Biochemical changes in the small intestine during development of naturally acquired wheat-sensitive enteropathy of Irish Setters were investigated. To distinguish primary biochemical abnormalities from secondary 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 sequentially obtained between weaning and 1 year of age; specific activity and reorientating sucrose density-gradient distribution of organelle marker enzymes were determined. Major primary biochemical abnormalities were not detected in affected progeny. In affected dogs fed wheat, there was a selective, but secondary, loss of the brush border alkaline phosphatase and aminopeptidase N activities. This loss was associated with the development of partial villus atrophy, but represented a specific effect of dietary wheat on the brush border, not merely a nonspecific effect of mucosal damage, because other brush border enzymes, including disaccharidases, were not similarly affected. Increased soluble activities of lysosomal and peroxisomal marker enzymes late in the disease process may represent alterations in these 2 organelles as a secondary consequence of mucosal damage.

Detection of capsular polysaccharide (CP) in milk of cows with natural intramammary infection caused by Staphylococcus aureus was attempted. Five quarters of 5 cows harboring S aureus strains that produce type-8 CP were selected. Using an ELISA with a monoclonal antibody, type-8 CP was not detected in extracts prepared from fresh milk collected aseptically. By contrast, CP was easily detectable after incubation of infected milk at 38 C for 20 hours. Quantitation of CP in extracts from incubated milk samples by use of ELISA indicated a great variation of CP expression by strains. Although an incubation step was necessary to detect CP, results of the study indicate that CP may be expressed in vivo during intramammary infection caused by S aureus.

Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P < 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia. The results indicated that young calves are susceptible to 3-methylindole-induced pulmonary injury and that nonciliated bronchiolar epithelial cells, type-I alveolar epithelial cells, and pulmonary endothelial cells are most susceptible to injury. The results failed to indicate that 3-methylindole pulmonary toxicosis significantly enhances respiratory disease induced by bovine respiratory syncytial virus.

Acute nephrotoxicosis was induced in ewes by daily SC administration of gentamicin. Activity of 3 urine enzymes, gamma-glutamyltransferase (GGT), beta-N-acetylglucosaminidase (AGS), and beta-glucuronidase (GRS), were measured during the development of aminoglycoside nephrotoxicosis. Measurements from timed, volume-measured urine samples were performed on days 0, 7, and 8. Measurements from urine samples obtained without volume measurement (spot samples) were performed daily. Urine GGT and AGS activities were high 3 days prior to detection of high serum creatinine concentration and 1.5 days before the appearance of casts in the urine sediment; values consistently remained in the abnormal range until termination of the study. High urine GRS activity was inconsistent and transient; serum GGT activity did not change during the course of the study. Urine GGT and AGS activities expressed as total excretion per unit time and body weight, enzyme activity per unit volume, and as ratio of urine enzyme activity to urine creatinine concentration were strongly correlated. Urine GGT and AGS, but not GRS activities, are suitable indicators of renal tubular cell damage in sheep with aminoglycoside nephrotoxicosis. Urine GGT and AGS activities indicate cellular changes occurring several days prior to the first indications of renal functional change.

Blood samples were obtained from 20 bison (Bison bison) from a ranch in northern lower Michigan, as well as from 20 free-ranging bison of the same sex and similar age from the Badlands National Park in South Dakota. Hematologic and serum biochemical values were determined. The values were comparable in both groups, except for those for BUN, aspartate transaminase, and phosphorus, which were significantly (P < 0.001) higher in the ranched bison than in the free-ranging bison. These differences were attributed to nutritional effects. Impact of age on blood characteristics was assessed in the ranched bison only by comparing values from calves weighing less than 185 kg with those from bison weighing more than 185 kg. Calves had significantly (P < 0.001) higher values for phosphorus and RBC counts and lower total protein values than adults. Adult bison had higher eosinophil and neutrophil counts with lower numbers of lymphocytes, suggestive of a stress leukogram, whereas calves had the typical bovine neutrophil:lymphocyte ratio.

