Gastric dilatation was experimentally induced in 6 anesthetized dogs maintained with constant-dose isoflurane in oxygen. An intragastric balloon was used to distend the stomach with a constant 30 mm of Hg for 3.5 hours. The PaCO2, was maintained between 35 and 45 mm of Hg, using intermittent positive-pressure ventilation. Cardiopulmonary measurements prior to stomach distension (baseline) were compared with measurements taken during 0.1, 0.5, 1.0, 1.5, 2.5, and 3.5 hours of stomach distension by analyzing the change from baseline in a randomized-block analysis with each dog as a block. After distending the stomach, cardiac index increased (P < 0.01) from 1.5 to 3.5 hours. Stroke volume did not change, thus the increase in the, cardiac index was attributable to an increase in heart rate. During inflation, increases were observed in systemic arterial, pulmonary arterial, and right atrial pressure. Respiratory frequency was unchanged; however, to maintain PaCO2, constant, it was necessary to progressively increase peak airway pressure. Although PaO2, tended to decrease during gastric dilation, the dogs were never hypoxemic. These results indicate that when our methods are used to maintain a constant anesthetic dose of isoflurane in oxygen, an observed increase in cardiovascular performance is expected. This differs from other studies in anesthetized dogs that have shown reduction in cardiovascular performance following gastric dilatation.

Luteinizing hormone (LH) and ACTH concentrations were measured in plasma from 7 cows to determine whether ACTH secretion changes with the phase of the estrous cycle, and to determine whether any ACTH peaks are associated with LH peaks. Blood was collected every 5 minutes for 190 minutes during the luteal and follicular phases of the estrous cycle. Radioimmunoassays were used to measure ACTH and LH in plasma. Mean concentration of ACTH in all cows did not differ significantly between luteal (35.1 +/- 8.0 pg/ml) and follicular (37.5 +/- 9.4 pg/ml) phases of the estrous cycle. Mean concentration of luteal-phase LH of all cows (2.0 +/- 1.1 ng/ml) was significantly (P < 0.01) lower than mean concentration of follicular-phase LH (5.4 +/- 1.6 ng/ml). Frequency of peaks in ACTH concentration was low during the sampling period. Mean number of luteal-phase ACTH peaks (0.29 +/- 0.49) was not significantly different from that of follicular-phase samples (0.43 +/- 0.53). Unlike ACTH, mean frequency of LH peaks was significantly (P < 0.05) higher in plasma from cows in the follicular phase of the estrous cycle (2.9 +/- 0.7), compared with that from cows in the luteal phase (0.29 +/- 0.49).

Forty-eight cattle were used in 4 experiments; 6-week-old calves in experiments 1-3 (n = 24) and 10-month-old heifers in experiment 4 (n = 24). In experiments 1-3, 7 groups of 3 calves each were inoculated SC with 5 strains of Brucella abortus: virulent strain 2308 (2 groups), vaccine strain 19 (2 groups), and mutant strains RB51, 19 delta 31K, and 19 delta SOD. Sera and lymph node tissues were examined at 2-week intervals for evidence of infection. At postinoculation (PI) week 12, 2 calves in each group were given dexamethasone for 5 days. Calves were then euthanatized and lymphoid tissue, spleen, liver, and bone marrow were examined for evidence of B abortus. Calves given strain 2308 had large numbers of bacteria in their lymph nodes, marked granulomatous lymphadenitis in the deep cortex, and loss of lymphoid cells in superficial cortical areas. In addition, they had high serum antibody titers at PI week 16. Calves given strain 19, or genetic mutants derived from strain 19, cleared bacteria from lymph nodes more rapidly, had less lymphoid destruction, and developed antibody titers that did not persist for 16 weeks. The RB51 strain (rough) was cleared most rapidly from lymphoid tissues and induced serum antibody responses only to the core of the lipopolysaccharide molecule. Treatment of calves with dexamethasone did not cause B abortus to reappear in tissues of any calves, nor did serum antibody titers increase. In experiment 4, designed to compare the effects of age, 4 groups (n = 4) of 10-month-old heifers were given 1 B abortus strain each (19, RB51, 19 delta 31K, or 19 deltaSOD), using the same methods. Results of bacteriologic culturing and antibody responses were similar to those in the calves, except that strain RB51 persisted longer in heifers. Results of these studies indicated that, in cattle, the genetically engineered deletion mutants of B abortus do not cause unusual lesions, do have characteristics that closely resemble the parental strain, and could be candidates for use in a live vaccine.

