The effects of coliform endotoxin (E) and recombinant ovine tumor necrosis factor a (TNF) were compared with respect to clinical signs of disease and changes in plasma metabolite and pituitary and pancreatic hormone concentrations in calves. In addition, changes in plasma TNF concentration during each challenge exposure were quantitated by use of radioimmunoassay. Healthy Holstein bull calves with mean body weight of 90 kg were each given, in order, on different days, saline solution (5.0 ml, IV, day 1, n = 4), E (type 055:B5, 1.0 microgram/kg of body weight IV, day 2, n = 4) and TNF (5.0 microgram/kg IV, day 9, n = 3). Jugular venous blood samples, rectal temperature reading, and PCV were obtained at hourly intervals before (2 hours) and after challenge exposure. The PCV increased (P < 0.05) after E and TNF administrations for the first 5 hours, then returned to normal in calves given E, but decreased and remained low in calves given TNF through 24 hours. Plasma triglyceride and nonesterified free fatty acids concentrations were increased through 10 hours (P < 0.05) after E administration, whereas triglyceride and nonesterified free fatty acids concentrations were not significantly affected by TNF administration. Increase in blood glucose concentration at 1 hour after administration of E and TNF was followed by prolonged hypoglycemia that lasted through 6 hours. Changes in plasma insulin concentration paralleled the observed changes in glucose concentration, initially increased at 2 hours after E and TNF (P < 0.05) administrations, but then tended to decrease below control values thereafter. Plasma growth hormone and luteinizing hormone concentrations decreased after E and TNF administrations to almost nondetectable values through 4 hours after dosing, returning to normal values by 8 hours. The data indicate similarities in physiologic response of calves to E and TNF and suggest a role for acute production of TNF as a mediator of E responses.

The efficacy of netobimin against digestive tract strongyles and the small lungworm Muellerius capillaris was tested in a dairy goat herd. The drenches were given orally at the rate of 20 mg/kg of body weight once, 10 mg/kg on 2 successive days, or 7.5 mg/kg on 3 successive days. Fecal egg counts and larval counts were done 8 days before and on the day of drenching; further counts were performed on postdrenching days 8 and 18. Two goats were necropsied, 1 on postdrenching day 5 and 1 on day 10 in the group treated on 3 successive days. The fecal egg counts were reduced by 44 to 79% depending on dosage on postdrenching day 18; the remaining worms were Trichostrongylus colubriformis. The larval counts of M capillaris were reduced by 72 to 92%, depending on dose. The reduction was significant in all the treated groups, compared with that in the control group. The use of netobimin at the dosage of 10 mg/kg given on 2 successive days or 7.5 mg/kg given on 3 successive days might be recommended to treat goats infected with Muellerius spp and digestive tract strongyles.

To test the effect of a parasite control program for cattle, 2 groups of similar composition were grazed on separate, but equivalent, improved pastures. Cattle in 1 group were treated with fenbendazole at 5.0 mg/kg of body weight at the time they were turned out on pasture in the spring and again at midsummer, when the cattle were moved to a new pasture. The control group was not treated. Parasite egg counts were significantly (P < 0.04) lower in the treated group. Trichostrongyle-type eggs were the most prevalent throughout the, year, except in the month of May, when Strongyloides papillosus eggs were predominant. The number of worms recovered from tracer calves was lower for those on pastures where the treated group grazed than for those on- the control group's pasture. The most consistently recovered parasite was Ostertagia ostertagi, and hypobiosis was observed.

To evaluate renal function and obtain reference values for measurements of urinary excretion of various substances, quantitative urinalysis was performed in healthy, growing kittens from 4 to 30 weeks after birth. Endogenous creatinine clearance, 24-hour urine protein excretion, and urine protein-to-creatinine ratio were determined. Additionally, fractional excretion to creatinine clearance was calculated for calcium, inorganic phosphorus, sodium, potassium, and chloride. Mean +/- SD endogenous creatinine clearance values (range, 3.80 +/- 0.48 to 4.74 +/- 0.61 ml/min/kg) were significantly (P < 0.0001) higher in kittens 9 to 19 weeks old, compared with younger (range, 1.39 +/- 0.85 to 3.59 +/- 0.86 ml/min/kg) and older kittens (range, 2.69 +/- 0.40 to 3.46 +/- 0.37 ml/min/kg). Mean values for all kittens for 24-hour urine protein excretion (range, 2.54 +/- 1.81 mg/kg at 4 weeks to 11.39 +/- 7.61 mg/kg at 14 weeks) and for urine protein-to-creatinine ratio (range, 0.14 +/- 0.03 to 0.34 +/- 0.18) varied from week to week of age. The urine protein-to-creatinine ratio in kittens greater than or equal to 9 weeks old correlated well (R2 = 0.861) with 24-hour urine protein excretion. Urinary fractional excretion of calcium, inorganic phosphorus, sodium, potassium, and chloride in kittens varied among age groups, being significantly (P < 0.01) different for potassium and calcium in young kittens (4 to 6 weeks) and older kittens (greater than or equal to 7 weeks).

