Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.

Nutritional and physiologic effects of clinically apparent and subclinical Ostertagia ostertagi infections were studied in 3 groups of 5 calves each. Group-1 calves were inoculated with 100,000 Ostertagia ostertagi third-stage larvae (L3)/calf/wk for 14 weeks. Group-2 calves were inoculated with 10,000 L3/calf/wk for 14 weeks, and group-3 calves were not inoculated. Calves in group 1 had decreased dry matter intake and feed utilization from 4 weeks after initial inoculation. Group-2 calves had no changes in dry matter intake, but had decreased feed utilization at 12 and 14 weeks. Calves with clinically apparent infections (group 1) lost a mean weight of 11.8 kg, whereas calves with subclinical infections (group 2) lost a mean of 46.6 kg, and control calves lost a mean of 60.7 kg. Calves with O. ostertagi infections (groups 1 and 2) also had decreased carcass quality at slaughtering, which was reflected in decreased dressing weights and increased water-holding capacity of the rib-eye muscle. Calves in groups 1 and 2 also had lower carcass yield and rib-eye muscle weight, and group-1 calves had decreased protein content. Results of hematologic, pathologic, parasitologic, and clinical examinations mirrored nutritional changes.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56. Leptomeres were observed in cardiac myocytes of ducklings that had been fed furazolidone, but not in those fed only the control ration. Our clinical, gross pathologic, and ultrastructural findings indicate that regression of the cardiac lesions of furazolidone toxicosis may be essentially complete by 28 days after cessation of furazolidone intake. Our ultrastructural findings indicate that furazolidone consumption may result in cardiac dilatation by altering myofibrillar/cytoskeletal attachments of myocytes.

The toxicity of zinc ethylene-bis-dithiocarbamate (zineb), a widely used fungicide, was studied in four 4-week-old Friesian calves with immature rumen function. Calves were first subjected to liver biopsy, and thereafter, 3 of them were orally administered 200 mg of zineb/kg of body weight daily for 80 days, whereas the fourth calf served as control and remained untreated. Clinical, hematologic, and pathologic (including ultrastructural) findings were recorded. The distribution in body fluids and tissues of the parent compound and one of its main metabolites, ethylenethiourea (ETU), also was examined. Treated calves had unthrifty appearance and reduction in weight gain. They also had remarkable impairment of thyroid function, as reflected by reduction in serum concentrations of triiodothyronine and thyroxine and increase in weight of the thyroid gland associated with epithelial vacuolization and foci of hyperplasia. Moderate increase in liver glycogen content and impairment in maturation of germ cells were recorded consistently. Whereas zineb was widely distributed in body tissues, ETU accumulated mainly in the liver and the thyroid gland, although noticeable concentrations also were attained in muscle. Data were consistent with involvement of ETU mainly in the pathogenesis of thyroid gland lesions, and indicate that unweaned calves given zineb develop a clinicopathologic syndrome that does not differ qualitatively from that already described in adult cattle exposed to zineb.

Fluctuations of serum vitamin E (alpha-tocopherol), cholesterol, and total lipids were monitored in 12 horses at 3-hour intervals for 72 hours. Mean coefficients of variation were 12, 5, and 15%, respectively. Statistical analyses were used to conclude that instrumentation error was accountable for only a small portion of the vitamin E variation. Results indicated that a single serum sample assay is an unsatisfactory indicator of vitamin E status in horses. These data have clinical application in the evaluation of horses suspected to be affected with equine degenerative myeloencephalopathy. The large variance of serum total lipids and the lack of correlation of it with serum vitamin E over time preclude the use of vitamin E/serum total lipids ratio in assessing vitamin E status.

Five 5 to 6 month old horses were surgically prepared with silver electrodes sutured to the serosa of gastric antrum, duodenum and proximal portions of the jejunum. Normal migrating motility complex (MMC) periodicity was determined during daytime hours in horses that were fed and horses from which food was withheld for 24 hours. Periodicity was defined as time span from the end of one period of regular spike activity (RSA) to the end of the next RSA in the MMC. The periodicity was 120.5 +/- 9.5 (SEM) minutes in horses from which food was withheld, and was 125.7 +/- 20.3 minutes in horses fed hay free choice. Coincident with each duodenal RSA, antral spike activity ceased. Xylazine (0.25 and 0.5 mg/kg), given IV during the period of intermittent spike activity of the MMC to either fed or unfed horses induced, within 2 minutes, a RSA complex in the duodenum that migrated to the proximal portion of the jejunum. This was followed by a period of no spike activity of normal duration, which proceeded on to a period of intermittent spike activity of varying duration to complete the MMC cycle. Pretreatment IV administration of an alpha 2-adrenergic antagonist, tolazoline (1 mg/kg) also provoked a RSA complex, but blocked the xylazine effect. The results indicated that xylazine resets the duodenal MMC in the horse, but does not seriously disrupt proximal gastrointestinal tract motility, and that control of MMC periodicity in this region probably involves more than alpha 2-adrenergic receptors.

