Effect of vaccine-induced immune activation on the performance of early-weaned pigs.

Two groups of 96 pigs were studied to determine the influence of weaning age, nursery site and a challenge to their immune system on their performance. The weaning ages were 11 to 16 days and 16 to 21 days. One nursery was on-site and the second nursery was off-site. Immune activation was stimulated by the administration of infectious bovine rhinotracheitis virus (IBR) vaccine to half of the pigs at each site. Serum virus neutralisation titres to IBR and total immunoglobulins were monitored in some of the pigs in each group. Performance was measured in terms of feed intake, average daily gain in weight, and feed conversion ratio (FCR). The mean serum immunoglobulin concentrations of all the groups of pigs tended to decrease in the first two weeks after weaning and then increase. Twelve of 20 pigs vaccinated with IBR had neutralisation titres to the virus. The site of the nursery did not significantly affect average daily gain in weight, feed intake or FCR. Pigs weaned at 16 to 21 days of age had a significantly better daily gain in weight than the pigs weaned at 11 to 16 days of age. Immune stimulation of the older weaned pigs did not influence their performance, but it had a significantly (P < 0.016) negative effect on the performance of the younger weaned pigs.

Depressed luteinizing hormone response to estradiol in vivo and gonadotropin-releasing hormone in vitro in experimentally diabetic swine.

The influence of the acute withdrawal of insulin therapy in streptozocin-diabetic female swine was examined for changes in 1) the in vivo pulsatile secretion of luteinizing hormone (LH), 2) the preovulatory-like gonadotropin patterns after exogenous estradiol, and 3) the in vitro LH secretion by cultured pituitary cells. In Experiment 1, ovariectomized diabetic pigs (n = 4) were maintained with insulin therapy until 4 d before estradiol benzoate (EB; 7 micrograms/kg body weight; subcutaneous) was administered. Four normal ovariectomized pigs, matched for age and weight, served as controls. The diabetic state was confirmed by the measurement of glucose and insulin concentrations during a glucose tolerance test. Pulsatile LH secretion was not influenced by experimental diabetes mellitus. However, the expected surge in LH was not induced by EB in diabetic gilts. In contrast, three of four normal gilts had a preovulatory-type surge in LH. Concentrations of follicle-stimulating hormone in serum were not affected by diabetes mellitus. Estradiol concentrations in serum after ER were influenced by diabetes mellitus (treatment by time interaction; P < 0.001). In individual estradiol profiles, maximum concentrations were similar (104 +/- 10.4 and 91 +/- 12.0 ng/ml for normal and diabetic pigs, respectively), but the interval to maximum concentration was delayed in diabetic pigs (27.5 vs. 9.0 h; SE = 3.0; P < 0.05). However, the duration of standing estrus (2.2 +/- .3 d) and the interval from EB to estrus (3.6 +/- 0.3 d) were not influenced by diabetes mellitus. In Experiment 2, LH secretion by cultured cells and residual cellular LH content were greater in the pituitaries of normal than diabetic pigs (P < 0.05), and only cells from normal pigs responded to gonadotropin-releasing hormone (GnRH), with increased production of LH (P < 0.05). In conclusion, diabetes mellitus did not affect pulsatile LH secretion but did lower the ability of exogenous estradiol to stimulate a surge in vivo and of GnRH to increase LH in vitro, suggesting that the pituitary response to estradiol and GnRH is more severely affected by diabetes than is the GnRH pulse generator.

Effect of diabetes mellitus during the luteal phase of the oestrous cycle on preovulatory follicular function, ovulation and gonadotrophins in gilts.

