Changes in erythrocytopoesis indices in dogs with babesiosis

Author:

Holovakha V. I.ORCID,Piddubnуak О. V.ORCID,Bakhur T. I.ORCID,Vovkotrub N. V.ORCID,Antipov A. A.ORCID,Anfiorova M. V.,Gutyj B. V.ORCID,Slivinska L. G.ORCID,Kurdeko O. P.,Macynovich A. O.

Abstract

Babesiosis is a common disease in dogs. Babesia canis (Piana & Galli-Valerio, 1895) (Sporozoa, Babesiidae) causes the destruction of erythrocytes, resulting in hypotensive shock and total tissue damage due to lack of oxygen. Because of babesiosis, anemia develops in dogs, and in the first hours of the disease it is normocytic, normochromic and nonregenerative, and on the 2–3rd day of the course, macrocytic, hypochromic anemia with reticulocytosis develops. Scientists have studied the most common indicators of evaluation of erythrocytopoesis during babesiosis (the number of red blood cells, hemoglobin, hematocrit index, indices of “red” blood MCH and MCV), but the age structure of erythrocytes, their acid resistance and the ferrum-transferrin complex for this parasitic pathology have not been sufficiently studied. We carried out research on dogs of service breeds, which were divided into two groups: the first (6–18 months old, n = 10) and the second (2–8 years, n = 15). According to the conducted studies, in dogs of different age groups with babesiosis revealed oligocythemia with anisocytosis and poikilocytosis, oligochromia, decreased hematocrit index and macrocytosis. Significant changes in the morpho-functional state of erythrocytes in dogs of both groups have been revealed, in particular, changes in the population (age) composition of red blood cells: the number of “old” erythrocytes increases (they are rapidly destroyed), the “young” forms of red blood cells decrease and the time for their hemolysis is reduced. As a result of the study of the ferrum-transferrin complex in dogs with babesiosis in both groups, an increase in the level of free ferrum (UIBC) and a decrease in the saturation of transferrin with the trace element was found, which makes it impossible to form a hemoglobin molecule in the bone marrow.

Publisher

Oles Honchar Dnipropetrovsk National University

Subject

General Engineering

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