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Medical records from 39 cats with hepatic disease, examined at the Veterinary Medical Teaching Hospital, University of Florida, between 1987 and 1992 were retrospectively evaluated for alterations in red blood cell (RBC) morphology. Diagnoses included: hepatic lipidosis, neoplasia, cholangiohepatitis, hepatitis/hepatopathy, systemic histoplasmosis, and portocaval shunt. A total of 56 laboratory data sets were studied which included complete blood counts and serum chemistry results. Stained blood smears were evaluated from 51 of the data sets. Twenty-two cats (56%) were determined to have poikilocytosis on the basis of blood smear evaluation. Eleven (28%) cats had moderate to marked poikilocytosis (2+ to 4+). Acanthocytes accounted for 62.6 -/+ 22.1% of morphologically abnormal RBC and were observed in blood smears from 100% of cats with poikilocytosis. Elliptocytes (ovalocytes) comprised 19.5 -/+ 15.8% of poikilocytes and were found in smears from 82% of cats with poikilocytosis. Keratocytes (7.0 -/+ 6.8%), schistocytes (3.6 -/+ 4.4%), and blister cells (2.6 -/+ 6.4%) were present in lower numbers and in fewer cats. Serum total cholesterol values were significantly greater (p < 0.05) in cats with moderate to marked alterations in RBC morphology. Cats with hepatic lipidosis were significantly (p < 0.04) more likely to have poikilocytosis than cats with other types of hepatic disease.

Erythrocyte binding and plasma protein binding of codeine in sickle cell patients and healthy controls were determined. A reversed-phase HPLC procedure was used for codeine analysis. Codeine was extracted from alkalinized plasma, separated on a CN column, and assayed by fluorescence detection. The erythrocyte-buffer partition coefficient was significantly higher in sickle cell patients (1.72 +/- 0.21) than in healthy controls (1.25 +/- 0.14). No time dependence of partitioning was observed. The fraction of codeine bound to plasma proteins, determined by ultrafiltration, was significantly higher in sickle cell patients (66.0% +/- 8.6%) than in healthy controls (30.5% +/- 2.7%). No concentration dependence of erythrocyte or protein binding was observed. Further studies were performed to elucidate the binding mechanisms. From a ghost cell binding study it was concluded that the major binding sites for codeine are in the cell membrane. A decrease in codeine binding was observed in the presence of bilirubin. Codeine binding to alpha 1-acid glycoprotein was found to be minimal. The levels of alpha 1-acid glycoprotein and other glycoproteins in sickle cell patients and healthy controls were measured by glycoprotein electrophoresis. The results showed no significant difference between the two groups. Plasma protein electrophoresis was performed for the two groups. The results showed a significant difference in gamma-globulin levels between sickle cell patients and healthy controls. Codeine is known to bind to gamma-globulin, a fact that may explain in part the observed increase in the plasma protein binding of codeine in sickle cell patients.(ABSTRACT TRUNCATED AT 250 WORDS)

cells; morbillivirus. Ante mortem diagnosis of canine distemper, a morbilli­ virus infection, is aided by demonstration of intracellular inclusion bodies in conjunctival epithelial cells and blood cells, particularly when these bodies are observed in con­ j unction with typical clinical symptoms."> Postmortem, characteristic histopathologic lesions may include the pres­ ence of intracytoplasmic and intranuclear viral inclusions in epithelial cells of the skin, gastrointestinal tract, lung, renal pelvis, urinary bladder, central nervous system (CNS), and eye, depending on the stage and severity of infection." The present case describes intracytoplasmic inclusions within large mononuclear cells in the cerebrospinal fluid (CSF) of a dog with clinical signs and histopathologic lesions consistent with those ofcanine distemper. The inclusions were detected using routine cytologic techniques and may be significant in de­ termining the prognosis of the disease.

Summary Bone marrow cells were identified in cytocentrifuge preparations of cerebrospinal fluid (CSF) obtained by lumbar punctures from two dogs. CSF analyses were characterized by normal or increased total cell counts, normal or increased total protein concentration and the presence of erythrocytes. Hematopoietic cells present included both erythroid and myeloid precursors and, in one case, an erythroblastic island was seen. Peripheral blood smear examination confirmed that the hematopoietic cells observed were not the result of blood contamination. Neither case was associated with a difficult tap procedure, nor with a specific disease process. Contamination may have resulted from actual marrow penetration or from extramedullary hematopoiesis in the dura mater. Accurate interpretation of CSF cytology requires the consideration of possible bone marrow contamination when hematopoietic cells are observed.

Despite the frequency of both oxidant drug-induced and spontaneous Heinz body formation in cats, the cellular and biochemical mechanisms by which Heinz bodies result in red blood cell (RBC) destruction and hemolytic anemia in this species remain unknown. Feline spleens are non-sinusoidal and inefficient at removing Heinz body-containing RBC from the circulation; therefore, alternative mechanisms must be involved in accelerated RBC destruction. Propylene glycol (PG) ingestion causes dose-dependent Heinz body formation and decreased RBC survival in cats. We investigated several aspects of Heinz body-containing RBC from three cats ingesting diets that provided 8.0 g PG/kg body weight for up to 3 weeks, in order to characterize cellular lesions that are associated with the presence of Heinz bodies and that might contribute to chronic, accelerated RBC destruction, as well as to gain insight into the mechanism by which PG induces Heinz body formation. Erythrocytes with PG-induced Heinz bodies had decreased levels of reduced glutathione and adenosine triphosphate and reduced deformability. There was no change in hemoglobin isoelectric focusing or membrane lipid peroxidation. Electrophoretic patterns of Heinz body-containing RBC membranes were significantly altered, and membrane surface charge distribution was disturbed. Progressively protruding Heinz bodies suggested that extrusion of Heinz bodies may be a means of cell healing and/or destruction in the absence of splenic pitting. When compared to results obtained using RBC from cats treated with the oxidant drug phenylhydrazine, significant differences were noted in packed cell volume, turbidity index, membrane heme, and morphologic appearance of Heinz bodies. Our results indicate that multiple cellular abnormalities develop in RBC with PG-induced Heinz bodies that do not cause acute hemolysis but that may shorten RBC survival. Propylene glycol-induced Heinz bodies provide an ideal model for studying the chronic effects of Heinz bodies on RBC structure and function and may be useful in understanding the mechanisms of formation and the consequences of endogenous Heinz bodies in cats.

