The breaking strength (stress at failure) of equine third metacarpal bones, with and without clustered drill holes, was determined in vitro. Paired ossa metacarpalia II-IV of 39 horses (n = 39) between 2 and 7 years old were tested in palmarodorsal 3-point bending. Four treatments were compared. Clustered 2.7- or 3.5-mm drill holes, in a 4- or 7-hole pattern, were made in the dorsal cortex of the distal diaphysis of the left third metacarpal bone. Undrilled right third metacarpi were used as controls. Bones with clustered drill holes failed by an oblique fracture through 1 or more drill holes, whereas undrilled bones failed with a middiaphyseal transverse fracture. Clustered drill holes acted as a stress concentrator and significantly (P < 0.05) decreased the stress required for failure. However, differences in breaking strength between treatment groups were not significant (P > 0.05).

During 1986 and 1987, electroencephalographic examinations were done on 8 dogs with intracranial mass lesions confirmed by computerized tomography, biopsy, necropsy, or a combination of these techniques. Tumor types included 1 astrocytoma, 1 undifferentiated glioma, 2 mixed gliomas, 2 meningiomas, 1 choroid plexus papilloma, and 1 cholesterol granuloma. It was found that no EEG pattern was pathognomonic for tumor type or location. Slow-wave activity was observed in the EEG of most of the dogs; asymmetry in amplitude or frequency was observed in approximately half the cases.

Subunit pseudorabies vaccines that contained only purified glycoproteins of either of 2 strains of pseudorabies virus (PRV) were prepared and subsequently tested for safety and efficacy. The strains of virus used for vaccine production differed in at least 2 properties. One strain (Kojnok) was virulent for pigs and was believed to code for the entire complement of viral glycoproteins. The other (Kaplan) was a deletion mutant that was unable to code for structural viral glycoproteins gI and gp63. Purified glycoproteins were dispersed in an oil-in-water emulsion and were administered IM to pigs. Both vaccines were found to be safe and effective immunogens. Neither caused any local or general reactions, as verified by examination of the injection site (local safety) and by vaccination of pregnant sows in PRV-infected and noninfected herds. Sows vaccinated with the gI+ or gI- vaccine protected their pigs at levels of 93 and 92%, respectively, against a severe challenge exposure that killed 98% of pigs born from nonvaccinated sows. Vaccinated pigs were tested for active immunity by intranasal challenge exposure with the NIA 3 strain. Protection was quantitated by measuring the relative daily weight difference, expressed in percent per day, between vaccinated and control pigs during the first week after challenge exposure (deltaG7); the estimated differences were 2.25 and 2.13% for gI+ and gI- vaccines, respectively. The absence of gI and gp63 did not affect the efficacy of this type of subunit glycoprotein vaccines. In pigs that were challenge-exposed intranasally 3 months after 1 injection with the gI- vaccine, the duration of viral excretion was highly reduced, compared with that in control pigs.

Twenty-two Hereford heifers were injected IM with prostaglandin F2 alpha(a), 11 days apart to synchronize estrous cycles. Twelve of 14 heifers that had signs of estrus were inoculated IV with 1 of 3 modified-live infectious bovine rhinotracheitis virus vaccines, and 2 were assigned to a nonvaccinated control group. Also, 6 of the 8 anestrous heifers were inoculated IV with 1 of the 3 vaccines on the fourth day after the last prostaglandin injection and the other 2 were assigned to the nonvaccinated group. Vaccine virus was isolated from the blood and nasal and vaginal secretions from the vaccinated heifers on postvaccination days 4, 7, and 9. On postvaccination day 9, all heifers were ovariectomized and ovarian tissues were processed for virus isolation and histologic examination. Vaccine virus was isolated from ovarian tissues of some heifers in each of the vaccine groups. Necrotic oophoritis characterized by multifocal areas of ovarian tissue necrosis, hemorrhage, and mononuclear lymphocytic infiltration was observed. The corpora lutea and surrounding ovarian tissues taken from vaccinated heifers in each group had varying amounts of necrotic and inflammatory change, but the changes appeared to be more severe in 1 group than in the other 2. Virus also was isolated from 2 of the controls; these heifers apparently became infected with vaccine virus that had been excreted from the vaccinated animals.

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.

