An immunoperoxidase technique was used to study the relationship between the necrotic lesions and causative bacteria found in lungs of 53 calves that had naturally acquired pneumonia. Four types of necrotic lesions were identified on the basis of morphologic characteristics as follows: type 1 had coagulation necrosis surrounded by a dense zone of numerous degenerated leukocytes; type 2 was similar to type 1, but the central area of the lesions was severely affected, had no alveolar architecture remaining, and was surrounded by a thin, sparse layer of degenerated leukocytes; type 3 had small swirling accumulation of degenerated leukocytes; and type 4 had necropurulent lesions resembling abscesses. By use of the immunoperoxidase technique, Pasteurella haemolytica serovar 1 antigen was confirmed to be associated with the necrotic lesions in many cases of type 1 and in some cases of types 2 and 3. Although some lesions were induced by other bacteria (Haemophilus somnus or Actinomyces pyogenes), the pneumonic lesions associated with P haemolytica could be differentiated from other pneumonic lesions in calves by use of the immunoperoxidase technique.

Ten adult dogs (5 Beagles and 5 mixed-breed dogs) were inoculated IV with canine platelets containing Ehrlichia platys. Inclusions and morulae of E platys developed in platelets of infected dogs at 10 to 14 days after inoculation, followed by marked thrombocytopenia at 14 to 21 days. Parasitemia and marked thrombocytopenia recurred at 24 to 28 days after inoculation. Increased numbers of megakaryocytes were observed in marrow aspirate smears from infected dogs, indicative of regenerative thrombocytopenia. Prior to infection, platelet-rich plasma from these dogs was determined to have similar aggregatory response to arachidonate. After infection with E platys, the aggregatory response of platelet-rich plasma to collagen or 3 dilutions of adenosine diphosphate was evaluated. A statistically significant (P < 0.05) inhibition of platelet aggregatory response to the lowest dilution of adenosine diphosphate was detected for mixed-breed dogs, whereas aggregation responses were unchanged in Beagles. Results indicate that platelet activation may occur in dogs with acute ehrlichial infection.

Intranuclear inclusions indicative of adenovirus infection were detected microscopically in formalin-fixed intestinal tissues from preweanling Syrian hamsters. The amphophilic intranuclear inclusion bodies were observed in ileal enterocytes from 16-to 24-day-old hamsters. Electron microscopy revealed large numbers of 72 +/- 3-nm viral particles typical of adenoviridae in enterocytic nuclei. Serum antibodies reacted with mouse adenovirus strains K87 and, to a lesser extent, FL, by indirect fluorescent antibody testing. Clinical disease was not associated with the adenoviral infections. Hamsters from 10 production colonies, including all major commercial Syrian hamster suppliers in the United States, were surveyed and all had serologic or histopathologic evidence of adenovirus infection.

Reference intervals are reported for feline CSF biochemical and serologic variables, IgG concentration, and electrophoretic fractionation, derived from 58 clinically normal adult cats that did not have histologic lesions of the CNS. There was no apparent effect of age on any variable. The CSF total protein concentration was significantly (P = 0.012) greater in males than in females, but all other variables were unaffected by gender. The only variable that had a statistically significant correlation with its corresponding blood concentration was IgG. Blood contamination of the CSF affected the following CSF variables: total protein concentration, activities of lactate dehydrogenase and creatine kinase, IgG ratio, and gamma-globulin percentage. The reference intervals proposed for feline CSF were derived from 33 cats with CSF RBC count < 31 cells/microliter. Reference limits for CSF with 31 to 1,700 RBC/microliter also are reported.

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.

