Quantitative evaluation of neutrophil chemotaxis was performed on cells obtained by hypotonic-lysis techniques from heparinized blood samples from clinically normal dogs. The techniques resulted in neutrophil recovery rates between 60 and 80%. Chemotaxis comparisons were based on cellular migration in microchambers equipped with polycarbonate membranes with 5-micrometer pores. Chemo-attractant comparisons were based on neutrophil migration to medium, normal canine plasma, zymosan-activated plasma, and xanthine oxidase. Cellular migration to zymosan-activated plasma in buffer (1:100 dilution) was significantly (P less than 0.001) enhanced over random baseline medium migration. Neutrophil migrations to normal canine plasma and xanthine oxidase were quantitatively less than to zymosan-activated plasma, but were equivalent to each other and significantly greater than for random migration. Migration to xanthine oxidase was maximal at concentrations near 1 U/ml within 30 minutes.

Laboratory rabbits from various commercial and private sources were found to have high serum antibody titers specific for lapine parvovirus (LPV). By both immunofluorescence and hemagglutination inhibition assays, 75% of these sera were positive for LPV. This finding, together with the recovery of LPV from kidneys of neonatal rabbits, suggested that LPV infection is common in commercially available rabbits in the United States. It was concluded that use of infected rabbits could interfere with research in which rabbit cell cultures or in vitro immunologic assays are used.

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity of the circular and longitudinal muscle layers of the cecal body were measured in 7 conscious healthy horses during IV infusion of physiologic saline solution for 60 minutes (control), during a 60-minute IV infusion of dopamine (at dosages of 1, 2.5, and 5 microgram/kg/min), and for 60 minutes after IV infusion of dopamine. The mean values for lateral cecal arterial blood flow during IV infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min were not significantly different from the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. The mean values for lateral cecal arterial blood flow, however, were significantly greater during IV infusion of dopamine at a dosage of 5 microgram/kg/min than the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. Intravenous infusion of dopamine at 1 and 2.5 microgram/kg/min did not significantly change the mean values for carotid arterial pressure. In contrast, the mean values for carotid arterial pressure were significantly less during IV infusion of dopamine at dosages of 2.5 and 5 microgram/kg/min than during infusion of saline solution. The mean values for heart rate were not significantly altered by infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min, but infusion of dopamine at a dosage of 5 microgram/kg/min significantly increased heart rate. Intravenous infusion of dopamine at dosages of either 1 or 5 microgram/kg/min did not significantly change the mechanical activity of the circular muscle layer of the cecal body, as measured by the area under the strain gauge deflection curve. Conversely, the mechanical avtivity of the circular muscle layer of the cecal body was significantly reduced by IV infusion of dopamine at a dosage of 2.5 microgram/kg/min. This reduction of circular muscle mechanical activity by dopamine infusion was attributable to a significant decrease in the total duration of contractions. The mechanical activity of the longitudinal muscle layer was not significantly altered by infusion of dopamine at any dose. These results suggest that IV infusion of dopamine at a dosage of 5 microgram/kg/min increased lateral cecal arterial blood flow by either increasing cardiac output or dilating the lateral cecal artery, an effect most likely mediated by dopaminergic or beta-adrenergic receptors. In addition, dopamine had a biphasic effect on contractile activity of the equine cecum.

The sensitivity of an indirect enzyme-linked immunosorbent assay (ELISA) for bovine IgG serum antibody to Pasteurella haemolytica was compared with that of an indirect hemagglutination (IHA) test. Pasteurella haemolytica serotypes were grown in a chemically defined cell culture medium, and soluble antigens released into the growth medium were used in the ELISA and IHA test. An ELISA with serotype-1 antigen consistently detected antibody in sera that were positive by IHA test (correlation, 99%). Sera reacting with serotype-1 ELISA antigens also reacted with ELISA antigens prepared from other serotypes. Although ELISA titers determined by the 2 methods were approximately linear. Titer increases detected in paired serum samples by either test were similar. The ELISA was more sensitive than was the IHA in detecting colostral IgG antibody in serum of newborn calves. The ELISA uses a simple, stable antigen preparation and detects antibody to P haemolytica serotypes that commonly infect cattle.

Four healthy cats were given clindamycin orally in daily doses of 25 or 50 mg/kg of body weight for 6 weeks. Significant change in Factor-VII activity was not found, compared with pretreatment values. In 2 cats tested, toxin produced by Clostridium difficile was not detected in fecal samples obtained before treatment and at 6 weeks after treatment, suggesting that intestinal overgrowth by C difficile did not develop. Results of the study seemed to indicate that orally administered clindamycin does not measurably reduce synthesis of vitamin K-dependent clotting factors in healthy cats.

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.

