The effects of coliform endotoxin (E) and recombinant ovine tumor necrosis factor a (TNF) were compared with respect to clinical signs of disease and changes in plasma metabolite and pituitary and pancreatic hormone concentrations in calves. In addition, changes in plasma TNF concentration during each challenge exposure were quantitated by use of radioimmunoassay. Healthy Holstein bull calves with mean body weight of 90 kg were each given, in order, on different days, saline solution (5.0 ml, IV, day 1, n = 4), E (type 055:B5, 1.0 microgram/kg of body weight IV, day 2, n = 4) and TNF (5.0 microgram/kg IV, day 9, n = 3). Jugular venous blood samples, rectal temperature reading, and PCV were obtained at hourly intervals before (2 hours) and after challenge exposure. The PCV increased (P < 0.05) after E and TNF administrations for the first 5 hours, then returned to normal in calves given E, but decreased and remained low in calves given TNF through 24 hours. Plasma triglyceride and nonesterified free fatty acids concentrations were increased through 10 hours (P < 0.05) after E administration, whereas triglyceride and nonesterified free fatty acids concentrations were not significantly affected by TNF administration. Increase in blood glucose concentration at 1 hour after administration of E and TNF was followed by prolonged hypoglycemia that lasted through 6 hours. Changes in plasma insulin concentration paralleled the observed changes in glucose concentration, initially increased at 2 hours after E and TNF (P < 0.05) administrations, but then tended to decrease below control values thereafter. Plasma growth hormone and luteinizing hormone concentrations decreased after E and TNF administrations to almost nondetectable values through 4 hours after dosing, returning to normal values by 8 hours. The data indicate similarities in physiologic response of calves to E and TNF and suggest a role for acute production of TNF as a mediator of E responses.

The efficacy of netobimin against digestive tract strongyles and the small lungworm Muellerius capillaris was tested in a dairy goat herd. The drenches were given orally at the rate of 20 mg/kg of body weight once, 10 mg/kg on 2 successive days, or 7.5 mg/kg on 3 successive days. Fecal egg counts and larval counts were done 8 days before and on the day of drenching; further counts were performed on postdrenching days 8 and 18. Two goats were necropsied, 1 on postdrenching day 5 and 1 on day 10 in the group treated on 3 successive days. The fecal egg counts were reduced by 44 to 79% depending on dosage on postdrenching day 18; the remaining worms were Trichostrongylus colubriformis. The larval counts of M capillaris were reduced by 72 to 92%, depending on dose. The reduction was significant in all the treated groups, compared with that in the control group. The use of netobimin at the dosage of 10 mg/kg given on 2 successive days or 7.5 mg/kg given on 3 successive days might be recommended to treat goats infected with Muellerius spp and digestive tract strongyles.

Twenty-four specific-pathogen-free Beagles were each given 50 cysticerci of Taenia pisiformis that had been harvested from experimentally infected rabbits. Quantitative fecal egg counts and fecal screening for recovery of passed segments were performed on postinoculation days 56 through 70. Twenty-three of 24 dogs fed cysticerci developed patent infections. The 23 dogs with patent infections were assigned to 1 of 2 groups and treated with nitroscanate or a placebo 60 days after inoculation. Egg counts in the treated dogs had markedly decreased by the second day after treatment, and by the sixth day after treatment, segments were not found in the feces of any of the treated animals. The control dogs continued to pass eggs and segments in their feces throughout the 9 days after treatment. The dogs were euthanatized and necropsied 70 days after being inoculated. At necropsy, the mean number of scolices recovered from control dogs was 24.6, the mean number of scolices recovered from treated dogs was 0.25. Worms recovered from the control dogs were intact, gravid cestodes. Efficacy of treatment with nitroscanate at a mean dosage of 56 mg/kg of body weight was 98.9%.

Two commercially available synthetic adjuvant systems, trehalose dimycolate (TDM) and TDM + monophosphoryl lipid A (MPL), were compared with Freund complete adjuvant (FCA) for the ability to stimulate antibody production in New Zealand White rabbits (Oryctolagus cuniculus). In addition, each animal was evaluated for adverse reactions. The antigen, rat liver microsomal epoxide hydrolase, was administered sc emulsified with FCA, TDM, or TDM + MPL. Serum antibody titers were stimulated with all 3 adjuvant-antigen combinations. The highest titer was produced by use of FCA; TDM + MPL produced an intermediate response, and TDM produced the lowest titer. All of the rabbits immunized with FCA developed sterile subcutaneous abscesses. Rabbits immunized with TDM or TDM + MPL developed no abscesses, and only slight reactions at the injection sites. The synthetic adjuvant system TDM + MPL is recommended for use in rabbits, considering its adequate stimulation of antibody production with minimal adverse reactions.

