Reasons for an increased number of circulating large platelets during inflammation may be twofold: (1) increased cytokine concentrations contribute to megakaryocytosis, resulting in the release of larger immature platelets regardless of the platelet concentration ( 11, 12) and (2) following activation, platelets undergo a shape change with small protuberances appearing on their surface, resulting in an increase in the platelet volume ( 10, 13). Optical based automated hematology analyzers are able to accurately measure platelet size and content and record various of these platelet indices that may serve as surrogate markers for platelet activation ( 8– 10). Platelet indices such as mean platelet volume (MPV), mean platelet mass (MPM), mean platelet component concentration (MPC), and platelet volume distribution width (PVDW) are recognized as surrogate markers of platelet activation ( 8, 9). Platelet activation, resulting in changes that lead to platelet adhesion and aggregation, only occur after stimulation with one of several physiological agonists, for example weak agonists such as adenosine diphosphate or stronger agonists such as thrombin or vessel wall collagen ( 8). Platelets normally circulate in blood in a resting state. Platelets are more than cytoplasmic fragments that participate in hemostasis, but have been reported to play a significant role in the host inflammatory response ( 8). Increased serum concentrations of CRP in CPV infected dogs has been shown to be associated with disease severity and outcome ( 7). C-reactive protein (CRP), a major acute phase protein in dogs, is considered an accurate indicator of systemic inflammation ( 6). Endotoxins, as well as proinflammatory cytokines, are powerful mediators of the systemic inflammatory response as well as triggers of the coagulation cascade ( 4, 5). This can ultimately progress to septic shock and death in severe cases ( 3). Systemic inflammation may occur in many cases due to bacterial translocation from the damaged intestinal tract with a subsequent bacteremia and endotoxemia ( 3). In susceptible populations, the viral infection most commonly manifests as a severe systemic and often life-threatening illness ( 2). Further studies are required to investigate the prognosticating ability of MPV in dogs with CPV enteritis.Ĭanine parvovirus (CPV) is an important pathogen worldwide and a significant cause of viral enteritis in dogs with associated high morbidity and mortality rates ( 1). 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. 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). 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). There was no significant difference for platelet count between the groups. EDTA whole blood samples were analyzed on an automated cell counter, ADVIA 2120, within 30-60 min from collection. CPV infection was confirmed with electron microscopy and concurrent blood-borne infections were excluded using PCR. Forty-eight dogs with CPV enteritis and 18 healthy age matched control dogs were included. 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. Increased MPV has been reported to be an indirect indicator of platelet activation and of bone marrow response in people and dogs with sepsis. Alterations in platelet indices, specifically mean platelet volume (MPV), is a consistent finding in critically ill people and dogs with and without sepsis. Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Pretoria, South Africaīacterial 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.Monique Engelbrecht *, Brogan Atkinson, Amelia Goddard, Paolo Pazzi and Vanessa McClure
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