The central arterial pharmacokinetics of alfentanil, a short-acting opioid agonist, were studied in rabbits, sheep, and dogs after short-duration infusion of the drug. Alfentanil was infused until a set end point (high-amplitude, slow-wave activity on the EEG) was reached. This required a larger alfentanil dose and a higher alfentanil arterial concentration in sheep, compared with rabbits and dogs. The plasma concentration-time data for each animal were fitted, using nonlinear regression, and in all animals, were best described by use of a triexponential function. In this study, differences in the disposition kinetics of alfentanil among the 3 species were found for only distribution clearance and initial distribution half-life. In dogs, compared with rabbits and sheep, the first distribution half-life was longer, probably because of pronounced drug-induced bradycardia (mean +/- SD, 48 +/- 21 beats/min). Distribution clearance was faster in sheep, compared with dogs, also probably because of better blood flow in sheep. Elimination half-life was similar in all species (rabbits, 62.4 +/- 11.3 minutes; sheep, 65.1 +/- 27.1 minutes; dogs, 58.3 +/- 10.3 minutes). This rapid half-life resulted from a small steady-state volume of distribution (rabbits, 908.3 +/- 269.0 ml/kg; sheep, 720.0 +/- 306.7 ml/kg; dogs, 597.7 +/- 290.2 ml/kg) and rapid systemic clearance (rabbits, 19.4 +/- 5.3 ml/min/kg; sheep, 13.3 +/- 3.0 ml/min/kg; dogs, 18.7 +/- 7.5 ml/min/kg). On the basis of these pharmacokinetic variables, alfentanil should have short duration of action in rabbits, sheep, and dogs. This may be beneficial in veterinary practice where rapid recovery would be expected after bolus administration for short procedures or after infusion for longer procedures.

Blood culture and serologic testing were used to study the prevalence of Trypanosoma cruzi infection in a group of 85 dogs from southern Louisiana rural environment. These dogs were known to have been in contact with wild mammalian hosts of the hemoflagellate. Results were compared with blood culture and serologic test results in 103 dogs from a rural environment and with limited known wild mammalian T cruzi host contact. Serologic test results for the 188 dogs from the rural environment were compared with results for 176 dogs from an urban animal shelter and for 100 household pet dogs from an urban southern Louisiana environment. Blood culture was not performed on urban dogs. Culture results were negative in all dogs from rural environments. Serologic evidence of infection was obtained for 4 of the 85 (4.7%) dogs of rural environment with known host contact. Of 176 dogs from the animal shelter, 4 (2.3%) had high antibody titer to T cruzi, and 11 others had low titer (< 2 adjusted ELISA units [aEU]). Two and 4 dogs of the housed urban and rural groups, respectively, had antibody titer to T cruzi that was < 2 aEU. Results indicate that prevalence for exposure to T cruzi antigen is higher in dogs with high potential contact with the vector and wild mammalian hosts of T cruzi, whether they are from rural or urban environment. Furthermore, results indicate that similar studies on high-risk human populations may be indicated.

Blood, feces, nasal secretions, and tears werecollected weekly from 5 randomly selected 1- to 8-week-old calves in a large commercial dairy herd. Clinical signs and bovine coronavirus (BCV) shedding from the respiratory and enteric tracts of calves were monitored through the 8-week period by direct immunofluorescence of nasal epithelial cells, protein A-gold immunoelectron microscopy on feces, and ELISA on nasal secretions and feces. All samples were analyzed for antibody isotypes to BCV structural proteins by immunoblotting. All calves had BCV respiratory tract infections and 4 of 5 calves shed virus in feces. Several calves had multiple or prolonged periods of BCV respiratory tract or enteric tract shedding or both. All calves (except 1) had passive IgG1 antibodies to some BCV proteins (mainly the E2 and E3 proteins) in their serum when they were 1 week old. The presence of these passive serum antibodies (mainly to the E2 and E3 BCV proteins) was associated with decreased or delayed systemic and mucosal antibody responses in calves, in particular IgA responses in nasal secretions and tears to the E2 and E3 BCV proteins, but not to the N protein. Moderate amounts of maternal BCV E2- and E3-specific antibodies in serum did not prevent BCV enteric tract or respiratory tract infections in calves, but may have delayed the development of active antibody responses to these BCV proteins. However, calves with BCV respiratory tract or enteric tract infections had no detectable passive antibodies to any BCV proteins in nasal secretions or feces.