The purpose of this in vitro study was to determine whether Pasteurella haemolytica capsular extract (CE) damages bovine pulmonary endothelial cells (EC) directly or through neutrophil-mediated mechanisms. Chromium 51-labeled EC were treated with the following variables: CE (1, 10, and 100 ng of protein/ml), CE and bovine neutrophils (10(6) cells/well), and CE and polymyxin B (500 U/ml). Although only minimal damage to EC occurred by 5 hours after treatment, by 22 hours after treatment, the 10-ng and 100-ng CE dose produced severe damage to EC, as indicated by 51Cr release, cellular detachment, and loss of monolayer confluency. The component in the CE that was toxic to the EC was lipopolysaccharide, evidenced by effective neutralization of the toxic effect with polymyxin B. Neutrophils inhibited the CE-mediated EC toxicity and were activated, as indicated by shape change and adhesion to EC monolayers. We concluded that the lipopolysaccharide component of CE causes direct damage to EC, which can be attenuated by neutrophils and polymyxin B.

Ceruloplasmin (Cp) was isolated from fresh equine plasma by precipitation, cellulose chromatography, and improved ion-exchange chromatography. Purified equine Cp is a glycoprotein having a molecular weight of approximately 115,000. In electrophoresis, equine Cp migrated to the alpha 1-globulin region, its isoelectric point was about 4.15 and consisted of about 890 amino acid residues. Serum Cp concentration was measured by use of the single radial immunodiffusion method. In clinically normal horses, the mean (+/- SD) serum Cp concentration of newborn foals was 2.87 +/- 0.40 mg/ml and that of 3-month-old foals was 5.02 +/- 0.92 mg/ml, which was similar to the adult value. It reached a peak of 6.06 +/- 0.74 mg/ml in 2-year-old horses. The Cp concentration in mares was not statistically different for the perinatal period, but it decreased immediately before and after delivery. Concentration of Cp increased at 6 days after IM administration of turpentine oil, castration, or jejunojejunostomy in adult horses, and increased to peak values twice as high as baseline values at 7 to 14 days, returning to baseline values at 28 days after treatment. We concluded that equine serum Cp is an acute-phase reactive protein increased in the intermediary or later phase of acute inflammation.

Progressive changes in serum enzyme activity and liver histologic features were monitored in calves fed tansy ragwort (Senecio jacobaea)-contaminated pellets. The experiments were designed to simulate natural intoxicant ingestion conditions in relationship to the dose and duration of exposure to the toxic plant to correlate early laboratory diagnostic changes with the natural progression of the disease, thereby facilitating early diagnosis and intervention by veterinary clinicians. Eight calves were fed tansy ragwort and 4 additional calves served as controls. In group 1, 4 calves were continuously fed dried tansy ragwort mixed in a pelleted feed at a 5% concentration by dry weight until terminal liver disease developed. Serum liver enzyme (alkaline phosphatase, glutamate dehydrogenase, and gamma-glutamyltransferase) activities were monitored at weekly intervals in these calves and in the 2 controls. In group 2, 4 calves were fed the same contaminated feed for only 60 days, with return to normal feed for the duration of the trial. Two additional calves served as controls. Their liver enzyme activities were monitored every other week in conjunction with percutaneous liver biopsies. All 8 calves fed tansy ragwort-contaminated pellets developed terminal hepatopathy in either a chronic pattern (n = 6) or a chronic-delayed pattern (n = 2), with the onset of a moribund state or sudden death at 11 to 17 weeks and 27 to 51 weeks, respectively. The calves were euthanatized when classic terminal signs of hepatic encephalopathy first became evident. The clinicopathologic patterns of chronic and chronic-delayed toxicoses were typical of over 5,000 cases of field tansy toxicosis diagnosed at the diagnostic laboratory. Serum glutamate dehydrogenase was the first enzyme to increase in most animals, with a short-term increase to peak values followed by a rapid return to normal. This enzyme change was followed by increases in alkaline phosphatase and gamma-glutamyltransferase. Serum enzyme changes preceded development of recognizable histologic lesions. Vacuolar changes in hepatocyte nuclei, biliary hyperplasia, and fibrosis sequentially developed in liver biopsy specimens from each animal, whereas megalocytosis was not a predominant feature until necropsy. On the basis of our finding we suggest that the optimal tests for diagnosis of pyrrolizidine alkaloid intoxication should consist of liver biopsy and determination of concurrent serum liver-enzyme activities.

