Hematological Alteration In Parvo-viral Enteritis of Dogs

Canine parvovirus is still most significant and highly fatal viral cause of enteritis in dogs of less than 6 months of age. The dogs get infection through the oro-nasal route and show various symptoms after an incubation period of 3–10 days. Parvovirus works by temporarily destroying the lining of the intestinal tract so that very little or no food or liquid can be absorbed. As a result, dogs that become infected with parvovirus may experience bloody diarrhea, severe vomiting, weight loss, and fever. In addition, because parvovirus also affects the immune system, limiting it from producing the white blood cells that protect against infection, dogs with the virus may develop other diseases. Purpose of present study was to investigate the hematological alteration in dogs affected with parvo-virus gastroenteritis. The CPV infection was diagnosed based on clinical findings and further confirmed by the rapid antigen test kits (standard immunochromatography assay kit by Intas Pharma. Ltd.) for detection of CPV antigen in dog feces. In positive cases, haematological parameters including white blood cells (WBC), red blood cells (RBC), and platelets, measurement of haematocrit values using an automated haematology analyzer were performed. In addition, the differential WBC counts were obtained manually. Result showed 10.50 ±1.83 (g%) haemoglobin, 42.56 ± 8.22 (%) PCV, 6.94 ± 2.75 10³/cumm) WBC, 5.50 ± 2.96 (10⁶/cub mm) TEC. The differential leukocyte counts were 62.78 ± 11.97% neutrophil, 29.78 ± 10.08% lymphocyte, 4.11 ± 2.72% monocytes, and 2.89 ± 4.01% eosinophils. Neutropenia frequently occurs following canine parvovirus infection as virus has a predilection for rapidly dividing cells, making the granulocyte precursor pool in the bone marrow a prime target for destruction. In addition, loss of neutrophils may occur through the damaged gastrointestinal tract, also there is massive demand for leukocytes (specifically neutrophils) in the inflammed gastrointestinal tract, which increases the risk of death due to sepsis. Although these changes are nonspecific and may be contributed by endotoxemia. Anemia seen in parvo virus infection is unlikely to be due to suppression of erythropoiesis, as circulating red blood cells have a long half-life relative to the short period during which the virus suppresses production in the bone marrow. Reduced hematocrit is more likely to be the result of a combination of intestinal hemorrhage and rehydration therapy. Increased levels of lipid peroxides and an alteration in antioxidant enzyme concentrations, indicating a state of oxidative stress in these patients, may also play a role in anemia pathogenesis. Platelet count in present study was 1.40 ± 0.96 lacs, suggested reason is the decreased platelet production or as a result of direct action of viruses or immunologic components on platelets or endothelium. Besides hemorrhagic manifestations (which are rare), subclinical thrombocytopenia may affect vascular permeability, which may potentiate extravascular dissemination of the virus.