Serologic recognition of common lipopolysaccharide core antigens has been related to enhanced resistance to gram-negative bacterial disease in several species. Class-specific titers (IgG, IgM) were determined by direct ELISA, using intact Escherichia coli (J5) as a plate antigen. Serum samples were obtained from 224 neonatal swine between the ages of 36 and 60 hours. The mean (+/- SEM) log(10) IgG titer against gram-negative core antigens was 1:1,713 +/- 0.4718 and the mean log(10) IgM titer was 1:202 +/- 0.5644. The IgG titer was directly related with litter size, birth weight, and serum total IgG concentration; IgM titer was directly related with dam parity and serum total IgG concentration.

Atracurium (0.4 mg/ml in isotonic NaCl solution) was administered by IV infusion to 7 healthy adult horses for 2 hours. Over the 2-hour period, a 95 to 99% reduction of train-of-four hoof-twitch response was maintained by 0.17 +/- 0.01 mg of atracurium/kg of body weight/h, for a total of 161 +/- 6 mg of atracurium (mean +/- SEM) for horses 1 to 4, 6, and 7. Horse 5, a mare in estrus, required 0.49 mg of atracurium/kg/h to maintain comparable relaxation. Hoof-twitch recovery time from 10 to 75% of baseline strength was 19.8 +/- 2.5 minutes for all horses. The 10 to 75% recovery time for horse 5 was 18 minutes. Recovery time from discontinuation of halothane until standing was 86 +/- 14 minutes (range, 55 to 165 minutes). Horse 5 had a 165-minute recovery. Regarding recovery from anesthesia, 3 recoveries were rated as excellent, 1 recovery good, and 2 recoveries as fair. Horse 5 laid quietly until she stood with 1 strong, smooth effort.

The effects of single IV administered doses of dexamethasone on response to the adrenocorticotropic hormone (ACTH) stimulation test (baseline plasma ACTH, pre-ACTH cortisol, and post-ACTH cortisol concentrations) performed 1, 2, and 3 days (experiment 1) or 3, 7, 10, and 14 days (experiment 2) after dexamethasone treatment were evaluated in healthy Beagels. In experiment 1, ACTH stimulation tests were carried out after administration of 0, 0.01, 0.1, 1, and 5 mg of dexamethasone/kg of body weight. Dosage greater than or equal to 0.1 mg of dexamethasone/kg decreased pre-ACTH plasma cortisol concentration on subsequent days whereas dosages greater than or equal to 1 mg/kg also decreased plasma ACTH concentration. Treatment with 1 or 5 mg of dexamethasone/kg suppressed (P less than 0.05) post-ACTH plasma cortisol concentration (on day 3 after 1 mg of dexamethasone/kg; on days 1, 2, and 3 after 5 mg of dexamethasone/kg). In experiment 2, IV administration of 1 mg of dexamethasone/kg was associated only with low (P less than 0.05) post-ACTH plasma cortisol concentration in dogs on day 3. In experiment 2, pre-ACTH plasma cortisol and ACTH concentrations in dogs on days 3, 7, 10, and 14 and post-ACTH plasma cortisol concentration on days 7, 10, and 14 were not affected by dexamethasone administration. The results suggest that, in dogs a single IV administration. The results suggest that, in dogs, a single IV administered dosage of greater than or equal to 0.1 mg of dexamethasone/kg can alter the results of the ACTH stimulation test for at least 3 days. The suppressive effect of dexamethasone is dose dependent and is not apparent 7 days after treatment with 1 mg of dexamethasone/kg. The magnitude of the decrease in post-ACTH plasma cortisol concentration did not exceed 35% (compared with control values), regardless of the dose of dexamethasone used.

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe, generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Altough the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (MH) had increased sensitivity to the membrane-perturbing effects of halothane that increase cytoplasmic calcium. Cytoplasmic concentration of ionized calcium in lymphocytes isolated from blood was determined in the presence and absence of halothane for 10 Pietrain X Poland China swine that were susceptible to MH and 20 Yorkshire swine that were resistant to MH. Calcium was determined by dual-emission spectrofluorometry and by measuring the ratio of free to calcium-bound form of the fluorescent calcium dye Indo-1. Mean values for calcium concentrations in lymphocytes from MH-susceptible (MHS) swine were 80% less than control values (40.5 +/- 38.8 and 185.3 +/- 91.6 nmol/L; P less than 0.01). Untreated lymphocytes from MHS swine accumulated calcium at half the rate observed for controls. Exposure to 1 mmol/L halothane resulted in a 3-fold increase of free calcium concentration to 127.9 +/- 81.9 nmol/L in the lymphocytes of MHS swine, but had no significant effect on lymphocytes from control swine (225.0 +/- 91.4; P less than 0.01). Exposure to 2 mmol/L halothane resulted in a 6-fold increase of free calcium concentration to 255.9 +/- 91.4 nmol/L in lymphocytes from MHS swine and a 63% increase in lymphocytes from controls (303.8 +/- 116). The rate of halothane-induced increase in cytosolic calcium was 13 times greater in lymphocytes from MHS swine, compared with controls. These data indicated that the molecular defect that results in halothane-hypersensitivity and is characteristic of muscle of MHS swine also occurs in lymphocytes from MHS swine.

