Pseudorabies is a porcine herpesvirus of major importance in the swine industry. Isoprinosine is an immunomodulating drug that has been shown to be beneficial in treating herpesvirus infections. Twenty-four 7-week-old pigs were allotted within litters to 1 of 4 groups: control, isoprinosine (ISO), pseudorabies virus (PRV), or isoprinosine and pseudorabies virus (ISO-PRV). Isoprinosine was administered daily for 16 days to the ISO and ISO-PRV groups (75 mg/kg of body weight/day, PO). Immunity in pigs in the PRV and ISO-PRV groups was challenged with pseudorabies virus (10(5) TCID50 units) on day 4. Rectal temperatures and viral excretion were monitored daily; total and differential leukocyte counts, lymphocyte response to mitogens, and interleukin-2 production were monitored every 4 days. Pigs challenge-inoculated with pseudorabies virus became ill, with the ISO-PRV group most severely affected. Rectal temperatures were high (P less than 0.05) in virally challenged pigs on days 5 to 12 and 14 to 16; isoprinosine did not alter this effect. Pseudorabies virus-infected pigs had leukocytosis (P less than 0.05) on days 12 and 16, primarily caused by neutrophilia. Concanavalin A-stimulated lymphocyte proliferation was decreased (P less than 0.06) in both PRV and ISO-PRV groups on day 12, compared with control pigs, but only in the PRV group on day 16. Pokeweed mitogen-stimulated lymphocyte proliferation was decreased (P less than 0.02) in ISO-PRV pigs on day 8 of the experiment. Interleukin-2 concentrations, pooled over all sampling days, were decreased (P less than 0.03) in pseudorabies virus-infected pigs. Viral excretion was not altered by isoprinosine treatment. These data suggest that pseudorabies virus infection decreased lymphocyte proliferative responses and interleukin-2 prodcution in pigs, and that isoprinosine did not mitigate these effects.

Serum complement activity and selected hematologic variables were evaluated in 5 newborn foals fed bovine colostrum (principal group) and 6 foals allowed to nurse their dam (control group). Also, bovine colostrum was evaluated for anti-equine antibodies. Precolostral serum hemolytic and conglutinating complement activities were low and increased similarly in foals of both groups to reach adult values between 1 and 3 weeks after birth. Bovine colostrum strongly agglutinated, but did not hemolyse principal foals' RBC and blood containing all known equine blood group alloantigens. Hemolysis was not detected after administration of bovine colostrum. Physiologic anemia developed in foals of principal and control groups during the first week of life. Erythrocyte osmotic fragility in foals of the principal group prior to and after the ingestion of colostrum remained unchanged. However, at 36 hours after birth, there was a significant decrease in erythrocyte osmotic fragility in foals fed homologous colostrum.

Immunodeficiency in neonatal and young pigs was studied in terms of T-cell function. Generalized T-cell deficiency did not exist in young pigs on the basis of the in vitro response of blood mononuclear cells to a polyclonal T-cell mitogen, phytohemmagglutinin. However, immunodeficiency that extended from birth up to 4 weeks, was observed in serum antibody concentration and in vitro proliferative responses of blood mononuclear cells from young pigs exposed to a low antigen dose of a T-cell dependent antigen, egg white lysozyme. The low in vitro proliferative response to lysozyme was not attributable simply to a lack of interleukin-2 production, because supplementation with human interleukin-2 did not enhance the in vitro cellular response. Also, pokeweed mitogen-stimulated B cells from young pigs up to the age of 5 to 6 weeks produced immunoglobulin concentration, which also was not affected by the addition of human interleukin-2 to the in vitro cultures. The blood mononuclear cells obtained from pigs within the first 5 to 6 weeks after birth and incubated with monoclonal antibodies reactive to all T cells (MSA4), helper T cells (74-12-4) or suppressor/cytotoxic T cells (76-2-11) did not yield consistent excess of suppressor/cytotoxic T cells. This observed immunodeficiency cannot be attributed to a simple lack of functional T cells or to an excessive number of suppressor/cytotoxic T cells, but may be a property of the ability of specific T-cell clones to respond t o low concentration of T cell-dependent antigens or may be attributable to the induction of a suppressor T-cell population in response to in vitro stimulation with the polyclonal T-cell-dependent pokeweed mitogen system.