Conditions necessary for establishment of a graft, posttransplant supportive care and complications, and lymphohematopoietic reconstitution after bone marrow transplantation were evaluated in 7 cats. Donor-recipient pairs were selected on the basis of low mutual reactivity in one-way mixed lymphocyte reactions. Before transplantation, cats were given marrow ablative (7 Gray) total-body gamma irradiation. Cyclosporine A was administered to cat 7, which was given marrow from an unrelated donor. Rapid hematologic recovery was attained in 5 of 5 (cats 1 to 5) sibling bone marrow recipients and 1 (cat 7; cyclosporine A-treated) of 2 recipients from unrelated donors. Lymphocyte recovery was prolonged, requiring up to 100 days to attain reference concentrations. Lymphocyte blastogenic responses were below reference range in 2 of 3 cats (cats 1 and 3) examined approximately 1 to 3 months after transplantation. Serum IgG concentrations determined 1 to 6 months after transplantation were within reference range in cats 1 to 5 which were given sibling bone marrow. Fatal infections did not develop in cats that had established grafts. Antimicrobial-responsive fevers did develop, but were generally detected only when granulocyte counts were low (< 1 X 10(9) cells/L). Clinical signs of disease in the immediate posttransplant period consisted of hepatic lipidosis (fatal) in cat 4, hepatitis (mild graft-vs-host disease) in cat 3, and immune-mediated hemolytic anemia and thrombocytopenia in cat 7. Cats with hepatitis and immune-mediated disease responded to immunosuppressive therapy.

Urinary indices of renal function and damage were measured in 6 healthy, mature ewes over a 48-hour period. Endogenous creatinine clearance, total and fractional electrolyte excretion rates, protein excretion, urine volume, and urine gamma-glutamyltransferase and beta-glucuronidase activities were measured. Significant variations in the excretion rates of creatinine, electrolytes, and protein were not found between intervals within the 48-hour urine collection period. Total urinary electrolyte excretion rates were significantly (P < 0.001) correlated with fractional electrolyte excretion rates normalized for creatinine concentration; however, coefficient of determination was low.

The connective tissue structures commonly referred to as the periorbita, orbital septum, muscular fasciae, and vagina bulbi or collectively, as the orbital fasciae were dissected then illustrated and described. Two sheets (layers) of the periorbita (endorbita) were found in our dogs. The periorbita should be renamed endorbita because of its anatomic relations. The periorbita did not always fuse with the periosteum of frontal and sphenoid bones. Rather, the periorbita and the periosteum were often distinct and separate; only medioventrally did several fibrous bands unite the superficial sheet of the endorbita with the periosteum. Two layers of the endorbita fused with the periosteum of the margin of the bony orbit and with the orbital ligament. The muscular fasciae were divided into 3 layers. The superficial layer extended caudally from the orbital septum, was thick, and was pierced by arteries, veins, and nerves. The middle layer was attached to the sclerocorneal junction and, at the temporal canthus of the eye, was divided into superficial and deep sheets. The deep portion was attached to the lateral angle of the third eyelid, similar to a strong ligament. The deep layer of the muscular fasciae extended caudally from the sclerocorneal junction in intimate contact with recti and oblique muscles of the eyeball. The deep portion of the deep muscular fascia covered the deep surface of all recti muscles and separated them from the retractor bulbi muscle. Intermuscular septa were observed between middle and deep muscular fascia layers. The body of the third eyelid was located between superficial and middle muscular fascia layers and was fixed ventrally to the lateral angle of the eye by the deep sheet of the middle muscular fascia.

Morphologic changes in the small intestine were investigated during development of naturally acquired wheat-sensitive enteropathy in Irish Setters. To distinguish underlying morphologic abnormalities from non-specific effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were taken sequentially between 4 months and 1 year of age. At 4 months of age, there were no differences in villus height, comparing the 3 groups, but increased numbers of intraepithelial lymphocytes and goblet cells were already present in biopsy specimens from the affected Irish Setters fed wheat. Dietary wheat resulted in a progressive reduction in virus height in the jejunum of affected Irish Setters from 6 months onward. Underlying morphologic abnormalities were not found, and the characteristic morphologic changes of this enteropathy were secondary to the presence of dietary wheat. However, development of partial villus atrophy was preceded by increased numbers of intraepithelial lymphocytes and goblet cells.

Canine circulating neutrophils, isolated by a blood lysing technique, were incubated with 7-S nerve growth factor (NGF), at final concentrations between 12.5 and 800 ng/ml, for 30 minutes at 37 C. Neutrophil cytosolic H2O2 production, measured by flow cytometry, after 7-S NGF incubation was not significantly different from that produced at 37 C (baseline temperature controls) alone. Phorbol myristate acetate (PMA; 100 ng/ml) stimulation of neutrophils produced cytosolic H2O2 concentrations almost 13 times that of baseline temperature control neutrophils. Preincubation of neutrophils with 7-S NGF (100 to 800 ng/ml, 30 minutes, 37 C) and subsequent stimulation by PMA resulted in augmented H2O2 production in excess of twice that of neutrophils treated with PMA alone, and almost 30 times that of baseline temperature controls.