The heart rate (HR) induced by maximal beta-adrenergic activation, which was elicited by infusion of isoproterenol, was studied in 8 healthy horses before (control) and after hyperthermia was induced by IV administration of 2,4-dinitrophenol (DNP). Isoproterenol was administered IV at 1.0 micrograms.kg-1.min-1 for 3 minutes and the HR was determined during the final 30 seconds of the infusion. As the rectal temperature increased (P < 0.001) from 38.2 +/- 0.1 C (mean +/- SEM; normothermic control) to 40.1 +/- 0.1 C at 60 minutes after DNP administration, the isoproterenol-induced HR also increased from 198 +/- 4 beats/min (control) to 214 +/- 4 beats/min (P < 0.001). It appeared that the values of HR achieved with maximal beta-adrenergic activation were augmented by the hypermetabolic, hyperthermic state induced by DNP.

Norepinephrine (NE) and epinephrine (EPI) collected from dogs were sequentially and temporally measured in blood and plasma at 24 C. Heparin and EDTA anticoagulants, in combination with reduced glutathione and EDTA as a preservative, were also compared. Norepinephrine and EPI concentrations were measured by high-pressure liquid chromatography with electrochemical detection. In heparinized plasma, NE and EPI concentrations were relatively stable in the absence or presence of preservative after 24 hours at 24 C. In EDTA plasma, NE and EPI values were less stable when compared with those in heparinized samples. Norepinephrine concentrations in EDTA plasma without preservative decreased by 163.2 +/- 8.88 pg over 24 hours, compared with an 86.6 +/- 7.92 pg loss of NE in heparinized plasma. The degradation of EPI in EDTA plasma without preservative was also twofold greater, compared with that in heparinized plasma. Addition of preservative had no stabilizing effect on NE or EPI in heparinized or EDTA plasma. During long-term storage at -70 C, plasma NE and EPI values decreased < 0.6 and < 0.1 pg/d, respectively. Norepinephrine and EPI values were stable in heparinized blood for 6 hours but decreased to < 25% and < 6% of initial base line values, respectively, when plasma separation was delayed 24 hours.

Serum IgA, IgG, and IgM concentrations were determined for Beagle sires and dams of 717 matings to assess the relationship of parental immunoglobulins with the morbidity and mortality of their pups. A significant relationship was not found between parental immunoglobulins and pup mortality. Pups born to dams with low serum IgA (P < 0.001) and IgM (P < 0.02) concentrations, however, were found to have an increased incidence of sneezing, coughing, nasal discharge, and conjunctivitis. Thirty-eight percent of pups born to dams with IgA less than or equal to 40 mg/dl developed these same conditions during the first 18 weeks of life, compared with 32% of pups of dams with IgA of 41 to 65 mg/dl and 27% of pups of dams with IgA > 65 mg/dl. Similarly, 41% of pups born to dams with low IgM (less than or equal to 135 mg/dl) developed abnormal respiratory tract signs, compared with 34% and 30% of pups born to dams with medium (136 to 175 mg/dl) and high (> 175 mg/dl) IgM, respectively. Serum IgA concentrations of the sires were also associated with abnormal respiratory tract signs in pups, but this influence was evident only at 10 to 18 weeks of age. To determine biologic variability of serum IgA, 60 Beagle dams were selected from 3 serum IgA categories, low (10 to 21 mg/dl), medium (60 to 80 mg/dl), and high (125 to 210 mg/dl). A second serum IgA was determined from a sample taken 2 years later. The intraclass correlation coefficient (rI) indicated considerable biologic variability in all 3 groups: rI = - 0.24, rI = 0.09, and rI = 0.46, for low, medium, and high IgA categories, respectively. In contrast, minimal variability was noticed between observers (rI = 0.98) and in the radial immunodiffusion test itself (rI = 0.96).

The cytotoxic effect of Moraxella bovis 118F on bovine neutrophils was evaluated and characterized by use of a 51Cr release assay. Neutrophils harvested from healthy adult cattle were labeled with 51Cr. The leukocidic activity produced by M bovis 118F, a hemolytic strain of M bovis, was heat-labile. A live culture of strain 118F, at a ratio of 100 bacteria/neutrophil, released 97.7% of the 51Cr from labeled neutrophils. Neither a heat-killed preparation of M bovis 118F nor a live or heat-killed preparation of M bovis IBH63 (a nonhemolytic and nonpathogenic strain) induced significant (P > 0.05) release of 51Cr. Moraxella bovis 118F broth culture filtrates prepared for evaluation of leukocidic activity also were evaluated for hemolytic activity. These 2 toxic activities had several characteristics in common. Both were filterable, heat-labile, produced by a hemolytic strain, and were released during early logarithmic phase growth from broth cultures. Leukocidic and hemolytic activities were protected from degradation by phenylmethyl sulfonyl fluoride, a serine protease inhibitor. Leukocidic and hemolytic activities were dependent on calcium ions. Filtrate resulted in 54.1% 51Cr release from labeled neutrophils and contained 646.7 hemolytic U/ml, respectively, when saline (0.85% NaCl) + 10 mM CaCl2 solution was used as diluent. Neither saline solution nor saline + 10 mM MgCl2 solution supported leukocidic or hemolytic activity. Serum, obtained from several calves 10 to 38 days after M bovis inoculation, substantially neutralized leukocidic and hemolytic activities, compared with paired preinoculation serum samples. In addition, no significant difference (P > 0.05) was detected when the ability of each calf's postinfection serum to neutralize leukocidic activity was compared with the ability of the serum to neutralize hemolytic activity.