To differentiate the origin of high total lactate dehydrogenase (LD) activity in canine sera, a spectrophotometric method based on the preferential inhibition of cardiac LD isoenzymes by pyruvate was performed. Comparison with the electrophoretic separation of LD isoenzyme activities and determination of the hydroxybutyrate dehydrogenase-to-LD ratio indicated that the method proposed gave a better discrimination between cardiac and hepatic LD activities than did the other tests.

Ovariectomized, nonlactating cows were treated with IM injections of either physiologic saline solution or prostaglandin F2 alpha. Plasma concentrations of cortisol increased significantly by 30 to 60 minutes after injection of prostaglandin F2 alpha, but there were no significant increases in plasma concentrations of estradiol, progesterone, or testosterone. After saline solution treatment, there were no increases in any of the hormones measured.

A field study was performed to determine the effectiveness of benzathine cloxacillin for the treatment of infectious bovine keratoconjunctivits in cattle from 2 farms located in northern California. The study was performed between June and September of 1987. Affected calves ranging from 2 to 9 months of age were selected from the main herd when signs of corneal ulceration were observed. The study was conducted in 2 phases. For phase I, the affected calves of herd 1 (n = 21; Holsteins) and herd 2 (n = 43 Angus crossbred), were randomly assigned to 1 of 3 groups, and were either treated with 250 (n = 23) or 375 mg (n = 21) of benzathine cloxacillin, or mineral oil (n = 20) on days 1 and 4. For phase II, affected calves (n = 16; Angus crossbred, 3 to 9 months of age) from herd 2 were treated with benzathine cloxacillin (250 mg). Eight of these calves were retreated on day 4. After treatment, all calves were examined every 72 hours for 16 days. For examinations, a clinical score was assigned to each eye, and the surface areas of photographed corneal ulcers were measured. The ocular secretions were collected and examined culturally for Moraxella bovis. On days 7, 10, and 13, the calves treated with benzathine cloxacillin had significantly (P less than 0.05) lower lesion scores, compared with the controls. The percentage of day-1 area measurements on posttreatment days 4, 7, and 10 were significantly larger in the controls than in the treated calves. The mean healing times of corneal lesions in the 2 antibiotic treatment groups were significantly (P less than 0.05) shorter than in the controls. In the treated calves, the healing times of corneal ulcers less than or equal to 0.05 cm in diameter on day 1 were significantly (P less than 0.05) shorter than the healing times of larger lesions. The healing times of the corneal ulcers in the Angus crossbred calves were significantly (P less than 0.05) longer than the healing times of the Holsteins. The controls had the greatest number of nonhealed corneal ulcers on day 16. The number of calves that remained infected with M bovis on days 4, 7, 10, and 13 was significantly less in both groups of treated calves than in the controls. The scores, surface area measurements, healing times, and the M bovis isolation frequency in the calves of the 250-mg and 375-mg and 1- and 2-dose treatment groups were not significantly different. The minimal inhibitory concentrations (MIC) of penicillin, cloxacillin, and ampicillin in the day-16 isolates from benzathine cloxacillin-treated herd-2 calves were greater than in isolates from corresponding calves on observation day 1; however, twofold increases of the respective MIC of pretreatment and day-16 specimens were not observed. The highest MIC of ampicillin, cloxacillin, gentamicin, oxytetracycline, and penicillin were 0.5, 8.0, 0.5, 2, and 1 migrogram/ml, respectively, for isolates collected during the final study week.