Muscle damage attributable to selenium (Se)/vitamin E deficiencies is known to develop at birth or later in lambs. The purpose of this study was to determine whether and when muscle damage develops in utero. Thirty pregnant ewes maintained on Se-deficient forages from birth were allotted to 3 equal groups. Half of each group was given a single IM injection of 0.056 mg of Se/kg of body weight, 1 month before parturition. At 3 weeks before parturition, cesarean section-derived fetuses from Se-deficient ewes did not have evidence of muscle damage. At 2 weeks before parturition, fetuses from Se-deficient ewes had biochemical evidence of congenital nutritional myopathy, as evidenced by low blood Se concentration (P < 0.05) and by increased plasma creatine kinase (P < 0.001) and lactate dehydrogenase (P < 0.01) activities, compared with fetuses from Se-treated ewes. Thus, for optimal protection of fetuses and newborn lambs in Se-deficient areas, Se should be administered to ewes at least 1 month before parturition.

Ten healthy sedentary Thoroughbreds with previous race training experience were trained conventionally for 9 weeks. Muscle biopsy samples were obtained before and after training and after 6 weeks of detraining pasture rest. Biopsy samples were obtained from the right deltoid, triceps, vastus lateralis, middle gluteal, biceps femoris, and semitendinosus muscles. The deep-frozen biopsy samples were analyzed for activities of succinate dehydrogenase (SDH), 3-hydroxy-acylcoenzyme A dehydrogenase (HAD), and phosphorylase (PHOS) and for glycogen concentration. The triceps and gluteal muscle samples were also serially sectioned and stained for myofibrillar actomyosin adenosine triphosphatase (ATPase) activity after alkaline (pH 10.3) and sequential acidic (pH 4.34) ATPase inactivation. Fiber types I (alkaline preincubation), IIA1, IIA2, and IIA3 (sequential acidic preincubation over 5 minutes) were identified and were evaluated for fiber-type distribution and fiber areas. Increases in response to training were observed in deltoid and vastus muscle SDH and gluteal muscle HAD activities, and deltoid muscle glycogen concentration (P < 0.05 to P < 0.01). Changes in PHOS activity were not observed. Type-IIA1, -IIA2, and -IIA3 fiber areas in triceps muscle were increased in response to training (P < 0.05 to P < 0.01). Changes in fiber-type distribution did not occur in response to training. Changes in muscle enzyme activities, glycogen concentration, fiber types, and fiber areas were not seen from posttraining to detraining. Further increases were observed when detraining values were compared with pretraining values in deltoid, triceps, vastus, gluteal, and biceps femoris muscle SDH activities and in gluteal muscle glycogen concentration (P < 0.05 to P < 0.01). It was concluded that the predominant failure to detect training-induced muscle enzyme changes, along with documentation of increases in fast-twitch muscle fiber areas, indicate that conventional Thoroughbred training is principally of a sprinting nature. A greater emphasis on longer, slow endurance work early in training might add greatly to Thoroughbred horses' abilities to withstand the rigors of sprint training.