Two commercially available infectious bovine keratoconjunctivitis (IBK) vaccines were evaluated for their effectiveness in protecting cattle from disease caused by experimental challenge exposure and natural transmission of Moraxella bovis infections. The study was conducted as 2 experiments, using a total of 81 cattle that were culture-negative for M bovis prior to vaccination. In each experiment, young adult cattle were randomly allotted to 4 groups. Each calf in groups 1 and 2 was vaccinated according to the vaccine manufacturer's directions. Groups 3 and 4 were unvaccinated controls. Three weeks after the last vaccination, each calf in groups 1 and 3 was experimentally challenge exposed by dropping a suspension of viable cells of a virulent strain of M bovis directly onto the corneal surface of each eye. Calves in all 4 groups were then commingled in open pastures so that calves in groups 2 and 4 could be naturally exposed to the calves with experimentally induced infections. Each calf was examined for signs of ocular disease on a regular basis by 2 experienced clinicians who scored each eye for severity of disease on the basis of a prearranged scale. Neither clinician was aware of the vaccination or exposure status of the calf nor to which experimental group they belonged. Lacrimal secretions were collected regularly to determine the number of eyes in which the virulent organism became established. Moraxella bovis with bacterial cultural characteristics similar to those of the virulent strain placed in the eyes of groups 1 and 3 was cultured from > 83% of the eyes of calves in all groups. The incidence of clinical IBK was > 50% in each group. There was no significant difference in the ability of vaccinated calves to resist experimental or natural challenge infection. Compared with that in nonvaccinated controls, no decreased incidence or severity of clinical IBK was noticed in vaccinated calves. Though the challenge strain used was not homologous to those used to prepare the vaccine, it was no different than those that may be expected to cause disease under field conditions.

Biological effects of staphylococcal protein A (SPA) immunotherapy were studied in 5 viremic and 6 nonviremic cats with induced FeLV infection and in 6 control cats. The SPA therapy neither reversed FeLV viremia nor resulted in consistent improvement in humoral immune responses to FELV antigens. However, SPA immunotherapy induced a proliferative response in bone marrow granulocytic lineage, possibly resulting in expression of FeLV-free mature neutrophils in the blood. Seemingly, viral burden and chemiluminescent responses were reversed in viremic cats during SPA immunotherapy.

Alterations in serum lipid and lipoprotein concentrations in ponies with experimentally induced liver disease were investigated. Hepatocellular damage was induced, using a nonlethal dose of carbon tetrachloride. In a separate group of ponies, obstructive jaundice was induced by surgical ligation of the common bile duct. Over a 6-day period, blood samples were obtained from ponies after treatment with carbon tetrachloride and for 12 days in ponies subjected to surgery. Serum cholesterol and triglyceride concentrations were unaffected in both groups of ponies, except for significantly (P < 0.01) high triglyceride concentration in ponies of the ligated group during the second postsurgical week. This increase was most likely attributable to anorexia observed during that period. Hyperbilirubinemia was observed early in ponies of the ligated group; most of the bilirubin was of the conjugated type. Using electrophoretic and ultracentrifugal methods, serum lipoprotein alterations were detected only in ponies of the ligated group. Increases of very low-density and low-density hpoprotein cholesterol concentrations and decrease in high-density lipoprotein cholesterol concentration were found. Although no changes were seen in total serum cholesterol concentration, a redistribution of lipoprotein cholesterol was observed in ponies of the ligated group. Similar alterations in lipoprotein distribution have been found in dogs, rats, and human beings with obstructive jaundice and cholestasis. The association between serum lecithin:cholesterol acyl transferase activities and these lipoprotein alterations remains to be elucidated.

Over periods of 22 and 14 months, IgG antibody concentrations in serum samples obtained monthly from 14 mares and 19 foals, respectively, were measured by use of ELISA against antigens of the following environmental microbes: Aspergillus umbrosus, Penicillium brevicompactum, Rhodotorula glutinis, Absidia corymbifera, Aspergillus fumigatus, Humicola grisea, Micropolyspora faeni, and Thermoactinomyces vulgaris. The mares and foals were on pasture from early June until early October, then were stabled during the winter season until the following June. In the mares, increased antibody concentrations against most microbes were observed typically in midwinter and late spring when the horses were stabled; antibody concentrations against R glutinis, however, peaked in August. Concentrations differed between the summer and winter seasons and, in most instances, between 2 consecutive years and correlated with amounts of rainfall during the previous harvest season. In the foals, circulating passively acquired antibodies disappeared within 3 to 4 months after birth. During the first year of life, substantially increased autogenous antibody concentrations were observed only against R glutinis. Antibody concentrations against the other microbes increased gradually toward the end of the indoor season. In a group of foals transferred indoors in autumn, 6 weeks later than the other foals, antibody concentrations were lower when measured in December. Results supported the view that, to minimize exposure to microbial spores during the winter season, horses should be kept outdoors as much as possible and attention should be focused on improving the ventilation in stables and the quality of feeds and beddings.