Thirty mares with normal estrous cycles were allotted equally to 5 groups and infused with 250 ml of saline (NaCl) solution in utero on the seventh day after ovulation to test the effects of temperature, osmolarity, or pH of the saline solution on prostaglandin F2 alpha (PGF2 alpha) release and luteolysis. Intrauterine infusion of phosphate-buffered saline solution failed to alter the duration of the luteal phase, compared with the control group. Similarly, increasing the temperature of phosphate-buffered saline solution to 42 C or increasing (600 mosm) or decreasing osmolarity (less than 10 mosm) did not change the duration of the luteal phase. Decreasing the pH of saline solution to 3 caused significant (P less than 0.0001) re leases of PGF2 alpha from the uterus within the first hour after infusion, and the luteal phase was shortened to 8.8 +/- 1.0 days (mean +/- SEM; control, 15 +/- 1.2 days). The results of this study showed that pH is main factor in eliciting PGF2 alpha release by intrauterine infusion of a saline solution, whereas increased temperature and osmolarity have no effect on the release of PGF2 alpha. The intrauterine infusion of sterile water or physiologic saline (NaCl) solution has been used to induce estrus in mares for the past 50 years. Many investigators 1-10 have reported that intrauterine infusion of physiologic saline solution or water at body temperature (37 C or warmer up to 45 C) causes most "anestrous" mares to return to estrus in 1 to 8 days. The mare's ability to respond to intrauterine infusion was further defined when Arthur 11,12 demonstrated that estrus could be initiated only in mares in middiestrus or in pseudopregnancy, and Ginther and Meckley 13 reported intrauterine infusion was effective only during days 5 to 9 of diestrus. We subsequently demonstrated that the effect of intrauterine infusion of saline solution involved shortening the luteal phase.

Colostrum-deprived lambs (10 to 20 days old) were inoculated with either ovine adenovirus type 6 (OAV-6; n = 6), Pasteurella haemolytica type A1 (n = 6), or OAV-6 followed by P haemolytica 5 days later (n = 10). Another group (n = 3) served as sham-inoculated controls. Lambs inoculated with OAV-6 or P haemolytica developed mild and moderate respiratory tract disease of 6 and 3 days' duration, respectively. Lambs inoculated with virus and bacteria developed clinical signs of respiratory tract disease of greater intensity and duration (9 days) than with either agent alone. Within 3 hours of bacterial inoculation, all lambs that received P haemolytica were anorectic, listless, and febrile, and had hyperpnea and dyspnea. Ovine adenovirus type 6 was isolated from all virus-inoculated lambs. Although P haemolytica was not recovered from all bacteria-inoculated lambs, it was recovered for a longer period in the group that received both agents. Antibody to OAV-6 was detected in virus-inoculated lambs as early as day 6 after inoculation. The control lambs remained clinically normal and neither virus nor bacteria were recovered at necropsy.

Gastric emptying of a radionuclide-labeled test meal was studied in 10 dogs that had been treated surgically for gastric dilatation-volvulus and in 10 clinically normal (control) dogs. There were no significant differences between the gastric emptying rates and patterns in treated and in control dogs. Thus, there are no indications that gastric emptying is delayed in dogs that have recovered from gastric dilatation-volvulus, and there is no reason for pyloric surgery in dogs with this condition.

The role of turkey complement in a serum bactericidal reaction was determined using serum-sensitive and serum resistant Escherichia coli isolated from turkeys. Inactivation of complement by heating serum (56 C for 40 minutes) or by treating serum with 10mM EDTA eliminated bactericidal activity. Serum sensitive E coli organisms were killed by turkey serum treated with 10 mM ethylene glycol-bis-beta-(aminoethyl ether)-N, N, N,' N,'-tetraacetic acid and 5 mM MgCl2. Exposure of normal turkey serum to serum-sensitive or serum resistant E coli resulted in equivalent reductions in hemolytic activity of serum. Treatment of serum-resistant E coli with antibody rendered the bacteria sensitive to bactericidal effects of normal turkey serum. Serum-sensitive E coli organisms were readily killed by an alternative complement pathway, serum-sensitive and serum-resistant E coli activated the complement system equally well, and antibody was required for complement-mediated killing of certain serum-resistant E coli organisms from turkeys.