The effect that topical administration of cyclosporine would have on the number and type of microorganisms isolated from the corneal surface of dogs with keratoconjunctivitis sicca was studied. Schirmer tear tests were performed on and corneal swab specimens were collected from 61 eyes of 31 dogs with keratoconjunctivitis sicca prior to and after 3, 6, and 12 months of treatment with cyclosporine. In eyes that responded to cyclosporine treatment (Schirmer tear test value increased by greater than or equal to 5 mm/min, compared with pretreatment value), the percentage of eyes from which bacteria were isolated after 3, 6, and 12 months of treatment was significantly (P < 0.001) less than the percentage from which bacteria were isolated prior to treatment. However, among eyes that did not respond to treatment, we did not detect a significant change over time in prevalence of bacteria or type of bacteria isolated. The percentage of eyes from which fungi were isolated decreased during treatment; however, the small number of eyes in which fungal culture results were initially positive precluded demonstration of a significant change. For all eyes, we did not detect any significant differences over time in the frequency with which specific bacterial genera were isolated, with the exception of beta-hemolytic Streptococcus spp. Opportunistic corneal infections were not detected even though none of the dogs received antibiotics. An increase in production of tears, which contain anti-infection proteins, was believed to be the primary factor responsible for the decrease in the percentage of eyes from which microorganisms could be isolated.

We studied the uptake and sequential transneuronal passage of pseudorabies virus (PRV) in rat CNS by use of a combination of immunohistochemistry and in situ hybridization. Protocols for rapid detection of PRV by immunohistochemistry and in situ hybridization in rats with PRV infection of the CNS after intranasal instillation of a wild-type strain of PRV were optimized in vitro, using porcine kidney-15 cells. Pseudorabies virus-specific hybridization signals appeared in the cytoplasm and nucleus of PRV-infected porcine kidney-15 cells by postinoculation (PI) hour 6. In tissue sections of PRV-infected rats, PRV nucleic acids were detected in areas of the rat brain in close proximity to the areas in which PRV antigens were evident. The PRV was initially found in the nucleus of trigeminal ganglion neurons at PI hour 24. At PI hour 72, PRV antigens were observed in the mid-brain, and 24 hours later, in the telencephalon. We also found evidence of specific progressive transsynaptic transmission of the virus, and, on the basis of that, we have constructed a map of the synaptic contacts and pathways in the brain. Therefore, combined use of immunohistochemistry and in situ hybridization was useful for characterizing the pathogenesis of PRV in the CNS of rats after intranasal inoculation, following a pattern that mimics PRV infection of the natural host.

Three laparoscopic procedures were performed on each of 6 adult jersey cows in the first trimester of gestation to describe normal laparoscopic anatomy of the bovine abdomen. Also, a technique for laparoscopy of the cranioventral portion of the abdomen was described. Right paralumbar fossa, left paralumbar fossa, and cranioventral midline laparoscopy were performed 72 hours apart on each cow. Physical examination findings, CBC, serum biochemical analysis, and peritoneal fluid analysis before and 72 hours after the first surgery were used to assess the effects of the procedures on the cows. Exploratory celiotomy was performed 2 weeks after the last laparoscopy. The cows were then reexamined 6 weeks after the last procedure. The t-test for paired data was used for statistical analysis; the level of significance was P < 0.05. Laparoscopy was performed without complication in all cows. Adverse effects of laparoscopy, individually or serially, were not observed. Significant differences were not found between CBC, serum biochemical, and peritoneal fluid variables taken before and 72 hours after surgery.

Lymphoscintigraphic evaluation of the thoracic duct (TD) was performed in 10 healthy and 12 dogs with experimentally created TD abnormalities (6 dogs with TD lacerations and 6 dogs with cranial vena ligations). Complete imaging took 4 hours and caused no adverse effects or complications. Lymphoscintigraphy of healthy dogs failed to image the TD; however, background activity in the abdomen and thorax, and radioactivity in the kidneys, bladder, liver, and heart were noticed. Lacerations and transections of the TD were experimentally created, in 6 dogs to ascertain whether TD rupture could be detected with lymphoscintigraphy. Lymphoscintigraphy was performed within 48 hours of creating the TD defect. There was no significant difference in the scintigraphic pattern of healthy dogs and those with experimentally created TD defects. Ligation of the cranial vena cava was performed in 6 dogs; 3 dogs developed chylothorax. In those 3 dogs, diffuse radioactivity was imaged in the thorax and was compatible with thoracic lymphangiectasia. In one of these dogs, linear activity consistent with the TD and localized regions of radioactivity cranial to the heart (compatible with the mediastina lymph nodes) were noticed. Lymphoscintigraphic findings in these dogs correlated with lymphangiographic findings.