The effect of dry, soft moist, and canned dog foods on immediate postprandial plasma glucose and insulin concentrations was evaluated in clinically normal dogs. Dogs were fed either dry (10 dogs; group I), soft moist (10 dogs; group II), or canned (8 dogs; group III) dog food for 5 consecutive days. On the fifth day, plasma glucose and insulin concentrations were determined in each dog prior to, during, and at 5, 10, 15, 30, 45, 60, 90, 120, 180, and 240 minutes after ingestion of the food. The alterations in plasma glucose concentrations were not significantly different from prefeeding values until 240 and 180 minutes after feeding for groups I and III, respectively. In contrast, the increments in plasma glucose were significantly (P less than 0.01) increased from basal concentrations at 30 and 45 minutes after feeding in group-II dogs. The maximal mean postprandial plasma glucose concentration was significantly (P less than 0.0001) less for group III, compared with concentrations for groups I and II, but there was no significant difference between concentrations for groups I and II. Although a bisphasic insulin secretory response was found in all 3 groups of dogs, the patterns of phase-2 insulin secretion and the total amount of insulin secreted during the study were significantly different. There was a rapid increase in the plasma insulin concentration immediately after phase 1 in group II, with maximal plasma insulin concentrations occurring 30 minutes after feeding, followed by a gradual decrease in concentrations throughout the remainder of the study. In contrast, plasma insulin concentrations increased steadily in groups I and III, after phase-1 insulin secretion, with maximal values occurring at 240 minutes after feeding. The maximal mean increase from basal insulin concentrations during phase-2 secretion was significantly (P less than 0.005) greater for group II (80 +/- 15 micro IU/ml) than for groups I and III (23 +/- 3 and 24 +/- 6 micro IU/ml, respectively). Whereas the integrated areas under the glucose response curves were not significantly different between groups, total insulin secretion and total insulin secreted during phases 1 and 2 were significantly (P less than 0.01) greater in group II than in groups I and III. Differences in dietary composition may offer the best explanation for differences in postprandial glucose concentrations and insulin secretory responses between groups. These findings emphasize the importance of dietary formulations when designing hormonal studies or interpreting research data when dogs are the animal model.

Growth indices were examined in 24 identically managed tanks, each containing 120 diploid juvenile rainbow trout (initial mean body weight, 9.3 g), during a 12-week study to examine tank effects associated with tank location in a multi-user research facility. Growth indices included mean body weight, feed intake, feed conversion index, and specific growth rate. The null hypothesis that tank effect had no effect on growth over the 12-week period was rejected (P = 0.038), and mean weight in individual tanks differed by as much as 18.7%. During the study, it was determined that the proximity of tanks to common-use walkways in the facility could affect growth indices. This was indicated by significant differences in the mean fish weights among blocks of tanks served by different header tanks after 4 (P = 0.001) and 8 (P = 0.024) weeks. The block containing tanks of fish with the highest mean weight was nearest to the 2 common-use walkways in the facility. Fish in this block of tanks, compared with those in other blocks, had significantly greater feed intake but no significant differences in conversion efficiency. Compensatory growth, a well known growth attribute in fishes, diminished the difference in mean weight between these blocks of tanks by the end of the study. Comparison of paired tanks within header tank blocks indicated that fish in those located nearest to walkways had higher feeding rates over the 12-week period (P = 0.048), but less efficient teed conversion (P = 0.040) than did fish in matched tanks located farthest from walkways. However, there were no differences in mean weight of fish. Results of this trial document the risks involved in identifying fish in a tank as the experimental unit when treatments are administered to the tank of fish, the latter being the true experimental unit.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.5 mg of OA/kg of feed; 8.0 mg of T-2/kg of feed; or 2.5 mg of OA plus 8.0 mg of T-2/kg of feed for 30 days. Production performance, serum biochemical, hematologic, immunologic, and pathologic evaluations were made. Body weight and body weight gain were decreased by all toxin treatments, but the combination toxin treatment reduced weight gain more than did either of the toxins administered singly and could be considered additive. Liver weight was decreased by combination treatment, whereas kidney weight was increased by OA treatment. Ochratoxin decreased serum cholesterol, inorganic phosphorus, and alkaline phosphatase values; reduced mean cell volume, hemoglobin concentration, and macrophage phagocytosis; and increased creatinine and total protein values. Consumption of T-2 toxin reduced hemoglobin and serum alkaline phosphatase values. The combination treatment decreased serum cholesterol, gamma-glutamyltransferase, alkaline phosphatase, mean cell volume, hematocrit, and hemoglobin values, as well as lymphoblastogenesis and phagocytosis, and increased serum nine concentration. We concluded that OA and T-2, singly or in combination, can affect clinical performance, serum biochemical, hematologic, and immunologic values, and organ weights of growing barrows. Although some analytes were affected more by the combination than by either toxin alone, the interactions could best be described as additive, not synergistic.