The beige (bgJ/bgJ) mouse is a well-described murine model of Chediak-Higashi syndrome. Platelet function was examined in normal and beige mice to better characterize the defective aggregation response in platelets from mice with Chediak-Higashi syndrome. Platelet aggregation after collagen, thrombin, and phorbol-12-myristate 13-acetate stimulation was significantly (P < 0.025) decreased in platelets from beige mice, relative to platelets from normal mice. Compared with beige and normal mice, those heterozygous for the bg trait had intermediate responses to collagen and thrombin, but not phorbol-12-myristate 13-acetate. The defect(s) in aggregation of platelets from beige mice was associated with a dense granule storage pool deficiency and decreased stores of serotonin and adenine nucleotides in platelets. Mice heterozygous for the bg trait had normal platelet serotonin and adenine nucleotide concentrations. Platelets from beige mice were approximately 10 times more sensitive to prostacyclin inhibition of collagen-induced aggregation than were platelets from control mice. However, a significant difference in platelet cyclic AMP concentration was not apparent between beige and normal mice after prostacyclin stimulation. Platelet endoperoxide synthesis measured by quantification of thromboxane B2, was normal in beige mice. Protein phosphorylation patterns in mouse platelets were similar to those seen in human platelets. Thrombin and collagen-induced [32P] phosphorylation of 40- and 20-kD proteins in platelets from normal and beige mice was similar. Results indicate that the biochemical defect(s) in platelet function in beige mice is partially attributable to storage pool deficiency and does not result in an absolute defect in phosphorylation of 40- and 20-kD proteins.

Two recently developed direct methods, radioassay-125I-labeled hyaluronic acid binding protein (125I-HABP)- and high-performance liquid chromatography (HPLC), were used to assess and compare the concentration of hyaluronate (HA) in synovial fluid of horses. Also determined were changes in the HA concentration in an experimental treatment model involving physiologic saline solution (PSS)-irrigated or methylprednisolone acetate-injected tarsocrural joints of clinically normal horses. Serum HA concentration was determined simultaneously, using the 125I-HABP assay. Synovial fluid HA concentration values obtained by use of the HPLC method were approximately double the values obtained by use of 125I-HABP assay. Correlation (r = 0.819) between the 2 methods was highly significant (P < 0.001; linear regression analysis) for all samples studied and for various experimental subgroups. When pure HA standards were used, correlation between the 2 methods was close to 1 (r = 0.965; P < 0.001), with higher values obtained by use of the 125I-HABP assay. It is suggested that the HA binding protein derived from endogenous cartilage proteoglycan interferes with the 125I-HABP assay on synovial fluid, resulting in excessively low values, compared with those obtained using the HPLC procedure. Intra-articular injection of methylprednisolone acetate significantly (P < 0.01) increased synovial fluid HA concentration at 24 hours after injection. Increase was also detected after PSS irrigation, but owing to wide intersubject variation, this increase was not significant. The HPLC procedure, which provides simultaneous information about the concentration and degree of polymerization of HA, is recommended for the study of synovial fluid, whereas the 125I-HABP assay is more suitable for serum HA analysis.

A morphologic and morphometric study was carried out on the facial nerve: to determine normal histologic data in myelinated fibers of clinically normal young adult dogs; to establish reference values for mean fiber diameter, and to delineate the relative diameter frequency distribution curve. Few degenerative changes were observed in single teased-nerve fibers and semithin cross-sectional nerve preparations. Statistical difference was not observed between left and right facial nerves. The distribution of fiber diameters in the facial nerve was unimodal. Mean (+/- SD) fiber diameter of the facial nerve was 3.92 +/- 1.18 micromole. Approximately 89% of fibers in the facial nerve had diameter between 3 and 6 micromole. Fiber diameter ranged from 2 to 12 micromole; however, < 1% of fibers had diameter > 8 micromole.