A prospective cohort study was undertaken in a farrow-to-farrow swine herd to describe patterns of pneumonia, and to identify host risk factors associated with the extent of pneumonic lesions in 2 weight groups of slaughter swine. The risk of coughing and pneumonic lesions increased with increasing age of pigs within the herd (P < 0.0001). The age-specific prevalence of pneumonic lesions was low (2.7%) in pigs < 16 weeks old at slaughter, but increased rapidly when pigs were between 16 and 22 weeks old (8.6 to 67.9%). After 22 weeks, the prevalence remained relatively constant at about 80%. Associations between possible risk factors and pneumonia were investigated by use of multiple-regression models. Age at weaning (< 24 days) and birth weight (< 1 kg) exerted small, but significant (P < 0.002), effects on the extent of pneumonic lesions in pigs slaughtered at 30 to 50 kg live weight. For pigs slaughtered at 90 to 110 kg, pneumonic lesions were more extensive (P = 0.007) in pigs sired by Yorkshire boars than pigs sired by non-Yorkshire sires (Duroc, Hampshire, Chester White, or American Spotted). Other host factor variables including weaning weight and clinical diseases (atrophic rhinitis, diarrhea, and arthritis) were not associated with pneumonia extent in either weight group. Higher pneumonia percentages were also associated with reduced growth rates in the grower/finisher phase. Pigs sired by Yorkshire boars grew significantly (P < 0.0001) more slowly from entry into shed 2 (mean, 38 kg) until about the time of exit (mean, 92 kg) than pigs sired by other breeds (747 g/d and 795 g/d, respectively).

Hematologic and serum biochemical values were determined in blood samples from 217 donkeys (Equus asinus). Donkeys were classified on the basis of size, sex, age, and whether they were domestic or feral. Parametric (mean +/- 2 SD) and nonparametric (2.5th to 97.5th percentile) reference ranges were calculated for each analyte. For all donkeys, 26 of 46 analytes significantly departed from gaussian distribution. Serum lactate dehydrogenase activity in miniature donkeys was higher than that in other donkeys. Differential leukocyte counts in feral donkeys differed from those in other types in ways that suggested that the former had smaller parasite loads or experienced greater stress. Erythrocyte, lymphocyte, and platelet counts and fibrinogen, glucose, inorganic phosphorus, and potassium concentrations decreased with age. Eosinophil counts, mean corpuscular volume, and plasma protein, serum protein, and serum globulin concentrations increased with age. Female donkeys had significantly (P < 0.05) higher mean corpuscular hemoglobin concentration and leukocyte and neutrophil counts than did male donkeys. Mean corpuscular hemoglobin increased with age, and females had higher values than did males of all age groups. An interaction between age and sex was observed for alkaline phosphatase activity, with a trend for decreased activity with age.

Thyroxine (T4), 3,5,3'-triiodothyronine (T3), and cortisol frequently are quantified in canine serum or plasma samples to aid in the diagnosis of hypothyroidism, hypoadrenocorticism, and hyperadrenocorticism. Many laboratories have established reliable references values for concentrations of these hormones in blood of clinically normal animals. However, nonpathologic factors that affect thyroidal and adrenocortical secretion may lead to misinterpretation of test results when values for individual animals are compared with reference values. The objective of the study reported here was to identify effects of age, sex, and body size (ie, breed) on serum concentrations of T3, T4, and cortisol in dogs. Blood samples were collected from 1,074 healthy dogs, and serum concentrations of the iodothyronines and cortisol were evaluated for effects of breed/size, sex, and age. Mean (+/- SEM) serum concentration of T4 was greater in small (2.45 +/- 0.06 microgram/dl)- than in medium (1.94 +/- 0.04 microgram/dl)- or large (2.03 +/- 0.03 microgram/dl)-breed dogs, the same in females (2.11 +/- 0.04 microgram/dl) and males (2.08 +/- 0.04 microgram/dl), and greater in nursing pups (3.04 +/- 0.05 microgram/dl) than in weanling pups (1.94 +/- 0.05 microgram/dl), rapidly growing dogs (1.95 +/- 0.04 microgram/dl), and young adult (1.90 +/- 0.06 microgram/dl), middle-aged adult (1.72 +/- 0.05 microgram/dl), or old adult (1.50 +/- 0.05 microgram/dl) dogs. Dogs > 6 years old had lower mean serum T4 concentration than did dogs of all other ages, except middle-aged adults. Mean serum T3 concentration in medium-sized dogs (1.00 +/- 0.01 ng/ml) was greater than that in small (0.90 +/- 0.01 ng/ml)- and large (0.88 +/- 0.01 ng/ml)-breed dogs. Serum T3 concentration was lowest in nursing (0.85 +/- 0.01 ng/ml) and weanling (0.77 +/- 0.02 ng/ml) pups, increased in rapidly growing dogs (0.99 +/- 0.01 ng/ml) and young adult dogs (1.10 +/- 0.04 ng/ml), and decreased slightly in middle-aged (0.98 +/- 0.02 ng/ml) and old (1.01 +/- 0.03 ng/ml) adult dogs. Serum T3 concentration was unaffected by sex. Mean serum cortisol concentration was greater in small (1.06 +/- 0.07 microgram/dl)- than in large (0.79 +/- 0.03 microgram/dl)-breed dogs. Serum from nursing pups 0.57 +/- 0.04 microgram/dl) contained less cortisol than did serum from older dogs (mean values greater than or equal to 0.92 microgram/dl). Serum cortisol concentration was not different between males and females. These effects of breed/size and age on serum T3, T4, and cortisol concentrations should be considered when evaluating thyroid and adrenocortical functions in dogs.

