The dataset for the inflammatory response during experimental infection and treatment of dogs with Babesia rossi.

Babesia rossi causes severe morbidity and mortality in dogs in sub-Saharan Africa. This was an experimental study designed to observe systemic changes caused by Babesia rossi infection within a canine disease model as well as investigate the influence of inoculum dose and treatment on the progression of inflammation and clinical disease. Six healthy male beagle dogs formed the study population, one dog was splenectomised and used to raise the infectious inoculum, three were administered a high B. rossi infectious dose and two a low infectious dose. Clinical examination, complete blood count (CBC) and C-reactive protein (CRP) were determined daily. Cytokines were quantified on stored plasma collected during the study, using a canine specific cytokine magnetic bead panel (Milliplex©). The experiment was terminated, and treatment administered once predetermined experimental or humane endpoints were reached. The data and information provided in the following article is the summary of all data points collected over the course of the eight-day experimental infection.

Mean Platelet Volume and Platelet Volume Distribution Width in Canine Parvoviral Enteritis.

Bacterial translocation from the damaged intestinal tract, reported in canine parvoviral (CPV) enteritis, is thought to be responsible for the systemic inflammatory response resulting from coliform septicemia, which could ultimately progress to septic shock and death. Alterations in platelet indices, specifically mean platelet volume (MPV), is a consistent finding in critically ill people and dogs with and without sepsis. Increased MPV has been reported to be an indirect indicator of platelet activation and of bone marrow response in people and dogs with sepsis. The study aim was to compare admission MPV and platelet volume distribution width (PVDW) in dogs with CPV enteritis to that of healthy aged-matched control dogs. Forty-eight dogs with CPV enteritis and 18 healthy age matched control dogs were included. CPV infection was confirmed with electron microscopy and concurrent blood-borne infections were excluded using PCR. EDTA whole blood samples were analyzed on an automated cell counter, ADVIA 2120, within 30-60 min from collection. There was no significant difference for platelet count between the groups. The MPV for CPV infected dogs (median: 14.0; IQR: 12.2-15.1) was significantly higher compared to controls (11.3; IQR: 10.3-13.1, P = 0.002). The PVDW for CPV infected dogs (66.9; IQR: 64.2-68.8) was significantly higher compared to controls (63.3; IQR: 60.2-65.1, P < 0.001). These findings suggest that significant platelet activation is present in dogs with CPV enteritis which may play a role in the disease outcome, similar to people with sepsis. Further studies are required to investigate the prognosticating ability of MPV in dogs with CPV enteritis.