The activity of leukocytes, determined by chemiluminescence (CL) emission, was compared with the somatic cell count (SCC) in 4,883 quarter-milk samples from 132 dairy cows. The presence of bacteria was determined by bacteriologic culture of samples in which SCC and CL were high. Chemiluminescence was measured with an automated illuminometer system at 37 C after separating the leukocytes from milk by allowing them to adhere to cotton-wool swabs. Chemiluminescence emission was induced by opsonized zymosan and enhanced by luminol. After luminol and zymosan were added to the measuring vials containing the swabs, CL emission increased rapidly, reaching its maximum usually at about 15 minutes of reaction time, and decreasing slowly thereafter. In general, good correlation was found between CL and SCC (r = 0.876; P less than or equal to 0.001; n = 4,883). Even milk samples with low SCC gave reliably measurable CL signals. Minor pathogens in the milk caused about a sevenfold increase in both SCC and CL, whereas major pathogens caused 14- and 25-fold increases in SCC and CL, respectively. The diagnostic situation that requires both sensitivity and specificity to be at least 90% was attained only by the CL assay for major pathogens. These results suggest that the measurement of milk leukocyte activity by CL assay applies well to the diagnosis of mastitis, and has the potential to become a large-scale laboratory test, as well as a simple cowside test.

In a 4 x 4 crossover-design study, pharmacokinetic variables of 2 injectable formulations of netobimin (trisamine salt solution and zwitterion suspension) were compared after SC administration in calves at dosage of 12.5 mg/kg of body weight. Netobimin parent drug was rapidly absorbed, being detected between 0.25 and 12 hours after treatment, with maximal plasma drug concentration (Cmax) values of 2.20 +/- 1.03 micrograms/ml achieved at 0.75 +/- 0.19 hour (trisamine) and 1.37 +/- 0.59 micrograms/ml at 0.81 +/- 0. 18 hour (zwitterion). Netobimin area under the plasma concentration-time curve (AUC) was 7.59 +/- 3.11 micrograms.h/ml (trisamine) and 6.98 +/- 1.60 micrograms.h/ml (zwitterion). Elimination half-life (tl/2 beta) was 2.59 +/- 0.63 hours (trisamine) and 3.57 +/- 1.45 hours (zwitterion). Albendazole was not detected at any time. Albendazole sulfoxide was detected from 4 hours up to 20 hours (trisamine) and from 6 hours up to 24 hours (zwitterion) after administration of the drug. The Cmax values were 0.48 +/- 0.16 micrograms/ml and 0.46 +/- 0.26 micrograms/ml for trisamine and zwitterion formulations, respectively, achieved at time to peak drug concentration (Tmax) values of 9.50 +/- 1.41 hours (trisamine) and 11.30 +/- 1.04 hours (zwitterion). Albendazole sulfoxide AUC was 3.86 +/- 1.04 micrograms.h/ml (trisamine) and 4.40 +/- 3.24 micrograms.h/ml (zwitterion); tl/2 beta was 3.05 +/- 0.75 hours (trisamine) and 3.90 +/- 1.44 hours (zwitterion). Albendazole sulfone was detected from 4 (trisamine) or 6 hours (zwitterion) to 24 hours after treatment. The AUC was 6.98 +/- 1.60 micrograms.h/ml (trisamine) and 10.51 +/- 7.41 micrograms.h/ml (zwitterion); Cmax was 0.76 +/- 0.21 micrograms/ml at Tmax of 12.00 +/- 1.85 hours (trisamine) and 0.70 +/- 0.24 micrograms/ml at Tmax of 12.50 +/- 2.33 hours (zwitterion). Albendazole sulfone t1/2 beta was significantly (P < 0.05) longer for the zwitterion formulation (7.77 +/- 4.72 hours) than for the trisamine salt (2.87 +/- 0.61 hours). Albendazole sulfone AUC was higher than albendazole sulfoxide AUC, resulting in AUC ratio of 1.8 (trisamine) and 2.4 (zwitterion). The 2 formulations were not significantly different in terms of AUC or Tmax for netobimin and albendazole sulfone, AUC for albendazole sulfoxide, or tl/2 beta for netobimin and albendazole sulfoxide. It was concluded that the 2 netobimin injectable formulations were bioequivalent. Experimental phase had a significant effect on the AUC and Cmax for albendazole sulfoxide and on the Cmax for netobimin. One possible explanation for the differences between phases could be induction of liver microsomal enzymes by netobimin and its metabolites, resulting in increased rate of metabolism during phase 2 of the study.