Efficacy of a 1% solution of sodium carboxymethylcellulose (CMC) infused into the peritoneal cavity of ewes was evaluated for prevention of intraperitoneal adhesions resulting from surgery of the reproductive tract. Six ewes were assigned to each of 4 groups. Group-1 ewes were controls that underwent ventral midline celiotomy and exploration of the abdominal viscera. Group-2 ewes were treated similarly to group-1 ewes, except that a 1% solution of CMC (14 ml/kg of body weight) was infused into the peritoneal cavity. This group was studied to determine whether CMC would cause changes in the peritoneal cavity. Group-3 comprised ewes representing a uterine trauma model. Ewes underwent abdominal exploration, but in addition had a standard embryo collection technique performed on 1 uterine horn and hysterotomy performed on the opposite uterine horn. Group-4 ewes were treated like group-3 ewes, except that, similar to treatment of group-2 ewes, CMC was infused into the peritoneal cavity. All ewes were euthanatized and necropsied 12 to 14 days after surgery. Abdominal adhesions were evaluated, and an adhesion severity score was assigned to each ewe on the basis of number and severity of the adhesions. Ewes of all groups had abdominal adhesions. Significantly (P < 0.05) lower adhesion score was observed in ewes given CMC (groups 2 and 4) than in the adhesion model (group 3). Significant difference was not observed in adhesion score when groups 1, 2, or 4 were compared. Though not statistically significant, fewer adhesions were observed in ewes of groups 2 and 4 than in group-1 ewes.

A prospective observational cohort study of 361 dairy goat kids was conducted to compare 2 methods of controlling caprine arthritis-encephalitis virus infection under commercial dairy conditions. To compare effectiveness of feeding kids pasteurized milk vs serologic testing and segregation in addition to pasteurized milk feeding, goats were monitored up to the age of 30 months by use of monthly agar gel immunodiffusion testing. Survival analysis methods were used to determine whether age at seroconversion differed between the 2 groups. Significantly lower rates of seroconversion were observed in the segregated group (P < 0.001), compared with the nonsegregated group. Of 193 goats in the pasteurized milk-only group, 146 (75.6%) seroconverted within the 30-month study period, whereas infection was detected in 39 (23.2%) of 168 goats in the test/segregated group. Nonsegregated goats were 3.37 times more likely to seroconvert by 24 months of age, and 70.3% of seroconversions by 24 months of age could be attributed to nonsegregation. For age-specific intervals beyond 180 days of age, 70 to 100% of seroconversions could be attributed to lack of segregation. Cohort life tables for age at seroconversion were reported for each group. Type of colostrum fed, sex, and weaning group (season) were not significantly associated with age at seroconversion. Saanen goats had lower age-specific risk of seroconversion in the nonsegregated group alone and overall. Non-Saanen goats were 1.5 times more likely to seroconvert than were Saanen goats, when adjusted for a possible confounding effect of weaning group. Results indicate that pasteurized milk feeding and routine test and segregation would be a substantially more effective means of control of the disease in dairy goat herds than would pasteurized milk feeding alone.

Six male Beagles were inoculated with Ehrlichia canis. Transient proteinuria was confirmed during the acute phase of infection by serial determination of urinary protein-to-creatinine ratio. Peak urine protein loss, consisting principally of albumin, was observed 2.5 to 3.5 weeks after inoculation. Renal biopsy specimens were obtained before inoculation, during peak proteinuria, and 10 weeks after inoculation when proteinuria had resolved. Renal tissue was evaluated by use of light, immunofluorescent, and electron microscopy to correlate specific glomerular lesions with development of proteinuria. Histologic examination revealed perivenular and interstitial infiltrates of lymphocytes and plasma cells localized principally to the renal cortex. Glomerular lesions were minimal to absent. Immunofluorescent staining revealed moderate to marked deposition of anti-canine IgG and IgM in the glomerular tufts and mesangium. Depositions of anti-canine complement factor C3 were not observed. Immunofluorescent staining persisted 10 weeks after inoculation, despite resolution of proteinuria, and probably represented passive trapping of immunoglobulins. Ultrastructural examination revealed fusion of podocyte processes that coincided with development of proteinuria. Electron-dense deposits or changes in the basement membrane were not observed. Morphometric measurements of average podocyte process length and percentage of coverage of basement membrane by podocyte processes were used to quantify the degree of process fusion. Both measurements increased significantly (P < 0.05) during peak proteinuria, and returned to preinoculation values when proteinuria had resolved 10 weeks after E canis inoculation. These findings indicated possible minimal-change glomerulopathy, rather than immune-complex glomerulonephritis, during acute E canis infection and could explain transient proteinuria without histologic evidence of glomerular disease.

Hematologic and rheologic changes were examined in 49 Thoroughbreds before and after competitive racing. Mean postrace values for RBC count, hemoglobin concentration, and PCV increased by 58 to 61%, whereas blood viscosity increased 2 to 3 times. Postrace echinocyte numbers were 162% greater than prerace values. Smaller, but statistically significant, changes were found for mean corpuscular hemoglobin concentration, red cell distribution width, plasma total protein concentration, total WBC count, neutrophil count, and lymphocyte count. Variables measured did not predict whether a horse was a bleeder not treated with furosemide, a bleeder treated with furosemide, or a nonbleeder.

