Three sheep, a foal, a pony, and a calf were anesthetized and ventilated for short periods, using a high-frequency oscillatory ventilator. The efficiency of CO2 elimination was characterized at various oscillatory frequencies (50 to 30 Hz) and various tidal volumes, although the tidal volume used was always less than the measured dead space of the animal. In general, increasing either the oscillatory frequency or tidal volume increased CO2 elimination, but increasing the tidal volume had more effect. The relationship between these 3 variables was best described by a power law equation. Ventilatory frequencies and tidal volumes required to maintain eucapnia in the species studied were extrapolated from the results and, when technically possible, the potential of the technique to maintain eucapnia was tested in extended runs. The animals were supported successfully over this period, with normal blood gas tensions and no detrimental effects to heart rate and rhythm or arterial blood pressure.

The detection of volatile fatty acids (VFA) by gas chromatography of 85 purulent specimens from abscesses or pyogenic infections in cats, dogs, rodents, and ruminants was compared with the results of bacteriologic culturing, and proved to be a rapid means of presumptively diagnosing anaerobic infections. Of 83 bacteriologically positive specimens, 52 (61%) yielded obligate anaerobes and in 50 specimens, 1 or more VFA (butyric acid, isobutyric acid, valeric acid, isovaleric acid, caproic acid, or isocaproic acid) was detected. Forty-six specimens were positive for culturing of anaerobes and for detection of 1 or more of these VFA. By contrast, pus from infections caused by (facultative) aerobic microorganisms contained no VFA or only acetic and/or propionic acid.

Four groups of 8 horses each had 1 midcarpal joint injected with 33 colony-forming units (CFU) of viable Staphylococcus aureus plus: 1 ml of saline solution (group 1, control), 250 mg of polysulfated glycosaminoglycan (PSGAG, group 2), 100 mg of methylprednisolone acetate (group 3), or 20 mg of sodium hyaulronate (group 4). Horses were euthanatized, and samples were obtained on the basis of clinical signs of septic arthritis that were nonresponsive to phenylbutazone administration. One group-1 horse, all 8 group-2 horses, 3 group-3 horses, and 4 group-horses 4 were culture-positive for S aureus and had clinical signs, results of synovial fluid analysis, and histopathologic findings that were consistent with sepsis. The addition of 250 mg of PSGAG increased the development of sepsis significantly (P = 0.001), compared with results in control horses. Differences in the development of sepsis between horses injected with methylprednisolone acetate or sodium hyaluronate and control horses were not significant.

The efficacy of ivermectin as an in-feed formulation was evaluated against naturally acquired gastrointestinal helmiths, lungworms, and sarcoptic mites (experiment 1; n = 24) and against induced infection with intestinal nematodes (experiment 2; n = 24) in pigs. Treatments consisted of ivermectin administered in feed at concentrations calculated to provide 100 or 200 microgram/kg of body weight/d for 7 days or of nonmedicated feed (controls) for 7 days. At concentration of 100 microgram of ivermectin/kg/d, efficacy against naturally acquired infections was 97.7% for Ascaris suum, 97.8% for Metastrongylus spp, greater than 99% for Oesophagostomum spp, 100% for Macracanthorhynchus hirudinaceus, and 89.7% for Ascarops strongylina. Against induced infections (fourth-stage larvae), efficacy was 100% for A suum and 96.9% for Oesophagostomum spp. At concentration of 200 microgram of ivermectin/kg/d, efficacy against naturally acquired infections was 100% for A suum, Hyostrongylus rubidus, Metastrongylus spp; and 85.9% for Macracanthorhynchus hirudinaceus. Against induced infection (fourth-stage larvae), efficacy was 100% for A suum and 95% for Oesophagostomum spp. At concentrations of 100 and 200 microgram of ivermectin/kg/d, efficacy against Sarcoptes scabiei var suis was evidenced by elimination of the mite by posttreatment day 14.

Chicken eggs at embryonation day (ED) 18 or newly hatched chicks were inoculated with turkey herpesvirus (HVT), Marek's disease virus (MDV), or virus-free diluent and, at intervals after inoculation, tissue homogenates of virus-exposed and virus-free chickens or chicken embryos were examined for interferon (IFN) activity. Homogenates of lung thymus and spleen specimens from chickens given HVT at ED 18 had IFN activity. Activity of IFN in the lungs was studied further. Homogenates of lung specimens from chickens exposed to HVT at hatching also had IFN activity, although the concentration of IFN was lower than that in chickens given HVT at ED 18. The pathogenic isolates of MDV (JM-(MDV)), but not the atenuated (Md11/75C-(MDV)) or nonpathogenic (SB1-(MDV)) isolates, inoculates at ED 18 also induced high lung IFN activity. Exposure to a combination of HVT and SB1-MDV induced IFN activity comparable with that in chickens given HVT alone. The IFN activity in homogenates of lung specimens from virus-exposed chickens was species specific and heat and pH stable, but was destroyed by trypsin treatment. Occassionally, low IFN activity also was detected in homogenates of tissus specimens from virus-free chickens or chicken embryos. This IFN activity could have been produced constitutively or may have been induced by substances (inducers) in the environment.