Summary The first known report of synovial fluid eosinophilia in a dog is described here. The occurrence of eosinophils in joint fluid is rare. Sporadic cases have been recorded in humans and most can be related to immune-mediated reactions, both parasitic and non-parasitic. The dog in this case report had 20–52% eosinophils in multiple joints, as well as hemarthrosis and marked mononuclear cell reactivity. An intense peripheral eosinophilia was demonstrated one week later. The associated lameness resolved with non-steroidal anti-inflammatory therapy. Lack of remarkable history or other clinical symptoms led to a diagnosis of idiopathic, eosinophilic, polyarthritis, likely immune-mediated.

A dog was presented with mandibular paralysis, photophobia, and diffuse atrophy of the cranial skeletal muscles. Physical examination also revealed glossal paralysis, reduction of the swallowing reflex, re- duction of the pupillary light response, and generalized lymphadenopathy. Cytologic and ultrastructural ex- aminations of blood films, bone marrow, and lymph node aspirates were consistent with acute myelomonocytic leukemia. Post-mortem examination revealed extensive, multisystemic neoplastic infiltration with marked in- volvement of the central and peripheral nervous systems, especially the cranial and lumbar spinal nerves and associated ganglia. Neurologic manifestations are unusual in acute myelomonocytic leukemia in the dog. Acute myelomonocytic leukemia is a rare myelo- proliferative disorder in the dog. Within the past ten years, however, increased utilization of differential cy- tochemical stains and electron microscopy have re- sulted in several reports of acute myelomonocytic leu- Acute myelomonocytic leukemia is characterized by an acute clinical course. Leukemic cells have features of both granulocytic and monocytic precursors.*J2 In the reported cases, extensive bone marrow replace- ment and leukemic dissemination with hepatospleno- megaly and generalized lymphadenopathy are consis- tent findings. Although involvement of the central nervous system is not uncommon in acute lympho- blastic leukemia in the dog,3 there are only two reports of nervous system involvement in canine acute myelo- monocytic leukemia. 1,1° Ataxia, circling, and brain me- tastases were reported in one case.l In the second case, leukemic blasts were identified in the cerebrospinal fluid, and post-mortem examination revealed neo- plastic infiltration of the extradural spinal tissues. lo The present report describes an unusual case of acute myelomonocytic leukemia in a dog where the symp- toms were predominantly those of cranial polyneu- ropathy and severe atrophy of the cranial skeletal mus- cles. Differential cytochemistry and ultrastructural examination of lymph node and bone marrow aspi- rates were diagnostic for acute myelomonocytic leu- kemia. Case History

A case of idiopathic aplastic anemia in a dog was characterized by pancytopenia and bone marrow aplasia. Erythroid colony-forming units (CFU-E) were not detected in bone marrow culture. Addition of the dog's serum to CFU-E culture from control dogs failed to suppress colony formation, suggesting that humorally-mediated suppression at the CFU-E level was not a cause of the aplastic anemia.

Some neoplastic cell lines are readily killed when incubated in the presence of polyunsaturated fatty acids (PUFA). In an attempt to elucidate this phenomenon, we studied PUFA-driven superoxide (O2-) production by cultured NS-1 cells (murine lymphoid tumor cells). We find: (1) Even in the absence of added PUFA, NS-1 cells generate O2- (i.e., reduce nitroblue tetrazolium). (2) addition of PUFA increases O2- by greater than 50%. (3) Artificial loading of NS-1 cells with liposome encapsulated superoxide dismutase prevents the majority of spontaneous and PUFA-driven NBT reduction. We conclude that PUFA drives O2- generation by tumor cells, that this generation is largely intracellular, and that this phenomenon may help explain toxicity of PUFA for tumor cells.

This prospective longitudinal study investigated the progression of haematological changes in 32 transfused and 54 non-transfused dogs naturally infected with Babesia rossi over the 1st 6 days following diagnosis and treatment. The effect of patient age on the results of complete blood counts was determined. Haematology data were analysed at presentation and at 24 hours, 3 days and 6 days after presentation. Dogs were treated with diminazene aceturate at diagnosis and a blood transfusion was given if deemed clinically required. Mildly to moderately regenerative normocytic normochromic anaemia was observed in all dogs throughout the study period. Transfused dogs more often had an inflammatory leukogram at presentation and at 24 hours, than dogs that were not transfused. In dogs with a left shift, a concurrent normal or decreased segmented neutrophil count was found more commonly than neutrophilia. Severe thrombocytopenia that resolved within a week was common. Blood transfusion alleviated the anaemia, but had no significant effect on white blood cell or platelet responses. Blood cell responses were not significantly influenced by age. In conclusion, the red blood cell and white blood cell responses were less than expected in dogs with babesiosis, given the degree of anaemia and inflammation present. The magnitude of thrombocytopenia and rapid return of the platelet count to normal suggested a possible immune-mediated mechanism for the thrombocytopenia.