The cardiopulmonary effects of dorsal recumbency were studied in awake cows restrained for surgical correction of left displaced abomasum. During the recumbent period, Pa(O2), Pa(CO2), arterial pH, and base excess values were significantly decreased. Heart rate, respiratory rate, blood hemoglobin concentrations, and rectal temperature increased significantly.

Serum antibody titers to canine parvovirus (CPV), canine adenovirus-1 (CAV-1), and canine distemper virus (CDV) were measured in dogs with known immunization status. The dogs represented 3 groups: nonvaccinated dogs less than 12 months old; vaccinated dogs less than 12 months old; and adult dogs greater than 12 months old. For practical reasons, the population from which the specimens were obtained could be considered as free from natural infection with CAV-1 and CDV. In nonvaccinated dogs less than 12 months old, antibodies against all 3 viruses were measured at the time the dogs were given their first vaccination. Altogether, 50.7% of the dogs had titer greater than or equal to 1:10 to CPV, and 26.1 and 46.2% had titer greaterthan or equal to 1:8 to CAV-1 and CDV, respectively. The concentration of maternal antibody seemed to be of major importance for failure of immunization with use of inactivated CPV vaccine, but not with CAV-1 and CDV vaccination. In dogs less than 12 months old and vaccinated against CPV infection with inactivated virus, only 11.5% had titer greater than or equal to 1:80. In dogs vaccinated against infectious canine hepatitis and canine distemper, 63.2 and 78.3%, respectively, had titer greater than or equal to 1:16. In adult dogs greater than 2 months old and vaccinated against CPV infection, less than 50% had titer greater than or equal to 1:80, regardless of time after vaccination. There was no significant difference in titer between vaccinated and nonvaccinated dogs. Approximately 60% of these dogs had titer greater than or equal to CAV-1 at all time intervals after vaccination. There was only a weak correlation between decrease of titers and time; this correlation could be explained by the fact that a proportion of the dogs had been vaccinated with inactivated CAV-1 virus. There was, however, no correlation between titer to CDV and time. The percentage of dogs with titer greater than or equal to 1:16 was at least 60%.

Monoclonal antibodies and microfluorimetry were used to determine the absolute number of B and T lymphocytes in the blood of bovine leukemia virus (BLV)-infected cows. The blood lymphocyte populations from BLV-infected cows were significantly higher than those from BLV-negative cows. The increase in the lymphocyte population in 3 BLV-infected nonlymphocytotic cows was attributed to a significant increase in the number of T lymphocytes; in 3 BLV-infected persistently lymphocytotic cows, the increase was attributed to a significant increase in the number of B and T lymphocytes. One persistently lymphocytotic cow had a high lymphocyte count, and lymphocytes from this cow contained cells that appeared to stain with markers specific for bovine B and T lymphocytes. We concluded that infection of cattle with the B-cell lymphotropic retrovirus, BLV, not only affected B cells, but also T cells.

Observations were completed over an 18-year period (1966 through 1983) in Thoroughbred mares (15/year) and yearlings (11 to 24/year) on a farm where benzimidazole-resistant small strongyles had emerged previously (1962 to 1965). This farm was operated as a closed, nonboarding type, which included a racing stable for its home-bred foals. At 2-week intervals, counts of worm eggs per gram of feces (EPG) and larvae per gram of feces were done to monitor strongyle infections and efficacies of bimonthly (every 8 weeks) antiparasitic treatments that were administered by stomach tube or were fed (dichlorvos pellets) to 1 group of yearlings during a 7-year period (1970 through 1976). The study included several drugs or mixtures, including thiabendazole (TBZ), phenothiazine (PTZ) + piperazine (PPZ)-carbon disulfide (CS2) complex, PTZ + PPZ + trichlorfon (TCF), dichlorvos, and pyrantel pamoate. These were used selectively in treated subgroups (usually 3/year) of mares and yearlings. The horses in drug treatment subgroups grazed together on common pastures; thus, efficacy comparisons between drugs were limited or nullified. However, annual mean EPG and larvae per gram of feces counts of mares and yearlings tended to increase over time, and for the yearlings treated with TBZ + PPZ and PTZ + PPZ-CS2, the buildup of these mean counts was statistically significant (P less than 0.05 for regression coefficients). These trends of annual mean counts to increase were a general index of loss of anthelmintic activity of the 3 drug mixtures containing PPZ (TBZ + PPZ, PTZ + PPZ-CS2, and PTZ + PPZ TCF); however, trends were indicated more definitively by 2 other indices: (1) loss of effectiveness in reduction of EPG counts 2 weeks after treatment and (2) decrease in performance for complete clearance of strongyle eggs (EPG, 0) 2 weeks after treatment. Loss of effectiveness over time was statistically significant (P less than 0.001) for the mares only when data was pooled for all 3 treatments (TBZ + PPZ, PTZ + PPZ-CS2, and PTZ + PPZ + TCF); however, the decreasing effectiveness was statistically significant (P less than 0.05) for TBZ + PPZ and PTZ + PPZ-CS2 treatment of yearlings. Statistically, clearance performance in mareswas significant for treatments with TBZ + PPZ (P less than 0.003) and PTZ + PPZ + TCF (P less than 0.005) and approached significance with PTZ + PPZ-CS2 (P greater than 0.06). Clearance performances in yearlings were highly significant (P less than 0.0003) for treatments with TBZ + PPZ and PTZ + PPZ-CS2. These analyses of data indicate that the intense and prolonged (greater than or equal to 18 years) use of PPZ as a common component in several of the drug mixtures had resulted in the selection of a segment of small strongyles resistant to PPZ. Multiple resistance of this population of small strongyles includes several drugs: PTZ, the benzimidazoles (except oxibendazole and albendazole), possibly pyrantel, and PPZ. Side effects of drug treatments were not apparent during the prolonged period of this study.