Antiparasitic efficacy of ivermectin against migrating Gasterophilus intestinalis was evaluated in 36 treated and 24 nontreated (n = 12) or vehicle-treated (n = 12) ponies experimentally and naturally infected with G intestinalis and naturally infected with G nasalis. Each pony was experimentally infected with 500 G intestinalis lst instars in 2 divided doses on days -14 and -7 before treatment. On day 0, ivermectin was administered at the rate of 200 microgram/kg of body weight by IV (n = 12) or IM injection (n = 12) or given as an oral paste (n = 12). Ponies were euthanatized and necropsied 21 days after treatment. In each nontreated or vehicle-treated pony, late lst-, lst- to 2nd-instar molt, and early 2nd-instars of G intestinalis were found in the mouth, and 2nd- and 3rd instars of G intestinalis and 3rd instars of G nasalis were found in the stomach. Bots were not found in any ivermectin-treated pony and, thus, ivermectin was 100% effective against oral and gastric stages. Adverse reactions were not observed in ponies given ivermectin by IM injection or orally, but 1 pony given the vehicle IV and 1 pony given ivermectin (in the vehicle) IV had an anaphylactic reaction, resulting in death of the ivermectin-treated pony. It was speculated that the adverse reaction was caused by histamines released in response to vehicle components given by IV injection.

The myoelectric activity of the cecum and right ventral colon (RVC) was studied in 4 female ponies. Eight, bipolar Ag-AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and RVC (2 electrodes), and recordings were begun 14 days after surgery. The myoelectric activity for each pony was recorded during 12, 60-minute recording sessions done during the interdigestive period (3 to 7 hours after the morning feeding). Coordinated series of spike bursts were recognized as independent motility patterns in the cecum and in the RVC. Local haustra-haustra myoelectric activity involving approximately 40 cm of the cecal body (0.45 +/- 0.03 spike bursts/min) were detected. A series of spike bursts started at the cecal apex and progressed to, but stopped at, the caudal cecal base (0.04 +/- 0.03 spike bursts/min). Infrequently, a series of spike bursts started at the apex and progressed to the cranial cecal base (0.09 +/- 0.01 spike bursts/min). More commonly, a series of spike bursts with a conduction velocity of 3.8 +/- 0.07 cm/s, began in the cranial base and progressed orally to the cecal apex (0.46 +/- 0.03 spike bursts/min). Spike bursts conducted aborally (propulsion) beginning at the origin of the RVC (0.05 +/- 0.07 spike bursts/min) and spike bursts conducted orally (retropulsion; 0.15 +/- 0.02 spike bursts/min) were seen independent of cecal myoelectric activity. A progessive series of coordinated spike bursts, which began at the cecal apex, were conducted through the cecolic orifice and continued into the RVC (0.42 +/- 0.02 spike bursts/min), representing the only pattern common to the cecum and RVC. This pattern, associated with a loud rush of ingesta heard on auscultation, had a conduction velocity of 5.65 +/- 0.12 cm/s and was always generated in the cecal body, near the apex. An apparent electrical pace-maker area was proposed in this area. Duration of spiking activity during the progressive pattern was significantly (P = 0.0001) greater at electrodes 7 and 8 in the RVC than at any electrode locus in the cecum. Coordinated orally directed spike bursts were detected frequently in the cecum before and after the progressive pattern, indicating a complex sequence of motility patterns may exist.

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.

Leukotoxin activity from culture supernatants of Pasteurella haemolytica serotype 1 in logarithmic growth phase caused rapid (less than 5 min) release of intracellular K+, uptake of extracellular Ca2+, and swelling of cultured bovine lymphoma cells (BL3 cells). Release of 51CrO(4)(2-) and lactate dehydrogenase (LDH) from BL3 cells began after 15 minutes of incubation with leukotoxin at 37 C and was completed between 60 and 120 minutes of incubation. In addition, leukotoxin exposure of BL3 cells resulted in cell aggregation and adherence to glass surfaces. Scanning electron microscopy indicated that after 10 minutes of leukotoxin exposure, BL3 cells increased in size, and large membrane defects developed between 20 and 60 minutes of exposure. The rate of release of LDH from leukotoxin-exposed BL3 cells was proportional to the amount of leukotoxin added. At high cell concentrations, the activity of LDH released at completion was directly proportional to the amount of leukotoxin added. Leukotoxin-induced release of LDH required a divalent cation, whereas K+ release and cell swelling did not. The addition of Ca2+, Mn2+, and Ba2+ resulted in increased leukotoxin-induced release of LDH. Divalent cation concentrations of 0.5 to 2.5 mM resulted in 50% of maximal stimulation. Ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid blocked increased release of LDH caused by Ca2+ addition, but had no effect on K+ release or cell swelling. Leukotoxin action on BL 3 cells (K+ release, cell swelling, Ca2+ uptake, and release of LDH) was prevented by incubation at 4 C.