The forelimb superficial digital flexor (SDF) tendons of 6 Thoroughbreds were examined clinically and ultrasonographically during the first 4 months of race training. Sonograms were interpreted clinically and by use of computer-aided analysis. Tendon tissue from all horses was examined histologically at the end of the study. Computer-aided analysis of sonograms of the SDF tendons revealed trends toward an increase in mean cross-sectional area and a decrease in mean echogenicity over time with training. An inverse relation was found between increase in cross-sectional area and decrease in mean echogenicity over time in training. Two of the trained horses developed clinical signs of mild SDF tendonitis. Ultrasonography revealed an increase in cross-sectional area and decrease in mean echogenicity of clinically affected areas of the SDF tendons of 1 horse, compared with changes observed prior to the onset of tendonitis (these changes were not statistically significant). Blood vessels and lymphatics supplying the clinically and ultrasonographically affected tendon sites were large and thick-walled. These changes were not observed in the tendons of the other horses at the end of the study. The authors conclude that equine SDF tendons adapt to the early months of race training by increasing in size and decreasing in echogencity, as determined by ultrasonography.

Approximately 45 Holstein cows that were Mycobacterium paratuberculosis-positive on the basis of fecal culture results were maintained at any one time in a 210-cow dairy herd. Farm management participated in the New York State Paratuberculosis Eradication Program. Paratuberculosis-positive cows were grouped separately from paratuberculosis-negative cows, but they were otherwise managed identically. During a 1-year study, 180 paratuberculosis-negative cows and 113 clinically normal paratuberculosis-positive cows were identified. Quarter milk samples (n = 6,100) were aseptically collected for microbiologic culture of mastitis pathogens from paratuberculosis-negative cows, and 3,129 quarter samples were obtained from paratuberculosis-positive cows. Dairy Herd Improvement Association (DHIA) records were used to monitor milk somatic cell count linear scores, mature equivalent milk production, new mastitis infections, and chronic mastitis infections. For second-lactation cows greater than 100 days in milk production, and increasing with age beyond that point, paratuberculosis-positive cows had lower mature equivalent milk production than did negative herdmates. Rates of new and chronic mastitis infections, as measured by DHIA linear scores were significantly (P less than 0.05, P = 0.05, respectively) lower in cows with nonclinical paratuberculosis. Infected cows were cuffed from the herd at a faster rate than were paratuberculosis-negative herdmates. Therefore, paratuberculosis was associated with financial loss attributable to reduced milk production and increased culling of infected cows.

Reciprocal embryo transfers were made between scrapie-inoculated and scrapie-free sheep (Cheviot and Suffolk breeds) to measure scrapie transmission via the embryo (using offspring from embryos of scrapie-inoculated donors and scrapie-free recipients) and via the uterus (using offspring from embryos of scrapie-free donors and scrapie-inoculated recipients taken by cesarean section). Two control groups of offspring, 1 from scrapie-free parents (negative) and 1 from scrapie-inoculated parents (positive), also were included. All sheep were observed for clinical signs of scrapie until death or for a minimum of 60 months. Final diagnosis was made on the basis of histopathologic findings or results of mouse inoculation and/or proteinase-K-resistant protein analysis. Thirty to 61% of the scrapie-inoculated donor/recipient sheep within groups developed scrapie within 8 to 44 months after inoculation. None of the scrapie-free donor/recipients, including those gestating embryos from scrapie-inoculated donors, developed scrapie. Also, none of the offspring observed to larger than or equal to 24 months of age from reciprocal cross, via embryo (0/67), or via the uterus (0/25), or from the negative-control group (0/33) developed scrapie. Fifty-six of the offspring via embryo, 19 of these via the uterus, and 31 negative controls survived to larger than or equal to 60 months of age. Of the 21 sheep in the positive-control group, 2 (9.5%) developed scrapie, 1 at 31 months of age and 1 at 42 months of age. In the Cheviot offspring, the percentage of sheep carrying the short incubation allele ranged from 24 to 44% and the percentage in the Suffolk offspring ranged from 61 to 83%. These proportions indicate high degree of susceptibility to the disease. Results indicate that under the conditions of these experiments, scrapie was not transmitted to the offspring via the embryo or the uterus.

Anesthesia was induced and maintained in 6 Suffolk wethers by continuous IV infusion of guaifenesin (50 mg/ml), ketamine (1 mg/ml), and xylazine (0.1 mg/ml) in 5% dextrose in water (triple drip) to assess the anesthetic and cardiopulmonary effects. All sheep were positioned in right lateral recumbency. Dosages of triple drip used for induction and maintenance of anesthesia were 1.2 +/- 0.02 ml/kg and 2.6 ml/kg/h, respectively. Lack of gross purposeful movement of sheep to electrical stimulation indicated that analgesia and muscular relaxation induced by triple trip were adequate for surgical procedures. Heart rates and arterial blood pressure remained unchanged from baseline values during a 1-hour period of anesthesia. Arterial blood pressures were measured indirectly, using an inflation cuff placed over the metatarsal artery at the heart level. Significant decrease in arterial partial pressure of O2 (PaO2), coupled with an increase in arterial partial pressure of CO2 (PaCO2), from baseline values was observed throughout the course of the study. Decrease in PaO2 was observed concomitantly with significant (P < 0.05) increase in respiration rate. Changes in arterial blood gas tensions observed in this study were attributed to respiratory depressant effect induced by anesthetic drugs and right-to-left shunting, perfusion/ventilation mismatch, or both caused by right lateral recumbency. Administration of 100% O2 via the endotracheal tube reduced the magnitude of the decrease in PaO2. All sheep recovered smoothly and stood within 96.3 +/- 48.9 minutes after termination of triple drip administration.