Three doses of sodium monoiodoacetate (MIA) were used to induce degenerative changes in articular cartilage in middle carpal joints of horses. Twelve young (2- to 5-year-old) horses, free of lameness, were randomly allotted to 3 groups. One middle carpal joint of each horse was injected with 0.9% NaCl solution (control joint). The contralateral middle carpal joint was injected with 0.09 mg of MIA/kg of body weight (group 1); 0.12 mg(kg (group 2); or 0.16 mg(kg (group 3). After MIA administration, horses were allowed ad libitum exercise in a 2-acre paddock for 12 weeks. At the end of the study, gross and microscopic tissue changes were evaluated and biochemical analyses of articular cartilage were done. Grossly, diffuse partial-thickness articular cartilage lesions were observed in group-2 (n = 2) and group-3 (n = 4) horses, but not in group-1 horses. Articular cartilage uronic acid content was significantly (P < 0.03) decreased in all MIA-injected joints, compared with controls. Articular cartilage matrix staining with safranin-O was decreased in 3 of 4 MIA-injected joints of group-1 horses and in all MIA-injected joints of group-2 and group-3 horses, compared with controls (P < 0.06). Microscopic degenerative changes in articular cartilage were not significantly different between MIA-injected and control joints in group-1 horses, but were increased (P < 0.06) in all MIA-injected joints of group-2 and group-3 horses, compared with controls. Qualitatively, decreased matrix staining and degenerative changes were more severe in group-3 horses. On the basis of articular cartilage gross and microscopic changes, as well as biochemical changes, 0.12 mg of MIA/kg injected intra-articularly was determined to induce moderate degrees of articular cartilage degeneration. This model of chemically induced articular cartilage injury could be useful for evaluating treatment effects of anti-arthritic drugs in horses.

Detection of autoantibody, complement, or both bound to RBC is an essential requirement for unequivocal diagnosis of immune-mediated hemolytic anemia in dogs. An enzyme-linked antiglobulin test was adapted for laboratory diagnosis of this disease. The refinement and routine use of this assay have allowed further observation of the pathogenesis of the disease process. In particular, degree of hemolysis can be related to the degree of RBC sensitization associated with primary immune-mediated hemolytic anemia, and this correlation is highest for IgG autoantibody. Results indicate that autoantibody isotype might have an important role in the hemolytic process.

Pregnant sows, immune against pseudorabies after vaccination, were inoculated at 70 days of gestation either with autologous blood mononuclear cells that had been infected in vitro with pseudorabies virus (PRV) or with cell-free PRV. The infected cells or cell-free PRV were inoculated surgically into the arteria uterina. Eight sows (A to H) had been vaccinated with an inactivated vaccine. The titer of seroneutralizing antibodies in their serum varied between 12 and 48. Five sows (A to E) were inoculated with autologous mononuclear cells, infected either with a Belgian PRV field strain or with the Northern Ireland PRV strain NIA. These 5 sows aborted their fetuses: 2 of them (B and C) 3 days after inoculation, and the other 3 (A, D, and E) 10, 11, and 12 days after inoculation, respectively. Sows F, G, and H were inoculated with a cell-free PRV field strain. They farrowed healthy Utters after normal gestation. Neutralizing antibodies were absent against PRV in the sera of the newborn pigs, which were obtained prior to the uptake of colostrum. The 23 fetuses that were aborted in sows B and C 3 days after the inoculation were homogeneous in appearance and size. Foci of necrosis were not detected in the liver. Viral antigens were located by immunofluorescence in individual cells in lungs, liver, and spleen of 15 fetuses. Virus was isolated from the liver, lungs, or body fluids of 12 fetuses. The 39 fetuses that were aborted in sows A, D, and E between 10 and 12 days after inoculation were of 2 types: 17 were mummified and 22 were normal-appearing. Foci of necrosis were found in the liver of all mummified fetuses and 13 of the normal-appearing fetuses. In fetuses with foci of necrosis in the liver, viral antigens were located in groups of cells in the liver, lungs, and spleen. Virus was isolated from 16 normal-appearing fetuses and from 11 mummified fetuses. Pseudorabies virus was isolated from vaginal excretions of sows A and D until 1 and 2 days after abortion, respectively, and of sows B and C until 4 and 5 days after abortion, respectively. Virus was not isolated from sow E. It was concluded that PRV can reach the uterine and fetal tissues, via infected mononuclear cells, in the presence of circulating antibodies induced on vaccination. This cell-associated spread led to abortion. Cell-free virus did not induce abortion under similar circumstances.