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P < 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P < 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P < 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P < 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P < 0.02), second 60 minutes (P < 0.001), and total 120 minutes (P < 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and cell responsiveness to stimuli (ie, glucose).

The purpose of this project was to study the effect of superalimentation in lactating sows through permanent, surgically placed, gastric cannulas. A surgical technique was developed to install gastric cannulas into pregnant sows to allow superalimentation by introducing feed through the cannula. After induction of general anesthesia, a flexible, T-shaped cannula (22 mm outside diameter) was surgically placed in the dorsal portion of the greater curvature of the stomach and exteriorized through the tenth intercostal space approximately 30 cm left of the dorsal midline. Cannulas were installed on day 85 5 days of gestation. Anesthesia, surgical procedures, and the subsequent presence of the cannula did not affect the size ornumber of live pigs at birth. In addition, the prevalence of stillbirths and mummified fetuses was not significantly different than that of noncannulated sows. The gastric cannulas did not affect lactation performance, as litter size and weight were unaffected when compared with that in noncannulated controls. Postmortem examination of euthanatized sows revealed adhesions of the gastric wall to the abdominal wall, thus eliminating the possibility of leakage of the gastric contents into the peritoneum. Detrimental effects of the cannulas on gastric function or capacity were not detected, and cannulas could be maintained through multiple parities.

Brain stem auditory-evoked responses were recorded in 9 male and 11 female clinically normal mature dogs, weighing between 2 and 36 kg. Mean wave latency for the entire group of dogs, using 60-dB hearing level click stimuli at 11/s for waves I to VII was: 1.41, 2.21, 2.85, 3.31, 3.71, 5.12, and 6.46 ms, respectively. The mean interpeak latency for waves I and V (IPLIV) was 2.32 ms. Neither gender nor ear effect was detectable. Positive correlation was observed between cranium length, cranium width, nasion-external auditory meatus interval, and body weight for wave-V latency and IPLIV. Such correlation was not documented for wave I. The regression equations for their effects on IPLIV were: cranium length, y = 0.05x + 1.85; cranium width, y = 0.07x + 1.32; nasion-external auditory meatus interval, y = 0.05x + 1.79; and body weight, y =0.05x + 2.15. On the basis of any of the 3 variables of cranium size or body weight, the study population could be classified into groups of large and small dogs, with the large group having significantly (P < 0.05) longer latency for wave V and IPLIV. It is recommended that the effect of size variation in dogs on brain stem auditory-evoked responses should be compensated for by use of the regression equation based on cranium length.

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire X Landrace X Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time. Treatment with T-2 toxin induced microcytic hypochromic anemia, increased numbers of circulating metarubricytes and decreased absolute numbers of lymphocytes. Hepatocellular lesions in barrows of the AF and the AF plus T-2 groups (2 and 4, respectively) were compatible with aflatoxicosis. When fed in combination, each toxin appeared to have a sparing action on certain effects of the other, and the responses elicited were either additive or less than additive.

Two experiments were conducted to determine changes in body composition and various physiologic variables in feeder pigs under simulated marketing conditions. In the first experiment, pigs were assigned to 1 of 4 treatment groups for 48 hours: (1) no water and feed; (2) water ad libitum, no feed; (3) no water, feed ad libitum; or (4) water and feed ad libitum. During a 48-hour recovery period, all pigs were allowed feed and water ad libitum. Plasma triiodothyronine decreased (P < 0.01) within the first 24 hours in groups-1 and -2 pigs, but increased (P < 0.01) within the first 6 hours of the recovery period. The circadian rhythm of plasma cortisol was disrupted in groups-1 and -3 pigs and during recovery in group-1 pigs. Packed cell volume increased (P < 0.05) in groups-1 and -3 pigs and returned to initial values within the first 24 hours of the recovery period. In the second experiment, body composition was estimated by the 40K technique for fat-free body mass, percentage of nitrogen, and percentage of fat. Body composition was determined before and after pigs were allotted to 1 of 2 groups for 48 hours: group-1 pigs were given feed and water ad libitum and group-2 pigs were not given feed and water. Group-1 pigs gained 2.2 kg of body weight (P < 0.01), 0.6% fat (P < 0.01), 0.7 kg of fat-free body mass, and 0.02% nitrogen (P > 0.01). Group-2 pigs lost 2.3 kg of body weight (P < 0.01), 0.6% fat (P < 0.01), 2.0 kg of fat-free body mass (P < 0.01), and 0% nitrogen.

Newly hatched chickens were treated with the trichothecene mycotoxin, T-2 toxin, during the first day of life. Control chickens were treated with other agents known to cause immunosuppression-cyclosporine, cyclophosphamide, and aflatoxin. Chickens were infected on day 6 (5 days after treatment with T-2 toxin) by intraperitoneal inoculation with Salmonella typhimurium. Blood samples were collected from treated chickens (noninfected) and used to assess the responsiveness of blood lymphocytes to T-cell or B-cell mitogens, phytohemagglutinin, or lipopolysaccharide, respectively. The T-2 toxin had a profound negative effect on the ability of the chickens to resist salmonellosis, as measured by survival. However, the toxin effect in reducing phytohemagglutinin- and lipopolysaccharide-stimulated mitogenesis, though significant (P > 0.05), was not severe. Our data indicate a direct effect of T-2 toxin on native resistance to systemic salmonellosis, which was not accompanied by marked alteration in T- or B-cell responses to mitogenic stimulation.