Bovine pulmonary artery endothelial cells (BPAEC) were labeled with 3H-arachidonic acid. Exposure of the labeled BPAEC to Pasteurella haemolytica lipopolysaccharide (LPS) resulted in a time- and dose-dependent release of radioactivity. The release was inhibited by 5 mM indomethacin, but inhibition was not caused by less than or equal to 500 micromole indomethacin or hydrocortisone, which suggests that the release was caused primarily by a mechanism other than cyclooxygenase or phospholipase A2 metabolism of arachidonic acid. Pasteurella haemolytica LPS also caused increased adherence of bovine neutrophils to BPAEC through independent effects on both cell types. The increased adherence was inhibited by treatment of either cell type with cycloheximide or actinomycin D prior to LPS exposure, indicating that de novo protein synthesis was required in both cell types to promote the LPS-induced adherence. Lipopolysaccharide may be an important factor in neutrophil-mediated effects in pneumonic pasteurellosis by causing increased neutrophil adherence and, thus, the vascular sequestration of neutrophils. Together, these experiments provide additional evidence for the involvement of LPS in pneumonic pasteurellosis. Moreover, they provide evidence of LPS-induced endothelial activation, which could have broad ramifications in the inflammatory and immune responses of pneumonic pasteurellosis.

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P < 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P < 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P < 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P < 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P < 0.02), second 60 minutes (P < 0.001), and total 120 minutes (P < 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and cell responsiveness to stimuli (ie, glucose).

Gentamicin sulfate, equivalent to 4 mg of gentamicin base/kg of body weight, was administered IV to 6 Thoroughbred foals on day 1 (12 to 24 hours of age) and at 5, 10, 15, and 30 days after birth. On day 40 after parturition, gentamicin was given to the mares at a dosage similar to that used in foals. Decay of serum gentamicin concentrations was best described by a 2-compartment model. Among foals, the overall elimination rate constant at 30 days of age was significantly (P less than 0.05) greater than at days 1, 10, and 15. There was, however, no difference in the overall elimination rate constant between foals and mares. The volume of distribution (Vd), determined on the basis of total area under the disposition curve, did not change between day 1 and day 30. Mean values of Vd of foals were between 1.5 and 2.5 times higher than the mean Vd of the mares; however, only values from the foals at days 5 and 10 were significantly greater. Both age and interindividual differences were reflected in the total body clearance (ClB) of gentamicin. Total body clearance of gentamicin of foals on day 1 was less than that of foals on days 5, 10, and 30. Additionally, ClB of gentamicin on day 15 was less than that on day 30. There was no significant difference between ClB of foals and mares except for the day-30 group, which had a higher clearance rate than did the adults. Protein binding of gentamicin was less than 30% in all groups, and there were no apparent age-related differences.

Spleen cells from a calf immunized with bovine herpesvirus-1 (BHV-1) were fused with the nonsecreting murine cell line SP2/0. Several bovine-murine hybridomas secreting bovine immunoglobulins were stabilized. Of these, 9 hybridomas secreted bovine monoclonal antibodies that specifically bound to BHV-1 in a radioimmunoassay. Two of these monoclonal antibodies reacted specifically with BHV-1 in an indirect fluorescent antibody test and immunoprecipitated a BHV-1 glycoprotein with molecular mass of 97 kilodaltons.

Colostrum-deprived lambs and CF1 mice were vaccinated with water-in-oil emulsion vaccines containing nonviable whole cells (WC) of Corynebacterium pseudotuberculosis with and without muramyl dipeptide (MDP). Efficacy of vaccines was determined from the survival of mice and lesions in lambs after IV injection of 10(4) colony-forming units of C pseudotuberculosis. In mice, protection was related to the concentration of WC in the vaccine. At 50, 100, or 150 micrograms of WC, protection was good (78.8%). At 10 or 25 micrograms of WC, protection was considerably less (54.7%). At high WC concentrations, protection could only be moderately increased to 82.3% with high (50 and 100 micrograms) concentrations of MDP or increased to 90% protection with low (5 and 10 micrograms) concentrations of MDP. At low WC concentrations, protection significantly decreased to 32% (P < 0.025) with high concentrations of MDP, but significantly increased to 72.5% (P < 0.025) with low concentrations of MDP. Therefore, the amount of protection with lower concentrations of WC and MDP was comparable with the amount of protection with higher concentrations of WC without MDP. In lambs, high prechallenge antibody titers (geometric mean titers from 5.1 to 5.4 by day 35) were observed after vaccination with WC. Protection and vaccination site abscesses in lambs were related to the concentration of WC and MDP. Pulmonary or vaccination site abscesses were not observed in 4 of 4 lambs vaccinated with 1 mg of WC + 50 micrograms of MDP.