Development of preovulatory follicles was studied during the oestrous cycle in two experiments designed to examine the effects of short-term lack of insulin on preovulatory follicular function and (Expt 2 only) ovulation. In Expt 1, on day 12 of the third postpubertal oestrous cycle, insulin treatment was discontinued in streptozocin-induced diabetic gilts (n = 4), and on day 18, ovaries were removed from the diabetic gilts and from four normal untreated gilts. Diabetic gilts had a higher percentage of macroscopically atretic follicles (29.4 versus 6.8%; SEM = 5.9, P < 0.03) than did normal gilts. Binding of 125I-labelled hCG by freshly collected granulosa cells from non-atretic follicles was similar in diabetic and normal gilts. Diabetic gilts had more LH peaks in 3 h on days 12-17 of the oestrous cycle than did normal gilts (2.3 versus 1.6; SEM = 0.12; P < 0.01). Serum oestradiol and progesterone concentrations were not affected by treatment, but serum testosterone was increased (P < 0.01) in diabetic gilts. In Expt 2, insulin treatment was withdrawn from nine diabetic gilts on day 12 of the oestrous cycle and ten normal gilts served as controls. On day 18, ovaries were removed from six diabetic and six normal gilts; four normal and three diabetic gilts were ovariectomized 25 days after oestrus. Follicular diameter of diabetic gilts tended to be smaller than that of control (control: 3.95 versus diabetic: 3.01 mm; SEM = 0.4, P < 0.08) and the proportion of follicles with histologic evidence of atresia was higher in diabetic gilts (control: 29 versus diabetic: 47%; SEM = 5; P < 0.05) on day 18. In both experiments, the insulin-like growth factor I (IGF-I) and oestradiol concentrations of follicular fluid of diabetic gilts untreated with insulin from day 12 to day 18 was lower than in nondiabetic gilts. After day 18 in Expt 2, normal gilts exhibited oestrus (duration of cycle was 20 +/- 0.5 days) accompanied by preovulatory surges in oestradiol and LH, whereas diabetic gilts did not exhibit oestrus or ovulate. In diabetic gilts, oestradiol concentrations were lower compared with those of normal gilts, and LH patterns were characterized by two (two gilts) or three (one gilt) increases of more than 2 ng ml-1 between day 18 and day 25. Thus, impaired follicular function in diabetic gilts is not explained by decreased function of the hypothalamo-pituitary axis, since LH was not decreased.(ABSTRACT TRUNCATED AT 400 WORDS)

Preweaning mortality.

A number of factors, both infectious and noninfectious, contribute to preweaning mortality in pigs. It is important to establish the causes of preweaning mortality and their distribution in investigating farm problems. The various causes, risk factors, and a step-by-step approach to solving the problem are discussed.

Intraosseous infusion of resuscitative fluids and drugs: long-term effect on linear bone growth in pigs.

We studied the effects of intraosseous (IO) infusion of a standard fluid bolus and resuscitative drugs on long-term bone growth and epiphyseal closure in the "pediatric" swine model. Eighteen weanling pigs were randomly assigned to six groups as follows: three animals received two normal saline boluses, 20 mL/kg IO over 20 minutes; three received sodium bicarbonate, 1 mEq/kg IO; three received a 10% sodium bicarbonate infusion IO at maintenance rate over 1 hour; three received epinephrine 1:10,000, 0.1 mL/kg IO; three received an epinephrine infusion IO at 1 microgram/kg/min for 1 hour; and three received a dopamine infusion IO at 10 micrograms/kg/min for 1 hour. All infusions were given in the left hindleg; the right hindleg was used as a control. Lateral radiographs of the hind extremities were obtained at the beginning of the study and at 1 and 3 months after infusion. Linear radiographic measurements of the infused and control tibias were compared. At 6 months after infusion, the tibias were harvested, measured directly, and radiographed to determine the degree of epiphyseal closure. Analysis of variance for the first 3 months' data yielded a nonsignificant time-by-treatment interaction (P = .84) and a nonsignificant main effect for time (P = .22). Separate analysis of the direct measurements taken at 6 months revealed no difference in growth between experimental and control tibias. In addition, no radiographic difference in epiphyseal closure was noted between the two groups at the conclusion of the study, nor were any structural defects discovered. Intraosseous infusion of fluids and resuscitative drugs does not adversely affect subsequent bone growth and development in the swine model.

Long-term local effects of intraosseous infusion on tibial bone marrow in the weanling pig model.

The weanling pig model was used to determine the long-term local effects, if any, on tibial bone marrow after intraosseous (IO) infusion of resuscitation fluid and drugs at standard dosages. One of six IO treatments (two normal saline boluses [20 mL/kg]; bolus sodium bicarbonate [1 mEq/kg]; 10% sodium bicarbonate infusion at a maintenance rate for 1 hour; bolus 1:10,000 epinephrine [0.01 mg/kg]; 1:10,000 epinephrine solution infusion, 1 microgram/kg/min for 1 hour; or dopamine infusion, 10 micrograms/kg/min for 1 hour) was randomly administered via the left tibia to 18 pigs at 4 weeks of age. The animals were subsequently followed for 3 months, after which marrow from the same space and peripheral blood were examined. Marrow from the right tibia of each animal served as control; untreated historic controls were also used for comparison. Examination of the marrow revealed normal cell differentials in all limbs in all groups. Overall cellularity was somewhat decreased in the experimental limbs of the normal saline bolus group when compared with same-animal control limbs, perhaps due to the pressure effect from rapid injection. Peripheral blood counts and differentials in these and all other animals were normal. The authors conclude that IO administration of commonly used resuscitative medications does not result in significant adverse effects in the tibial bone marrow in this model.

