An experiment was conducted to determine whether baby pigs develop hypersensitivity to dietary soybean proteins. Thirty-two pigs were orally infused with either dried skim milk (5 g/d; control) or soybean meal (48% CP; 5 g/d) from d 7 to 14 after birth. Sows were fed a corn-corn gluten meal-based diet supplemented with lysine and tryptophan to avoid exposure of pigs to soybean proteins. Pigs were weaned at 21 d of age and fed diets containing either soybean meal or milk proteins until d 56. One half of the pigs were killed at 28 d of age and the rest at 56 d of age. Segments of small intestine were collected, and intraepithelial lymphocytes were isolated. At 28 d of age, pigs fed diets containing soybean meal had lower (P less than .05) villus height (221 vs 298 microns) and rate of gain (86 vs 204 g/d) than control pigs did. Pigs fed a diet containing soybean meal had higher (P less than .05) immunoglobulin G (IgG) titers to soybean protein than did pigs fed a milk protein-based diet. Blood and intestinal lymphocytes collected on d 28 and 56 did not exhibit any proliferative response when cultured with purified soy proteins (2.5 or 5 microns/ml). Phytohemagglutinin- and pokeweed mitogen-induced lymphocyte proliferations were higher (P less than .05) at d 56 than at d 28, but there were no differences attributable to protein source. There were no differences (P greater than .05) in skin-fold thickness measurements following intradermal injection with soy or milk proteins. Decreased villus height and increased serum IgG titers to soybean proteins coinciding with inferior performance of early weaned pigs fed diets containing soybean meal indicate that conventionally processed, commercial soybean meal may retain some antigens that can cause transient hypersensitivity in piglets.
Multiparous sows (n = 307) were used to evaluate the effects of added dietary L-carnitine, 100 mg/d during gestation and 50 ppm during lactation, on sow and litter performance. Treatments were arranged as a 2 (gestation or lactation) x2 (with or without L-carnitine) factorial. Control sows were fed 1.81 kg/d of a gestation diet containing .65% total lysine. Treated sows were fed 1.59 kg/d of the control diet with a .23 kg/d topdressing of the control diet that provided 100 mg/d of added L-carnitine. Lactation diets were formulated to contain 1.0% total lysine with or without 50 ppm of added L-carnitine. Sows fed 100 mg/d of added L-carnitine had increased IGF-I concentration on d 60 (71.3 vs. 38.0 ng/mL, P<.01) and 90 of gestation (33.0 vs. 25.0 ng/mL, P = .04). Sows fed added L-carnitine had increased BW gain (55.3 vs 46.3 kg; P<.01) and last rib fat depth gain (2.6 vs. 1.6 mm; P = .04) during gestation. Feeding 100 mg/d of added L-carnitine in gestation increased both total litter (15.5 vs. 14.6 kg; P = .04) and pig (1.53 vs 1.49 kg; P<.01) birth weight. No differences were observed in pig birth weight variation. Added L-carnitine fed during gestation increased litter weaning weight (45.0 vs. 41.3 kg, P = .02); however, no effect of feeding L-carnitine during lactation was observed. No differences were observed in subsequent days to estrus or farrowing rate. Compared to the control diet, feeding added L-carnitine in either gestation, lactation, or both, increased (P<.05) the subsequent number of pigs born alive, but not total born. In conclusion, feeding L-carnitine throughout gestation increased sow body weight and last rib fat depth gain and increased litter weights at birth and weaning.