Twenty-five strains of Escherichia coli isolated from turkeys were characterized for their serum resistance and virulence. An in vitro bactericidal assay was used to determine the serum resistance of E coli. Virulence was determined by survival time after IV inoculation of each strain into 3-week-old turkeys. Serum-resistant E coli strains were generally found to be virulent for turkeys, whereas serum-sensitive E coli strains were avirulent. Of the 25 strains, 18 strains were placed in the 2 categories of serum-resistant/virulent and serum-sensitive/avirulent. Five strains were serum-resistant and avirulent, and 2 strains were serum-sensitive and virulent. Serum resistance appears to be an important determinant of virulence for E coli in turkeys; however, the requirement for other virulence factors, in addition to serum resistance, was suggested by the finding that 5 serum-resistant strains were avirulent in turkeys.

The effect of Fusarium-produced T-2 toxin on tumor growth was evaluated in ICR, CFW, and C57B6/6 mice inoculated with murine sarcoma, Ehrlich ascites carcinoma, or B16F1 melanoma tumor cell lines. Mice were given T-2 toxin intragastrically either at the rate of 2 mg of toxin/kg of body weight daily for 5 days or a single dosage of 4 mg of toxin/kg and were inoculated SC with tumor cells 1 or 2 days after administration of toxin. Tumor growth was assessed 15 to 41 days after tumor challenge by determining the frequency of tumor development and tumor weights. Significant increases in the frequency of development of murine sarcoma (P < 0.005). Ehrlich ascites carcinoma (P < 0.01), and B16F1 melanoma tumors (P < 0.05) were detected in toxin-treated mice, compared with control mice. Murine sarcoma and B16F1 melanoma tumor weights also were significantly (P < 0.01) higher in toxin-treated mice. The effect of T-2 toxin on tumor growth was more marked after 5 daily treatments than after a single dose.

Primigravid swine were vaccinated orally with a live enterotoxigenic Escherichia coli (ETEC) strain that produces pilus antigen K99. The titers of K99 antibody in colostrum and milk of vaccinates remained higher than those of nonvaccinated controls through the first lactation after vaccination (4 weeks). Some control swine had low titers of K99 antibody in colostrum or developed low titers of K99 antibody in milk during lactation. Lacteal K99 antibody titers of vaccinates dropped to control levels during the second lactation, 6 months after vaccination. Pigs suckling vaccinates and controls were equally susceptible to challenge exposure to K99+ ETEC during the second lactation. Orally vaccinated swine given a parenteral booster vaccination (with killed K99+ ETEC) during their second gestation had K99 antibody in milk through their second lactation. During the second lactation, these orally vaccinated parenterally revaccinated swine had higher titers of K99 antibody in postcolostral milk than did nonvaccinated controls, controls given only the parenteral booster injection, or controls vaccinated parenterally during both gestations.

