Postnatal ossification of the atlas and axis was studied in Miniature Schnauzers by examining alizarin-stained bone clearings, cleaned dry bones, radiographs, histologic sections, and arterially perfused bone clearings. Sixty-two pups (1 day to 16 weeks old) and 4 adults were examined. In 1-day-old pups, the atlas consisted of 3 separate ossification centers: a left and right neural arch center and midventrally, the intercentrum 1, which formed the body of the atlas. The axis contained 4 separate ossification centers: a left and right neural arch center; centrum 2 in the main part of the axis body; and centrum 1, which formed the caudal part of the dens and the cranial part of the axis body. By 6 weeks of age, the epiphysis on the caudal end of the axis body had begun to ossify. At this time, the intercentrum 2, which developed as a cuboidal ossification center intercalated between centrum 1 and centrum 2 in the middle of the cranial half of the axis body, also began to ossify. The centrum of the proatlas, which formed the apex of the dens, was first seen ossified in a 9-week-old pup. These 10 ossification centers were seen as constant and separate elements. In all dogs, the dens developed from 2 separate ossification centers: the centrum of the proatlas formed the cranial one-quarter, and centrum 1 formed the caudal three-quarters. Dens dysplasia is unlikely to be a result of failure of development of one of the ossification centers for the dens. Seemingly, vascular-related ischemia may lead to postnatal resorption of at least the middle part of the dens and result in dens dysplasia, with subsequent atlantoaxial subluxation. This condition in dogs may be a suitable animal model for the study of the pathogenesis of odontoideum and related conditions in man.

Plasmid profiles were compared between nonpiliated and piliated forms of Moraxella bovis isolates. The piliated form of M bovis isolate IBH64 contained 1 fewer plasmid than did the nonpiliated form. Piliated and nonpiliated cells of IBH64 contained plasmids having molecular size of 45, 32.8, 4.9, and 4.6 kilobases (kb). Single- and double-restriction endonuclease digestion by Ava I and Nde I indicated that the size of the additional plasmid carried by the nonpiliated form of IBH64 was approximately 43.6 kb. The M bovis isolates, Newport and GRS, contained the same number of plasmids in either their piliated or nonpiliated form.

Alterations in serum lipid and lipoprotein concentrations in ponies with experimentally induced liver disease were investigated. Hepatocellular damage was induced, using a nonlethal dose of carbon tetrachloride. In a separate group of ponies, obstructive jaundice was induced by surgical ligation of the common bile duct. Over a 6-day period, blood samples were obtained from ponies after treatment with carbon tetrachloride and for 12 days in ponies subjected to surgery. Serum cholesterol and triglyceride concentrations were unaffected in both groups of ponies, except for significantly (P < 0.01) high triglyceride concentration in ponies of the ligated group during the second postsurgical week. This increase was most likely attributable to anorexia observed during that period. Hyperbilirubinemia was observed early in ponies of the ligated group; most of the bilirubin was of the conjugated type. Using electrophoretic and ultracentrifugal methods, serum lipoprotein alterations were detected only in ponies of the ligated group. Increases of very low-density and low-density hpoprotein cholesterol concentrations and decrease in high-density lipoprotein cholesterol concentration were found. Although no changes were seen in total serum cholesterol concentration, a redistribution of lipoprotein cholesterol was observed in ponies of the ligated group. Similar alterations in lipoprotein distribution have been found in dogs, rats, and human beings with obstructive jaundice and cholestasis. The association between serum lecithin:cholesterol acyl transferase activities and these lipoprotein alterations remains to be elucidated.

Eleven adult goats and 32 adult outbred mice were inoculated IV with Cowdria ruminantium-infected blood (Kwanyanga isolate), monitored clinically, then serially euthanatized. Predominant clinical signs of disease in goats were depression, head tremors, seizures, and dyspnea. In mice, dyspnea and depression were the only clinical signs of disease noticed. Tissues were examined histologically and immunohistochemically for C ruminantium colonies or antigen. In goats, C ruminantium was detected only in endothelial cells of the brain, even though gross and microscopic lesions were confined to the thorax. In mice, C ruminantium was detected only in endothelial cells of the heart and lungs.

Biological effects of staphylococcal protein A (SPA) immunotherapy were studied in 5 viremic and 6 nonviremic cats with induced FeLV infection and in 6 control cats. The SPA therapy neither reversed FeLV viremia nor resulted in consistent improvement in humoral immune responses to FELV antigens. However, SPA immunotherapy induced a proliferative response in bone marrow granulocytic lineage, possibly resulting in expression of FeLV-free mature neutrophils in the blood. Seemingly, viral burden and chemiluminescent responses were reversed in viremic cats during SPA immunotherapy.