The effect of dry, soft moist, and canned dog foods on immediate postprandial plasma glucose and insulin concentrations was evaluated in clinically normal dogs. Dogs were fed either dry (10 dogs; group I), soft moist (10 dogs; group II), or canned (8 dogs; group III) dog food for 5 consecutive days. On the fifth day, plasma glucose and insulin concentrations were determined in each dog prior to, during, and at 5, 10, 15, 30, 45, 60, 90, 120, 180, and 240 minutes after ingestion of the food. The alterations in plasma glucose concentrations were not significantly different from prefeeding values until 240 and 180 minutes after feeding for groups I and III, respectively. In contrast, the increments in plasma glucose were significantly (P less than 0.01) increased from basal concentrations at 30 and 45 minutes after feeding in group-II dogs. The maximal mean postprandial plasma glucose concentration was significantly (P less than 0.0001) less for group III, compared with concentrations for groups I and II, but there was no significant difference between concentrations for groups I and II. Although a bisphasic insulin secretory response was found in all 3 groups of dogs, the patterns of phase-2 insulin secretion and the total amount of insulin secreted during the study were significantly different. There was a rapid increase in the plasma insulin concentration immediately after phase 1 in group II, with maximal plasma insulin concentrations occurring 30 minutes after feeding, followed by a gradual decrease in concentrations throughout the remainder of the study. In contrast, plasma insulin concentrations increased steadily in groups I and III, after phase-1 insulin secretion, with maximal values occurring at 240 minutes after feeding. The maximal mean increase from basal insulin concentrations during phase-2 secretion was significantly (P less than 0.005) greater for group II (80 +/- 15 micro IU/ml) than for groups I and III (23 +/- 3 and 24 +/- 6 micro IU/ml, respectively). Whereas the integrated areas under the glucose response curves were not significantly different between groups, total insulin secretion and total insulin secreted during phases 1 and 2 were significantly (P less than 0.01) greater in group II than in groups I and III. Differences in dietary composition may offer the best explanation for differences in postprandial glucose concentrations and insulin secretory responses between groups. These findings emphasize the importance of dietary formulations when designing hormonal studies or interpreting research data when dogs are the animal model.

The use of lipoarabinomannan (LAM; obtained from Mycobacterium paratuberculosis) in an ELISA (LAM-ELISA) to test 75 sheep sera from a paratuberculosis-infected flock resulted in an approximate threefold increase in sensitivity (from 23.5% to 70.6%), compared with the use of Annau's polysaccharide in a complement fixation test (P-CFT). Even after manipulation of the LAM-ELISA cut-off value to produce a specificity of 100% to match that of the P-CFT, the sensitivity still was approximately twofold greater than that of the P-CFT. Anti-bovine monoclonal antiglobulin-enzyme conjugates matched commercially available anti-ovine polyclonal antiglobulin-enzyme conjugates with respect to sensitivity and specificity. False-positive results were found to be less frequent after combining 2 serodiagnostic tests, LAM-ELISA and D antigenagar gel immunodiffusion, resulting in an increase in specificity from 88.1% to 95.2%. The repeatability of true seropositive and seronegative results was found to be 89.5% and 91.1%, respectively, for sera obtained less than or equal to 1 month prior to slaughter and 91.7% and 95.5%, respectively, for reanalysis of sera obtained at the time of slaughter.

Fifteen newborn germ-free pigs were inoculated with 2 strains, D-282 and T-15, of Streptococcus suis type II. Some pigs also were preinoculated with Bordetella bronchiseptica, which successfully predisposed them to S suis infection. The 2 streptococcal strains were differentiated by muramidase treatment, which released certain high molecular-weight proteins, termed muramidase-released proteins (MRP), from the cell wall of strain D-282, but not from the cell wall of strain T-15. Only strain D-282 (MRP-positive) induced clinical signs of disease and markedly increased neutrophil numbers in pigs. Streptococci were more frequently isolated from fecal swab specimens obtained from pigs inoculated with strain D-282 (MRP-positive) than from specimens obtained from pigs inoculated with strain T-15 (MRP-negative). Both strains were isolated from nasal swab specimens obtained from all infected pigs. Postmortem examination revealed fibrinopurulent meningitis, polyserositis, and polyarthritis in pigs inoculated with strain D-282; this strain was isolated from the CNS, serosae, visceral organs, heart, and joints. Whereas strains D-282 caused several pathologic changes, strain T-15, isolated from the lungs, caused only pneumonia. Both strains were isolated from the tonsils of all pigs. Virulence differed distinctly between the MRP-positive and the MRP-negative strains.

Antibodies to bovine serum albumin were detected in swine sera by use of an immunoblotting technique. Such sera had false-positive reactions, as determined by results of African swine fever virus serodiagnostic techniques when bovine serum albumin was a contaminant in the soluble cytoplasmic antigen obtained from infected cells cultured in the presence of bovine serum. The soluble cytoplasmic antigen obtained from cell cultures infected with African swine fever virus in the presence of porcine serum did not react with the false-positive sera and, therefore, was used for African swine fever virus serodiagnostic methods, with 0% false-positive results.

Fluctuations of serum vitamin E (alpha-tocopherol), cholesterol, and total lipids were monitored in 12 horses at 3-hour intervals for 72 hours. Mean coefficients of variation were 12, 5, and 15%, respectively. Statistical analyses were used to conclude that instrumentation error was accountable for only a small portion of the vitamin E variation. Results indicated that a single serum sample assay is an unsatisfactory indicator of vitamin E status in horses. These data have clinical application in the evaluation of horses suspected to be affected with equine degenerative myeloencephalopathy. The large variance of serum total lipids and the lack of correlation of it with serum vitamin E over time preclude the use of vitamin E/serum total lipids ratio in assessing vitamin E status.