Pharmacokinetics and recovery characteristics of propofol in Greyhounds and mixed-breed dogs were compared. In all dogs, disposition of propofol was adequately described by a 2-compartment open model, with a rapid distribution phase followed by a slower elimination phase. When findings in Greyhounds were compared with those in mixed-breed dogs, significant differences were observed in mean concentrations of propofol in blood, recovery characteristics, and estimates for apparent volume of distribution, volume of distribution at steady state, and total body clearance. In addition, Greyhounds recovered from anesthesia at higher concentrations of propofol than did mixed-breed dogs. A secondary peak in blood propofol concentration was observed in 8 of 10 Greyhounds and in 5 of 8 mixed-breed dogs. This peak corresponded to the time of return of the righting reflex.

A murine IgM monoclonal antibody causing bacterial agglutination was used in an immunoaffinity procedure to purify a serotype 1-specific polysaccharide epitope from Pasteurella haemolytica. The P haemolytica serotype 1-specific antibody was precipitated from peritoneal ascitic fluid, dialyzed, and covalently attached to cyanogen bromide-activated Sepharose 4B beads. Retention of purified antibody activity and coupling efficiency were > 99% when evaluated by ELISA, agglutination testing, and protein determination. Potassium thiocyanate was selected as an eluant on the basis of reversible dissociation of bacterial agglutination and was titrated for the lowest effective concentration. Immunobead activity was observed microscopically by immobilization of encapsulated P haemolytica serotype 1 and its reversible dissociation after elution with 0.4M potassium thiocyanate. Specificity of immobilization was visualized, using P haemolytica serotypes 2 and 5, which were not bound, and by blocking serotype-1 binding with homologous capsular material. Saline-extractable capsular material from P haemolytica serotype 1 was used as an antigen source. After elution of the serotype 1-specific polysaccharide epitope, the product was dialyzed and analyzed, using chemical and immunologic methods. The immunoaffinity product contained no detectable protein and greater than half the original hexosamine content. Using defined monoclonal antibodies in ELISA, titration of the original capsular material and the immunoaffinity product revealed specific retention of lipopolysaccharide, a 10- to 30-kd polysaccharide antigen common to all P haemolytica and P multocida serotypes, and serotype 1-specific capsular polysaccharide, indicating possible epitope sharing among polysaccharide antigens of P haemolytica serotype 1.

Hemagglutinins HA) of H1N1 swine influenza viruses isolated in the United States have remained antigenically and genetically conserved for many years. In contrast to such conservation, the RA of A/Swine/Nebraska/1/92 (Sw/Neb) could readily be distinguished from those of contemporary porcine viruses. Twenty-eight amino acid mutations differentiated the HA of Sw/Neb and A/Swine/Indiana/1726/88, the most recent H1N1 swine influenza virus for which HA sequence data were available. Among these differences were mutations at potential asparagine-linked glycosylation sites and charge changes at many residues. The Sw/Neb virus also could be differentiated from other swine influenza viruses in hemagglutination-inhibition assays with monoclonal antibodies to recent H1 swine HA. Nonetheless, overall sequence analysis of the HA and the nucleoprotein genes of Sw/Neb indicated that this virus was more closely related genetically to classic H1N1 swine influenza viruses than to H1N1 avian or human viruses. Infection of swine with Sw/Neb under experimental conditions induced clinical signs and lesions typical of swine influenza. However, affected swine in the field had high, persistent fevers, but relatively mild signs of respiratory tract disease. This study indicated that an antigenically and genetically novel variant of swine influenza virus was detected in the United States.

Somatosensory evoked potentials in response to tibial nerve stimulation were recorded from the scalp of 31 clinically normal mixed-breed dogs. The latency and amplitude of a main positive potential (P18), recorded with a frontal electrode referenced to the nose, were measured in subjects with body length ranging from 316 to 962 mm. A linear relation to body size explained the variations in latency among dogs (r2 = 0.81); the amplitude variations were explained in part by body size (r2 = 0.44). Bilateral tibial nerve stimulation significantly (P < 0.05) increased the amplitude of P18, but its latency was unaffected, compared with unilateral stimulation. Results of unilateral right and left tibial nerve stimulation were compared and were not different. Replacing acepromazine with xylazine as premedication before thiopental anesthesia did not influence the recordings.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.

Prednisone was administered orally for 4 weeks at a dosage of 1.1 mg/kg of body weight/d, in divided dose every 12 hours, to a group of healthy adult dogs (n = 12). Intravenous glucose tolerance testing was performed before and after the 28-day regimen in each dog, as well as in dogs of a control group (n = 6). Glucose metabolism was evaluated by measurement of preprandial plasma insulin and glucose concentrations, total insulin secretion, and fractional clearance of glucose. Mean preprandial plasma insulin and glucose concentrations were not increased after the 4-week regimen of prednisone. Total insulin secretion in response to an IV administered glucose load was not increased in treated dogs, compared with pretreatment values or with values for control dogs. The fractional clearance of glucose was also not altered in dogs given prednisone. Results indicate that anti-inflammatory doses of prednisone, given orally for 4 weeks, probably do not alter insulin sensitivity or glucose tolerance in clinically normal dogs.