Four virgin heifers were experimentally inoculated intravaginally with 7 X 10(6) Tritrichomonas foetus, and 2 heifers served as uninfected controls. The durations of infection were 13, 20, 21, and 28 weeks, respectively. An ELISA that used whole T foetus antigen was used to detect anti-T foetus immunoglobulins (IgA, IgG1, IgG2, and IgM) in vaginal, cervical, and uterine secretions, and sera during the course of infection. The vaginal and cervical antibody responses were characterized by significantly increased T foetus-specific IgA and IgG1 at 7 to 9 weeks of infection, whereas uterine IgA and IgG1 responses peaked at 10 to 12 weeks. The antibody response in serum was predominantly of the IgG1 and IgG2 subclasses. In all reproductive tract regions, IgA persisted at least until the time of T foetus clearance, and usually longer. The next most persistent isotype was IgG1, lasting longest in the vagina, then cervix, and for the shortest time in the uterus. In local secretions, IgG2 was seen only transiently, increasing at weeks 13 to 15 in the vagina, and at weeks 10 to 12 in the cervix. Little IgM, relative to that present before infection, was detected in any secretion or serum, although cervical secretions had the greatest amount. Eight to 12 weeks after clearance, the 4 experimental heifers were inoculated intravaginally with 1 x 10(5) T foetus, transient infections (2 to 3 weeks' duration) were established in only 2 of 4 heifers, as determined by culturing of reproductive tract secretions. The lag times of antibody responses during this reinfection were shorter than in the initial infection, and ELISA optical densities were at least as high as during the primary infection, suggesting an anamnestic response.

Four virgin heifers were experimentally inoculated intravaginally with 7 X 10(6) Tritrichomonas foetus, and 2 heifers served as uninfected controls. The durations of infection were 13, 20, 21, and 28 weeks, respectively. An ELISA that used whole T foetus antigen was used to detect anti-T foetus immunoglobulins (IgA, IgG1, IgG2, and IgM) in vaginal, cervical, and uterine secretions, and sera during the course of infection. The vaginal and cervical antibody responses were characterized by significantly increased T foetus-specific IgA and IgG1 at 7 to 9 weeks of infection, whereas uterine IgA and IgG1 responses peaked at 10 to 12 weeks. The antibody response in serum was predominantly of the IgG1 and IgG2 subclasses. In all reproductive tract regions, IgA persisted at least until the time of T foetus clearance, and usually longer. The next most persistent isotype was IgG1, lasting longest in the vagina, then cervix, and for the shortest time in the uterus. In local secretions, IgG2 was seen only transiently, increasing at weeks 13 to 15 in the vagina, and at weeks 10 to 12 in the cervix. Little IgM, relative to that present before infection, was detected in any secretion or serum, although cervical secretions had the greatest amount. Eight to 12 weeks after clearance, the 4 experimental heifers were inoculated intravaginally with 1 x 10(5) T foetus, transient infections (2 to 3 weeks' duration) were established in only 2 of 4 heifers, as determined by culturing of reproductive tract secretions. The lag times of antibody responses during this reinfection were shorter than in the initial infection, and ELISA optical densities were at least as high as during the primary infection, suggesting an anamnestic response.

The in vivo effects of a single prophylactic dose of recombinant bovine interferon (rBoIFN)-alphaI1 in calves with salmonellosis were investigated, using a Salmonella typhimurium infection model. Treatment with rBoIFN-alphaI1 reduced the degree of septicemia compared with that in control groups, and, in one experiment, using disease of reduced severity, body temperature was lower in treated calves than in controls.

The in vivo effects of a single prophylactic dose of recombinant bovine interferon (rBoIFN)-alphaI1 in calves with salmonellosis were investigated, using a Salmonella typhimurium infection model. Treatment with rBoIFN-alphaI1 reduced the degree of septicemia compared with that in control groups, and, in one experiment, using disease of reduced severity, body temperature was lower in treated calves than in controls.

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.

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.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.