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BackgroundThrombocytosis is a hematologic abnormality in dogs that has been associated with various neoplastic, metabolic, and inflammatory conditions.ObjectiveTo classify thrombocytosis in dogs based on severity and evaluate whether there are associations between severity and underlying disease processes.AnimalsSeven hundred and fifteen dogs with thrombocytosis and 1,430 dogs with normal numbers of platelets.MethodsRetrospective study. Medical records of dogs with increased (>500 × 103/μL; thrombocytosis group) and normal (300–500 × 103/μL; control group) platelet counts between 2011 and 2015 were reviewed. Dogs were characterized by severity of platelet increase and diagnosis. Diagnostic categories included neoplasia, endocrine disease, inflammatory disease, or miscellaneous.ResultsA total of 1,254 complete blood counts with thrombocytosis from 715 dogs were included in the study. Median platelet count in this population was 582 × 103/μL (500–1,810 × 103/μL). No correlation between severity of thrombocytosis and diagnosis was identified. Causes of secondary thrombocytosis included neoplasia (55.7%), endocrine disease (12.0%), and inflammatory disease (46.6%). Immune‐mediated disease was common (22.2%), associated with frequent glucocorticoid administration, and had a significantly higher median platelet count (636 × 103/μL [500–1,262 × 103/μL] versus 565 × 103/μL [500–1,810 × 103/μL]) when compared to the other inflammatory processes (P < 0.001). The diagnoses in the thrombocytosis dogs differed significantly from the control population (P < 0.001).Conclusions and Clinical ImportanceThrombocytosis is commonly associated with carcinoma and immune‐mediated disease in dogs.

Two male North American elk from a commercial herd were evaluated because of a sudden onset of lethargy, anorexia, and voiding of red urine. These 2 elk were kept in the same pen as 4 other male elk that had died during the preceding 2 months. Laboratory analyses revealed anemia and intraerythrocytic parasites, later confirmed as Babesia odocoilei (a protozoal hemoparasite of cervids). Of the 240 elk remaining in the herd, 59 were screened for B odocoilei by microscopic evaluation of blood smears, protozoal culture of blood, and immunofluorescent antibody testing of serum. Of those 59 elk, 34 (58%) were infected with B odocoilei. Babesia odocoilei infection in elk can be fatal and should be considered in cases of sudden death or acute hemolytic anemia. Familiarity with the disease in elk is essential for practitioners because of the increasing popularity of commercial elk farming.

The partial pressure of oxygen constitutes an important factor in the regulation of human erythrocyte physiology, including control of cell volume, membrane structure, and glucose metabolism. Because band 3 is thought to be involved in all three processes and because binding of hemoglobin (Hb) to the cytoplasmic domain of band 3 (cdb3) is strongly oxygen-dependent, the possibility that the reversible association of deoxyhemoglobin (deoxyHb) with cdb3 might constitute an O 2 -dependent sensor that mediates O 2 -regulated changes in erythrocyte properties arises. While several lines of evidence support this hypothesis, a major opposing argument lies in the fact that the deoxyHb binding sequence on human cdb3 is not conserved. Moreover, no effect of O 2 pressure on Hb− band 3 interactions has ever been demonstrated in another species. To explore whether band 3−Hb interactions might be widely involved in O 2 -dependent regulation of erythrocyte physiology, we undertook characterization of the effect of O 2 on band 3−Hb interactions in the mouse. We report here that murine band 3 binds deoxyHb with significantly greater affinity than oxyHb, despite the lack of significant homology within the deoxyHb binding sequence. We further map the deoxyHb binding site on murine band 3 and show that deletion of the site eliminates deoxyHb binding. Finally, we identify mutations in murine cdb3 that either enhance or eliminate its affinity for murine deoxyHb. These data demonstrate that despite a lack of homology in the sequences of both murine band 3 and murine Hb, a strong oxygen-dependent association of the two proteins has been conserved.

We have evaluated senescence related changes in canine red blood cells (RBCs) using the biotinylation system, where RBCs are labeled in vivo with biotin at the beginning of their life span, and retrieved from circulation on immobilized avidin at the end of their life span. This approach avoids the controversial use of density gradient centrifugation to collect presumably old RBCs. Furthermore, the dog is an appropriate model for human RBC senescence because it has a low degree of random RBC loss and a similarly long RBC life span (approximately 110 days). Two dogs had 97% to 100% of their circulating RBCs biotinylated by infusion of N-hydroxysuccinimido biotin (Clontech, Palo Alto, CA; Calbiochem, La Jolla, CA) dissolved in dimethyl sulfoxide. At postbiotinylation days 104 and 107 for one dog and day 110 for the other dog, biotinylated RBCs were isolated by magnetic cell sorting and analyzed for the presence of autologous IgG using 125I- labeled sheep-antidog IgG (SAD IgG). On all 3 days, there were at least three times more SAD IgG molecules per RBC on senescent biotinylated RBCs than on control (unfractionated) RBCs (day 104: 11,677 v 3,399; day 107: 6,710 v 2,115; day 110: 6,042 v 1,838 molecules of SAD IgG per senescent v control RBC). Furthermore, it is unlikely that an immune response to the conjugated biotin had been elicited, because fresh in vitro biotinylated RBCs that were incubated in autologous plasma (taken after exposure to circulating biotinylated RBCs for 113 days) and then exposed to the SAD IgG showed no increase in antibody binding over control (non-biotinylated) RBCs (1,431 v 1,378 cpm/10(8) biotinylated v control RBCs; P > .20). These results suggest that senescence of canine biotinylated RBCs is characterized by binding of autologous IgG and that antibiotin antibodies do not contribute to this process.