Pharmacokinetic variables were calculated from time-concentration data obtained after IV (10 mg/kg of body weight; n = 9) and oral (12.5 mg/kg to group A [n = 3]; 25 mg/kg to group B [n = 3]; and 50 mg/kg to group C [n = 3] pigs) cyclosporine (formerly, cyclosporine A) administration. Resulting mean (+/- SD) pharmacokinetic variables were as follows: half life of distribution, 0.96 (+/- 0.7) hours; half life of elimination, 7.71 (+/- 2.6) hours; volume of distribution at steady state, 4.47 (+/- 2.22) L/kg; volume of the central compartment, 1.71 (+/- 0.78) L/kg; and systemic clearance, 8.95 (+/- 2.7) ml/kg/min. Oral bioavailability was: overall 57 (+/- 19) %; group A, 44 (+/- 11) %; group B, 78 (+/- 15) %; group C, 48 (+/- 6) %. Time to peak concentration was 3.55 (+/- 0.88) hours. During the 22 days of daily oral cyclosporine administration, blood 24-hour trough concentrations were: group A, 224.3 (+/- 78.4) ng/ml; group B, 640.7 (+/- 174.6) ng/ml; and group C, 2,344 (+/- 1,095) ng/ml. Lymphoblast transformation stimulation index was suppressed in all pigs except 1, which had a corresponding cyclosporine concentration of 92.4 ng/ml. Minimal, although statistically significant, decreases in serum albumin and magnesium concentrations and increases in serum creatinine and urea nitrogen concentrations were evident in pigs of some treatment groups. Histologic examination of necropsy specimens revealed mild hepatic necrosis (n = 1 pig), renal tubular dilatation (n = 5), and pulmonary inflammation (n = 2). Pigs given 25 and 50 mg of cyclosporine/kg failed to gain weight.

Changes in clotting time (CT) and fibrinolytic activity (FA) were evaluated in 6 mature, female horses during exercise. Two trials were performed on consecutive days, using a randomized crossover design. Each mare was assigned to either an exercise trial or a control trial on the first day, and to the alternate trial 24 hours later. Mares exercised for 20 minutes on a treadmill at an elevation of 2 degrees and a velocity of 5 m/s. Venous blood samples were collected immediately before exercise, at 4, 8, 12, 16, and 20 minutes during exercise, and 15 minutes after cessation of exercise. Blood was placed into plain glass tubes for determination of CT, and into chilled, citrated tubes for determination of FA, plasminogen/plasmin complex activity (PLG), one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), and antithrombin-III (AT-III) activity. There were significant differences (P < 0.05) between the control and exercise groups for CT, FA, and PLG. During exercise, clotting time decreased from 21.5 +/- 1.6 minutes to 9.9 +/- 1.6 minutes (mean +/- SD; P < 0.05), without significant changes in OSPT, APTT, or AT-III. Fibrinolytic activity and PLG increased (P < 0.05) during exercise. Changes in CT, FA, and PLG were significant at 4 minutes of exercise, remained altered until the end of exercise, and returned to baseline values by 15 minutes of recovery. Clotting time, OSPT, APTT, FA, AT-III, and PLG did not change (P > 0.05) during control trials.

Clinicopathologic manifestations of induced infection of the feline lower urinary tract with bovid herpesvirus-4 (BHV-4, strain FCAHV) were characterized in 6 conventionally reared adult cats (2 sexually intact males, 2 castrated males, and 2 females). Two additional control cats were exposed with noninfected cell culture control inoculum. Clinical and radiographic signs of lower urinary tract disease were not observed in exposed or control cats. Microscopic hematuria was detected in urine samples collected by cystocentesis from 4 of 6 exposed cats and 1 of 2 control cats. Results of culture of urine for bacteria, mycoplasmas, ureaplasmas, and viruses were consistently negative. Low titer of serum BHV-4 (strain FCAHV)-neutralizing antibodies was detected in 4 of 6 exposed cats, but not in controls. Gross abnormalities of the urinary tract were not observed in any cat. Light microscopic examination of serial sections of the lower urinary tract revealed mild focal lymphoid cystitis in 2 of 6 exposed cats, one of which also had increased amounts of connective tissue and proliferation of blood vessels in the urinary bladder lamina propria. Ninety days after initial exposure, BHV-4 (strain FCAHV) was reisolated from explanted urinary bladder tissues of 5 of 6 exposed cats. Virus was not isolated from tissues of control cats. It was concluded that BHV-4 (strain FCAHV) establishes persistent urinary tract infection in conventionally reared adult male and female cats. However, persistent BHV-4 infection in cats may remain clinically inapparent.