Three Beagles with chronic anemia and reticulocytosis were studied. The dogs originated from a large breeding colony and appeared clinically normal with the exception of splenomegaly. The PCV ranged from 30 to 39% (normal, 46 to 56%), with reticulocyte indices of 2.3 to 9.9. Red blood cells were morphologically normal, and examination of marrow aspirates revealed erythroid hyperplasia. Shortened chromium-51 RBC life-spans (7.2 to 15.4 days in anemic dogs; 22.2 to 25.2 days in control dogs) documented a hemolytic anemia. Acquired causes of hemolytic anemia were ruled out. Red blood cells had normal glycolytic enzyme activities, no evidence of unstable or abnormal hemoglobin, and had altered osmotic fragility curves. The breeding of 2 anemic dogs resulted in off-spring with anemia and reticulocytosis. Polyacrylamide gel electrophoresis revealed no abnormalities in RBC membrane cytoskeletal proteins in all anemic adult dogs and in 3 offspring.

Protein profiles of whole homogenates of anconeus (slow twitch) and biceps femoris (fast twitch) muscles of clinically normal dogs and of Labrador Retrievers with hereditary myopathy (HM) were resolved on flat bed polyacrylamide isoelectric-focusing gels. Three methods of sample solubilization were performed. The solubilization buffer, with high concentrations of urea, precipitated the zwitterionic detergent, but use of the buffer containing 3% NP-40, 9.2M urea, and 0.1M arginine resulted in better resolution and stability of pH gradient. Gels of anconeus muscle from clinically normal dogs contained 2 protein bands specific to anconeus muscle, whereas gels of biceps femoris muscle from clinically normal dogs contained 3 protein bands amplified in biceps femoris muscle that were barely detectable in anconeus muscle. The staining intensity of protein bands in biceps femoris muscles from Labrador Retrievers with HM was decreased, relative to controls. The quantitative analysis of peak height ratios of biceps femoris muscle revealed significant (P less than 0.05) differences between profiles of clinically normal dogs and Labrador Retrievers with HM.

Leukocytosis (34,600 WBC/microliter of blood) was detected in an apparently healthy 7-day-old Holstein heifer. Analysis of blood samples obtained over the next 41 days revealed chronic progressive neutrophilia, which peaked at greater than 85% neutrophils and exceeded 100,000 WBC/microliter. In vitro assessment of isolated blood neutrophils obtained from the heifer at 38 and 45 days of age revealed selected functional abnormalities. Endocytosis of immunoglobulin-opsonized Staphylococcus aureus and killing of this test organism by the calf's neutrophils were significantly diminished, as were phagocytosis-associated superoxide generation, chemiluminescence activity, and myeloperoxidase-catalyzed iodination. Diminished H2O2 elaboration by the calf's neutrophils was evident during ingestion of opsonized zymosan or on exposure to phorbol myristate acetate. Extracellular release (secretion) of elastase during ingestion of zymosan was also diminished, although total cell content of elastase was normal, compared with that of neutrophils from age-matched calves, and granular or other morphologic abnormalities of the calf's neutrophils were not evident by ultrastructural examination. Abnormalities of random migration were inconsistently detected, and normal or high degree of antibody-dependent cytotoxicity or natural killing by the calf's neutrophils was observed. Similar in vitro assessment of neutrophils obtained from the calf's dam revealed no functional abnormalities. The calf died at 48 days of age, with persistent fever and chronic diarrhea despite administration of antibiotics. Histologic examination at necropsy revealed large numbers of intravascular neutrophils in most tissues, including massive neutrophil sequestration in spleen. However, a striking lack of extravascular neutrophils was evident in inflamed submucosa mucosa adjacent to intestinal ulcers heavily contaminated with enteric microorganisms. Bone marrow examination revealed diffuse myeloid hyperplasia, but no other abnormalities. The clinical and pathologic features in this calf were similar to those in previously reported human patients or Irish Setters with genetic deficiency of the CD11/CD18 leukocyte glycoprotein complex, thus prompting further postmortem evaluations. Results of immunoblot analyses of the neutrophil lysates of the heifer calf (isolated and stored prior to death) documented severe deficiency of Mac-1 (CD11b/CD18). Results of immunofluorescent analyses indicated substantially diminished (intermediate) amounts of the Mac-1 beta subunit (CD18) on blood neutrophils of the calf's dam and sire and on neutrophils of 8 of 15 paternal half-siblings; findings were consistent with an autosomal recessive trait in the proband's kindred. Findings also indicate that genetic abnormalities of CD11/CD18 proteins may underlie the molecular pathogenesis of disease in this calf as well as other previously described examples of the granulocytopathy syndrome in Holstein cattle.

Immunochemical methods that are used to assess von Willebrand factor in human beings and dogs were used to assess von Willebrand factor in 3 cat species. Our findings indicated that the expression and multimeric composition of von Willebrand factor in plasma and platelets of cats were similar to those reported in human beings and dogs. We suggest that these methods may be used to evaluate von Willebrand disease in members of the cat family used in this study.