The effect of glucocorticoids on early follicular growth in sows undergoing normal estrous cycles was evaluated by administration of dexamethasone during the middle of the luteal phase. Plasma specimens were obtained for measurement of luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and estradiol-17 beta concentrations. Fifteen sows were used. Control sows (n = 5) were given physiologic saline solution twice daily from day 9 to day 14 of the estrous cycle. Sows of the second group (n = 5) were given dexamethasone (30 microgram/kg of body weight, IM) similarly, and those of the third group (n = 5) were given dexamethasone plus gonadotropin-releasing hormone (GnRH+ 50 microgram at 6-hour intervals, IV). Plasma specimens, obtained twice daily from day 8 through day 26, indicated that progesterone production and luteal regression were not inhibited by any of the 3 treatment regimens. Although preovulatory plasma estradiol concentration increased in control sows, such was not observed in the sows treated with dexamethasone or dexamethasone plus GnRH (P less than 0.01). Ovulation, with formation of corpora lutea, occurred in gilts given saline solution. Dexamethasone administration resulted in persistence of 19 to 41 follicles/ovary (2 to 4 mm in diameter), and dexamethasone-plus-GnRH treatment resulted in 6 to 18 follicles/ovary (5 to 6 mm in diameter). Plasma was obtained at 15-minute intervals for 12 hours to compare the effect of treatmenton hormone concentrations on day 12 of the estrous cycle with the values on day 8. Glucocorticoid administration had no significant effect on mean concentration, final concentration excluding those hormone concentrations that constituted part of a pulse (referred to as base line), number of pulses, pulse amplitude, and area under the pulse for either gonadotropin. Addition of GnRH to dexamethasone treatment significantly (P less than 0.01) increased all plasma LH values, but only base-line concentration of FSH. For estradiol, pulse amplitude and mean pulse area were increased (P less than 0.05), and although the frequency of pulses was not significantly altered, base-line concentration in glucocorticoid-treated sows was significantly reduced, compared with that of control sows. In sows treated with GnRH plus dexamethasone, the pulse frequency of estradiol was significantly (P less than 0.01) increased, but pulse area and amplitude were similar to those of sows given saline solution. Dexamethasone treatment was associated with an increase in mean and base-line concentrations of progesterone. The results suggest that high midcycle glucocorticoid concentrations (1) do not inhibit luteal function or regression, (2) have little influence on LH and FSH secretion during the middle of the luteal phase, (3) alter the pattern of estradiol secretion, (4) are associated with the persistence of small ovarian follicles, and (5) result in the development of fewer but larger follicular structures when GnRH is administered concurrently.

Using an avidin-biotin-peroxidase complex immunoperoxidase staining method, respiratory syncytial virus (RSV) antigen was demonstrated in glutaraldehyde-fixed, parraffin-processed lung sections from calves with induced RSV pneumonia. The virus also was detected in formalin-fixed, paraffin-processed lung sections from calves with naturally occurring RSV pneumonia. Specific immunoperoxidase staining was detected within the cytoplasm of epithelial cells and syncytia in small bronchi, bronchioli, and alveoli. Staining also was detected within exudates in airway lumina and in mononuclear and multinucleate cells within alveolar lumina. Optimal intensity of staining was achieved by proteolytic enzyme treatment of lung sections, using 0 .1% pronase and overnight incubation in diluted primary antiserum. The distribution of antigen had a close correlation with presence of lesions. Antigen-staining patterns were similar in lung tissue from calves with naturally occurring and induced RSV disease.

Neuromuscular and cardiovascular effects of atracurium, a nondepolarizing neuromuscular blocking agent, were evaluated in 10 halothane-anesthetized adult horses. Hind limb digital extensor tension (hoof twitch) was measured with a strain gauge to quantitate the muscle relaxant effects of atracurium. Response of facial muscles was compared with hoof twitch. Five injections of atracurium were given. Initial mean (+/- SEM) dosage of 0.07 +/- 0.01 mg of atracurium/kg of body weight caused 98.6 +/- 0.8% reduction of the preinjection hoof twitch. Subsequent dosages of 0.04 +/- 0.003 mg/kg induced a degree of relaxation similar to that induced by the initial dose. Duration of paralysis from maximal effect to 10% recovery of twitch was 12.2 +/- 1.5 minutes for the first injection. This was significantly (P less than 0.05) different from subsequent paralysis periods, which lasted approximately 7 miutes. The 10% to 75% recovery time after all injections was similar--approximately 16 minutes. The facial muscles were less affected objectively by atracurium than was the hind limb. Atracurium did not cause cardiovascular changes. When the hoof twitch had recovered to 95% of its tension before atracurium administation, 0.5 mg of edrophonium/kg, was given to antagonize neuromuscular blockage. Within 5 minutes of edrophonium administration, twitch tension exceeded that measured before atracurium administrations. Within 2 minutes of edrophonium administration blood pressure began to increase and continued to increase approximately 10 mm of Hg above the value measured before edrophonium administration. Heart rate was not affected by edrophonium. Other muscarinic side effects of edrophonium were not observed. Of the 10 horses, 9 had good, unremarkable recovery to standing position. One horse had a violent recovery period.