Ten healthy sedentary male Thoroughbreds with previous race training experience were studied for 14 weeks. Horses were trained for 9 weeks, using a program designed after those used commonly in the United States. Horses were trained conventionally by slow trotting (250 m/min) for 2 weeks and galloping (390 to 450 m/min) for 4 weeks, followed by 3 weeks of galloping (440 to 480 m/min) and intermittent sprinting exercises (breezes) at distances between 600 and 1,000 m (900 to 950 m/min). The horses were then pasture rested for 5 weeks. A standardized exercise test (SET) involving an 800-m gallop at 800 m/min was administered before and after the 9-week training period and after the 5-week detraining period. Heart rate (HR) was monitored during exercise and at standardized intervals after exercise for 60 minutes. Venous blood for determination of plasma lactate concentration was obtained at 5 minutes after exercise. Heart rate was monitored daily at rest, during exercise, and through the first 60 minutes of recovery. Venous plasma samples (for lactate determination) were obtained 5 minutes after the sprinting exercises. Horses were observed daily before exercise for signs of lameness and were not allowed to train if lame. Differences after 9 weeks' training were seen in the SET recovery HR at 0.5 through 5 minutes after exercise (P < 0.05 to P < 0.01). Differences after detraining were seen in the SET recovery HR at 40 and 60 minutes after exercise (P < 0.05 to P < 0.01). Neither training nor detraining resulted in differences in plasma lactate concentration after the SET gallop. A training-induced resting bradycardia was not observed. The mean maximal HR (HRmax) during workouts was 238 +/- 3.4 beats/min (n = 9). When exercise HR was expressed as a function of HRmax, 22% of trotting, 89% of galloping, and 100% of sprinting workouts were performed at the greater than or equalto 60% HRmax value characterized by the onset of blood lactate accumulation. Plasma lactate concentration further documented that all the sprinting exercises were performed with concentration above the point of onset of blood lactate accumulation. Mean postsprinting lactate concentration was not different over time and ranged from 13.4 +/- 0.9 to 15.6 +/- 0.6 mmol/l. As training progressed, some of the horses had days on which they were lame after exercise. Some lameness was judged sufficient to warrant phenylbutazone (PBZ) administration. Retrospective analysis of the daily HR data indicated that there were no differences in HR during workouts for lame horses given PBZ, compared with those not given PBZ. Using analysis of variance, HR for horses that were lame during workouts was significantly higher than that for horses that were sound during workouts, during and 0.5 minutes after trotting; 0.5, 1, 2, 20, 40, and 60 minutes after galloping; and 0.5 and 20 minutes after sprinting (P < 0.05 to P < 0.01).

An immunoperoxidase technique was used to study the relationship between the necrotic lesions and causative bacteria found in lungs of 53 calves that had naturally acquired pneumonia. Four types of necrotic lesions were identified on the basis of morphologic characteristics as follows: type 1 had coagulation necrosis surrounded by a dense zone of numerous degenerated leukocytes; type 2 was similar to type 1, but the central area of the lesions was severely affected, had no alveolar architecture remaining, and was surrounded by a thin, sparse layer of degenerated leukocytes; type 3 had small swirling accumulation of degenerated leukocytes; and type 4 had necropurulent lesions resembling abscesses. By use of the immunoperoxidase technique, Pasteurella haemolytica serovar 1 antigen was confirmed to be associated with the necrotic lesions in many cases of type 1 and in some cases of types 2 and 3. Although some lesions were induced by other bacteria (Haemophilus somnus or Actinomyces pyogenes), the pneumonic lesions associated with P haemolytica could be differentiated from other pneumonic lesions in calves by use of the immunoperoxidase technique.

Ten adult dogs (5 Beagles and 5 mixed-breed dogs) were inoculated IV with canine platelets containing Ehrlichia platys. Inclusions and morulae of E platys developed in platelets of infected dogs at 10 to 14 days after inoculation, followed by marked thrombocytopenia at 14 to 21 days. Parasitemia and marked thrombocytopenia recurred at 24 to 28 days after inoculation. Increased numbers of megakaryocytes were observed in marrow aspirate smears from infected dogs, indicative of regenerative thrombocytopenia. Prior to infection, platelet-rich plasma from these dogs was determined to have similar aggregatory response to arachidonate. After infection with E platys, the aggregatory response of platelet-rich plasma to collagen or 3 dilutions of adenosine diphosphate was evaluated. A statistically significant (P < 0.05) inhibition of platelet aggregatory response to the lowest dilution of adenosine diphosphate was detected for mixed-breed dogs, whereas aggregation responses were unchanged in Beagles. Results indicate that platelet activation may occur in dogs with acute ehrlichial infection.

Intranuclear inclusions indicative of adenovirus infection were detected microscopically in formalin-fixed intestinal tissues from preweanling Syrian hamsters. The amphophilic intranuclear inclusion bodies were observed in ileal enterocytes from 16-to 24-day-old hamsters. Electron microscopy revealed large numbers of 72 +/- 3-nm viral particles typical of adenoviridae in enterocytic nuclei. Serum antibodies reacted with mouse adenovirus strains K87 and, to a lesser extent, FL, by indirect fluorescent antibody testing. Clinical disease was not associated with the adenoviral infections. Hamsters from 10 production colonies, including all major commercial Syrian hamster suppliers in the United States, were surveyed and all had serologic or histopathologic evidence of adenovirus infection.

Reference intervals are reported for feline CSF biochemical and serologic variables, IgG concentration, and electrophoretic fractionation, derived from 58 clinically normal adult cats that did not have histologic lesions of the CNS. There was no apparent effect of age on any variable. The CSF total protein concentration was significantly (P = 0.012) greater in males than in females, but all other variables were unaffected by gender. The only variable that had a statistically significant correlation with its corresponding blood concentration was IgG. Blood contamination of the CSF affected the following CSF variables: total protein concentration, activities of lactate dehydrogenase and creatine kinase, IgG ratio, and gamma-globulin percentage. The reference intervals proposed for feline CSF were derived from 33 cats with CSF RBC count < 31 cells/microliter. Reference limits for CSF with 31 to 1,700 RBC/microliter also are reported.