Decreased follicular steroids and insulin-like growth factor-I and increased atresia in diabetic gilts during follicular growth stimulated with PMSG.

Four streptozotocin-diabetic gilts (maintained on exogenous insulin for 3 months) and 4 normoglycaemic gilts were treated with 600 i.u. PMSG. Diabetic gilts had insulin therapy removed at the time of PMSG administration. Plasma glucose averaged 463 +/- 5 mg/100 ml for diabetic gilts and 82 +/- 4 mg/100 ml for control gilts over the 72-h sampling period. Serum insulin was lower in diabetic than in normoglycaemic gilts (glycaemic state by time interaction; P less than 0.0001). At ovary removal 75 h after PMSG, numbers and percentages of large (greater than or equal to 7 mm) and medium (3-6 mm) non-atretic follicles were similar for diabetic and control gilts (31 vs 68%; s.e.m. = 7; P less than 0.05). Diabetic gilts had a greater percentage of atretic follicles over all size classes (50 vs 21%; s.e.m. = 7; P less than 0.03). After PMSG, LH was suppressed within 12 h in control gilts and remained similar to values in diabetic gilts until 72 h, when LH was elevated in 2 diabetic gilts (glycaemic state by time interaction; P less than 0.001). Pulsatile LH patterns during 52-55 h after PMSG were not affected by glycaemic state. Serum concentrations of IGF-I tended (P less than 0.1) to be lower in diabetic gilts. Concentrations of oestradiol and FSH in serum were similar in diabetic and control gilts. Follicular fluid concentrations of oestradiol in follicles greater than or equal to 7 mm were lower in diabetic than normoglycaemic gilts (341 vs 873 ng/ml; s.e.m. = 86; P less than 0.05). Testosterone was higher in follicles 3-6 mm in diameter in diabetic than in normoglycaemic gilts (142 vs 80 ng/ml; s.e.m. = 26; P less than 0.05). Progesterone concentrations in follicular fluid were not affected by glycaemic state. Concentrations of IGF-I in follicles greater than or equal to 7 mm were lower in diabetic than control gilts (150 vs 200 ng/ml; s.e.m. = 13; P less than 0.05). We conclude that follicles of diabetic gilts respond to external gonadotrophic stimulation with decreased hormone production and increased ovarian follicular atresia, despite an absence of effects on circulating gonadotrophin and oestradiol concentrations.

Prepubertal exposure to dietary zearalenone alters hypothalamo-hypophysial function but does not impair postpubertal reproductive function of gilts.

At an average age of 70 d, 60 Yorkshire gilts born either in July (Trial 1; n = 30) or August (Trial 2; n = 30) received a diet containing zearalenone for 0 (control), 45 or 90 d. The concentration of zearalenone in diets was 2 ppm for 2 wk and 1.5 ppm for the remainder of the study. Vulval swelling and reddening was evident within 7 d after zearalenone was first fed. Zearalenone consumption had no effect on BW or backfat depth. Puberty occurred in Trial 1 at 219 +/- 6 d and was not influenced by zearalenone. Gilts in Trial 2 were divided into two groups; blood samples were taken from 12 gilts to assess pulsatile LH patterns and LH response to estradiol benzoate (EB) and 18 were handled similarly to those in Trial 1. Of this latter subgroup, age at puberty was younger (P less than .05) with zearalenone (217 +/- 7.0, 193 +/- 9.1 and 185.6 +/- 8.2 d for 0-, 45-, and 90-d treatments). Prepubertal consumption of zearalenone did not affect conception rates, ovulation rates, number of fetuses or percentage of embryo survival following mating at pubertal estrus. Two days before the 90-d experimental period ended for Trial 2, blood samples were taken from 12 gilts (four/treatment) every 15 min for 4 h prior to injection of EB (10 micrograms/kg) and every 6 h for 108 h after EB. Analysis of pulsatile patterns of LH revealed no influence of zearalenone on the number of peaks/4 h, baseline concentration or peak height.(ABSTRACT TRUNCATED AT 250 WORDS)