of 12 young dogs were used. Group A was composed of healthy dogs (n = 5), and group B consisted of animals infected with R vitalii (n = 7). Blood samples were collected on days 0, 10, 20, and 30 post-inoculation and stored in EDTA tubes for a full hematology profile, including a reticulocyte count. On days 10 and 20, bone marrow samples were collected, stained, and examined.
In infected dogs anemia was identified on days 10 and 20 post-inoculation (P < .01), and on day 20 reticulocytosis was present. Infected dogs had leukopenia due to neutropenia and eosinopenia, along with lymphocytosis and monocytosis, when compared with control animals. In bone marrow, the myeloid:erythroid ratio was significantly decreased (P < .05) in infected dogs due to increased erythroid precursors.
Dogs experimentally infected with R vitalii develop regenerative extravascular hemolytic anemia accompanied by erythroid hyperplasia in the bone marrow. During the acute phase of the disease, leukopenia due to neutropenia and eosinopenia suggests intense tissue recruitment of these cells in response to the endothelial damage caused by this parasite.