Thoracic compliance measurements by use of readily available equipment were determined to be practical and safe in dogs. Twenty healthy dogs (age 1 to 16 years, weight 2.3 to 49.5 kg) were anesthetized for routine procedures such as dentistry or neutering. The animals were first hyperventilated to reduce pulmonary atelectasis, to check for leakage at the endotracheal tube cuff, and to induce mild hypocarbia, thus minimizing voluntary respiratory efforts. Total thoracic compliance measurements were calculated as the difference between exhaled volumes at static inspiratory pressures of 15 and 20 cm of H2O, divided by the pressure difference, and expressed as a function of body weight. The procedure was easy, took 5 to 10 minutes, and caused no recognizable ill effects in any of the dogs studied. Mean total thoracic compliance was 42.25 +/- 32 ml/cm of H2O. There was a significant correlation with weight, but no significant relationship was seen between compliance and age, or gender. The mean weight-adjusted total thoracic compliance was 1.85 +/- 0.56 ml/cm of H2O/kg. In studies in a small group of dogs with documented respiratory tract disease, 4 of 7 had a mean compliance > 2 SD below the normal range. Thus, this test may become part of the routine workup of any animal being anesthetized for procedures such as bronchoscopy to evaluate respiratory tract disease. Routine monitoring of animals on ventilators could provide early warning of complications such as pneumonia, pleural effusion, or pulmonary edema.

Epidemiologic data were evaluated from all dogs admitted to the University of Minnesota, Veterinary Teaching Hospital (UMVTH) between June 1981 and November 1989. Of 69,890 admissions, 2,077 were Miniature Schnauzers. Uroliths were retrieved from 63 of the 2,077 Miniature Schnauzers admitted. In 20 of the 63 urolith episodes, calcium oxalate was the predominant mineral identified. By comparison, calcium oxalate uroliths were identified in only 56 of the remaining 67,813 non-Miniature Schnauzer canine admissions. The odds that uroliths from Miniature Schnauzers were composed of calcium oxalate was 11.8 times greater than for other canine breeds evaluated at the UMVTH (95% confidence interval = 6.8 to 20.1). Data also were evaluated from files of uroliths retrieved from dogs and submitted to the Minnesota Urolith Center for quantitative mineral analysis between June 1981 and November 1989. Of 3,930 uroliths analyzed, 615 (15.6%) uroliths were obtained from Miniature Schnauzers. Of the 615 uroliths, 175 (28.4%) were calcium oxalate. By comparison, only 550 (16.6%) of the remaining 3,315 from dogs of breeds other than Miniature Schnauzers were calcium oxalate. The odds that uroliths submitted for analysis were composed of calcium oxalate was 2 times greater for Miniature Schnauzers than for dogs of other breeds (95% confidence interval = 1.6 to 2.4). Calcium oxalate uroliths were retrieved more frequently in males than females. The risk for males developing calcium oxalate uroliths was > 3 times the risk for females in both groups of data evaluated. The mean age of all Miniature Schnauzers admitted to the UMVTH with calcium oxalate uroliths was 9 years. Calcium oxalate uroliths were not detected in Miniature Schnauzers younger than 1.7 years.

Axial length and corneal curvature were determined by use of A-scan ultrasonography and keratometry on both eyes of dogs of various breeds, sizes, and ages. Mean axial length was 20.43 +/- 1.48 mm; axial length was not related to age or sex, but was significantly greater (P = 0.047) in dogs of larger breeds. Mean corneal curvature was 39.94 +/- 2.61 diopters. Dogs of large breeds had significantly (P < 0.001) flatter corneas. Mild, roughly symmetric astigmatism was detected in a majority of dogs. Use of mean values in a theoretic artificial intraocular lens power equation suggests that aphakic dogs require an implant of approximately 40 diopters to achieve emmetropia.