The relationships of various iron-related analytes were evaluated in 95 dogs. Liver and spleen nonheme iron content was determined coulometrically on acid-digested tissue specimens. Serum iron concentration and total iron-binding capacity also were measured coulometrically, whereas serum ferritin concentration was measured by ELISA. Significant (P less than 0.0002) correlation was found between serum ferritin concentration and nonheme iron stores. Significant correlation was not found between nonheme iron stores and serum iron concentration or total iron-binding capacity. Serum ferritin concentration should provide a convenient and relatively noninvasive means of estimating iron stores in dogs.

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0,4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, pro-thrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on Pid 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.

Influence of supplemental Se on humoral immune response was measured in 60 weaned beef calves with marginal blood Se status. Calves were fed a Se-deficient diet consisting of corn silage, corn grain, and soybean meal. Blood Se concentrations, primary and secondary humoral immune responses to hen egg lysozyme inoculation, and weight gain were determined in a 70-day trial. Calves fed 20 mg of Se/kg of mineral mixture ad libitum had lower antibody responses (P less than 0.02), compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM, or with calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture. Calves fed 80, 120, 160, or 200 mg of Se/kg of mineral mixture had higher (P less than 0.001) blood Se concentrations on day 70, compared with calves fed 20 mg of Se/kg of mineral mixture and given 0.1 mg of Se and 0.22 IU of vitamin E/kg of body weight, IM. Selenium supplementation had no effect on weight gain.

Possible immunomodulation by low-level infection with Ostertagia ostertagi was studied in 4-month-old calves. Six groups of 4 calves each were subjected to the following regimes: group 1--nonparasitized controls; group 2--nonparasitized, but challenge exposed at day 64 with Brucella abortus strain 19 vaccine (BA) and at day 78 with IV administration of a soluble third-stage larval (L3) antigen preparation of O. ostertagi (OAG); group 3--nonparasitized, but challenge exposed at day 78 with 75 X 10(3) L3 of O ostertagi; group 4--continuously parasitized by weekly dosing with 30 X 10(3) L3 of O ostertagi; group 5--continuously parasitized by weekly dosing with 30 X 10(3) L3 of O ostertagi, then challenge exposed on day 64 with BA and on day 78 with IV inoculation of OAG; and group 6--continuously parasitized by weekly dosing with 30 X 10(3) L3 of O ostertagi, then challenge exposed on day 78 with 75 X 10(3) L3 of O ostertagi. Over the initial 10 weeks of the study, nonparasitized calves, (groups 1, 2, and 3) had higher body weight, blood lymphocyte (BL) response to phytohemagglutinin (PHA), and significantly (P less than 0.05) higher feed consumption and lymphocyte numbers, whereas parasitized calves (groups 4, 5, and 6) had higher BL responses to pokeweed mitogen (PWM) and significantly (P less than 0.05) higher neutrophil and eosinophil numbers, plasma pepsinogen (PP) values, and BL response to OAG. During the challenge-exposure period (weeks 10 through 13), group-5 calves had significantly (P less than 0.05) higher eosinophil numbers and PP values for week 11 (BA challenge exposure) and for week 13 (OAG challenge exposure) than did group-2 calves, but differences were not observed in BL responses to PHA, PWM, and OAG. Oral L3 challenge exposure at week 13 induced significantly (P less than 0.05) lower lymphocyte numbers, higher eosinophil numbers (P less than 0.05), and higher PP values, but lower BL response to PHA, PWM, and OAG in group-6, compared with group-3 calves. In continuously parasitized calves, comparison of IV OAG challenge exposure with oral L3 challenge exposure indicated that group-6 (L3) calves has significantly lower (P less than 0.05) lymphocyte numbers and higher PP values than did group-5 (OAG) calves. Results of ELISA revealed significantly (P less than 0.05) higher antibody titer to OAG in parasitized calves, compared with nonparasitized calves. Abomasal mucosal pathologic changes were most severe in the continuously parasitized calves. Calves of groups 4, 5, and 6 had thicker mucosae (edema), significantly (P less than 0.05) higher eosinophil numbers, and higher globule leukocyte and mast cell numbers in the fundic and pyloric regions than did calves of groups 1, 2, and 3. Calves of groups 4, 5, and 6 also had significantly (P less than 0.05) larger abomasal lymph node masses than did nonparasitized calves. In group-1 calves, nodes had the lowest mass. Differences were not observed among groups for lymphocyte responses to proliferative and suppressive assays performed on the abomasal lymph node lymphocytes.

Three independent 1-year studies were conducted during 3 consecutive years to better define the prevalence of bluetongue virus (BTV) infection in Mexico. Serologic data were obtained by use of agar-gel immunodiffusion for identification of BTV group-reactive antibodies, and virologic data were obtained by virus isolation. Samples were obtained from sheep in 6 states over a 1-year period, with 9% seropositive; samples were obtained from cattle in 11 states during the same 1-year period, with 35% seropositive. Two years later, samples were obtained from cattle in 4 additional states, with 69% seropositive. Virus isolation was conducted on pooled blood samples obtained from cattle in 7 states. Six virus isolates were recovered and included 2 isolates each of BTV serotypes 11 and 13 and 1 isolated each of serotypes 10 and 17. All virus isolates were partially characterized by electrophoretic analysis of genomic RNA migration profiles (electropherotypes) in polyacrylamide gels. All Mexican isolates of BTV differed considerably in electropherotype profile, as compared with their respective US prototype strain of the same serotype. Such differences appeared to be much more extensive than those described to exist between numerous California isolates of the same serotype.