To determine the role of thromboxane A2 in the pathogenesis of experimentally induced immune complex glomerulonephritis, 12 concanavalin A-immunized Beagles were infused with 1 mg of concanavalin A via each renal artery and treated twice daily for 8 days with either 30 mg of CGS 12970/kg, PO, a specific thromboxane synthetase inhibitor, or placebo. The effect of treatment was assessed by measuring endogenous creatinine clearance and urine protein and eicosanoid excretion, and by evaluating changes in glomerular morphometric characteristics. On postinfusion day 8, urine protein, thromboxane B2, and 11-dehydro-thromboxane B2 excretion, glomerular epithelial crescent formation, and glomerular cell proliferation in the CGS 12970-treated dogs were significantly decreased when compared with values in the placebo-treated group. Differences were not observed in endogenous creatinine clearance, urine prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion, or glomerular polymorphonuclear leukocyte infiltration between groups in this study. These findings suggest thromboxane A2 has a role in the development of immune complex glomerulonephritis and that thromboxane synthetase inhibition may be beneficial in attenuating some of the functional and histologic changes associated with immune complex glomerulonephritis.

Immunoglobulin E is produced in response to parasitic nematodes that undergo blood and tissue migrations. Results of our previous studies indicated that IgE and IgG respond to Dirofilaria immitis in experimentally infected dogs. To determine the association between treatment with the larvicide, diethylcarbamazine (DEC), and antibody responses and to examine the potential influence of infection with a nonfilarid intestinal nematode on isotype-specific immune responses, we monitored, by use of isotype-specific ELISA, separate IgE and IgG responses against D immitis in 4 groups (A-D) of 8 dogs experimentally coinfected with D immitis and Ancylostoma caninum. All dogs were monitored from 2 weeks before inoculation with D immitis, through postinoculation (PI) week 20. Group-B dogs received a daily regimen of 6.6 mg of DEC/kg of body weight. Group-C dogs received 4.95 mg of oxibendazole/kg daily. Group-D dogs received DEC and oxibendazole, equivalent to the daily doses given to dogs of groups B and C. All dogs given oxibendazole had no A caninum at necropsy. Of the groups receiving DEC, 3 group-B dogs each had 1 to 2 D immitis at necropsy. When results of chronologic IgE determination for all groups were statistically compared, only groups B and C had significant (P = 0.0148 and P << 0.00005, respectively) increases in IgE values. Group-C dogs had the highest IgE values from PI week 10 until the end of the study, whereas IgG values were statistically identical to those of group-A dogs. Group-B dogs given only DEC and having the least number of D immitis of all groups, had IgE values that peaked at PI week 6; values were significantly (P = 0.0002) higher than those for all other groups. In Group-B dogs, IgG values increased significantly (P << 0.00005) only at PI week 20 and were significantly (P << 0.00005) decreased after PI week 6, compared with values for all other groups. Group D containing 6 dogs infected with 1 to 18 D immitis found at necropsy had IgE values betwee.

Using catheter mounted microtip manometers, right atrial, pulmonary artery, and pulmonary artery wedge pressures were studied in 8 horses while they were standing quietly (rest), and during galloping at treadmill speeds of 8, 10, and 13 m/s. At rest, mean (+/- SEM) heart rate, mean right atrial pressure, mean pulmonary artery pressure, and mean pulmonary artery wedge pressure were 37 (+/- 2) beats/min, 8 (+/- 2) mm of Hg, 31 (+/- 2) mm of Hg, and 18 (+/- 2) mm of Hg, respectively. Exercise at treadmill belt speed of 8 m/s resulted in significant (P < 0.05) increments in heart rate, right atrial pressure, pulmonary artery systolic, mean, diastolic and pulse pressures, and pulmonary artery wedge pressure. All these variables registered further significant (P < 0.05) increments as work intensity increased to 10 m/s, and then to 13 m/s. Pulmonary artery diastolic pressure was, however, not different among the 3 work intensities. During exercise at belt speed of 13 m/s, heart rate, mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery pulse pressure, and mean pulmonary artery wedge pressure were 213 (+/- 5) beats/min, 44 (+/- 4) mm of Hg, 89 (+/- 5) mm of Hg, 69 (+/- 4) mm of Hg, and 56 (+/- 4) mm of Hg, respectively. Assuming mean intravascular pulmonary capillary pressure to be halfway between the mean pulmonary arterial and venous pressures, its value during exercise at 13 m/s may have approached 72.5 mm of Hg. Transmural pressure (intravascular minus alveolar pressure) across pulmonary capillaries may be even higher because of the large negative pleural pressure swings in galloping horses. High transmural pressures may cause stress failure of pulmonary capillaries, resulting in exercise-induced pulmonary hemorrhage.