Two trials were conducted to determine the suitability of soybean products for baby pigs. Weanling pigs (n = 40 and 48 in Trials 1 and 2, respectively) were infused orally (6 g/d) with dried skim milk, soybean meal (SBM, 48% CP); soy protein concentrate, moist extruded soy protein concentrate, or soy protein isolate from d 7 to 12 of age. Pigs were then fed a diet containing the same protein source for 1 (Trial 1) or 2 (Trial 2) wk after weaning (d 21 of age). To avoid exposure of pigs to soybean proteins, the dams of pigs were fed a corn-corn gluten meal-based diet supplemented with lysine and tryptophan from d 109 of gestation. All pigs in Trial 1 were killed at 28 d of age, and samples of ileal digesta and small intestine were obtained. In Trial 2, the soy protein isolate was not included, and all pigs were fed a diet containing 4% soybean oil and 1.25% lysine for the last 3 wk of the trial. Growth performance, skin-fold thickness, after intradermal injection of extracts of the corresponding proteins, and anti-soy immunoglobulin G (IgG) titers were measured. Results indicated that pigs fed diets containing SBM had lower (P less than .05) villus height and xylose absorption but higher (P less than .05) serum anti-soy IgG titers and increased skin-fold thickness compared with the mean of pigs given milk and all other soy treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
Three experiments, using 344 pigs, were conducted to evaluate the influence of beta-glucan on growth performance, neutrophil and macrophage function, haptoglobin production, and resistance to Streptococcus suis challenge in weanling pigs. In Exp. 1, 144 pigs were used to evaluate the influence of .1% dietary beta-glucan in a soybean meal- or milk protein-based diet on growth performance and neutrophil function. Pigs fed beta-glucan from d 7 to 14 after weaning had lower ADFI (P < .01) and, although not significant, ADG was lower for pigs fed beta-glucan than for pigs fed control diets. However, no differences were observed in growth performance or neutrophil function for pigs fed control or diets containing beta-glucan from d 7 to 35 after weaning. Experiment 2 was a 28-d growth assay in which pigs were fed a diet with or without .1% beta-glucan, containing 7.5% spray-dried plasma protein and 25% dried whey from d 0 to 14 after weaning. Pigs then were fed corn-soybean mealbased diets containing 2.5% spray-dried blood meal and 10% dried whey. No differences in growth performance were observed. Experiment 3 was a 35-d assay to evaluate growth performance, neutrophil and macrophage function, and plasma haptoglobin concentration. Pigs were challenged on d 28 postweaning with intravenous S. suis. In Exp. 3, pigs were fed diets without or with .025 or .05% beta-glucan. Dietary beta-glucan did not influence neutrophil or macrophage function. However, pigs fed diets containing .025% beta-glucan had increased (P < .05) ADG and ADFI and were heavier (P < .05) on d 28 after weaning than pigs fed the control diet. No differences in feed efficiency (G/F) were detected between treatments. Pigs fed beta-glucan had decreased (P < .10) plasma haptoglobin on d 14, 21, and 28 after weaning. However, Fisher's Exact test revealed that more (P < .04) pigs fed a diet containing .025% beta-glucan died by d 12 after challenge with S. suis. In conclusion, these data suggest the existence of a complex interaction involving growth performance and resistance to S. suis in pigs fed .025% beta-glucan.
Three growth assays were conducted to determine the efficacy of replacing dried skim milk and(or) dried whey in diets of starting pigs with commercially available spray-dried porcine plasma, spray-dried porcine blood, spray-dried bovine plasma, or spray-dried extracted meat protein. In Exp. 1, 236, 24-d-old crossbred pigs were fed diets containing either skim milk and whey or porcine plasma from 0 to 14 d postweaning and whey or porcine plasma from 14 to 28 d. Although pigs fed diets containing porcine plasma had greater ADFI and ADG than those fed milk products from 0 to 7 d, no differences were observed from d 0 to 14 or from 14 to 28 d postweaning. In Exp. 2, 204, 21-d-old pigs were fed corn-soybean meal-based diets using the following supplemental protein source combinations: skim milk and whey; skim milk, whey, and casein; porcine plasma, whey, and lactose/starch (10%); porcine plasma and lactose/starch (24.4%); or whey. A common diet (1.25% lysine, 10% whey) was fed from 14 to 35 d postweaning. Pigs fed diets containing porcine plasma consumed more feed and had greater ADG than others (P < .05) from 0 to 14 d and from 0 to 35 d. Both ADG and ADFI were highest when the diet contained 10.3% porcine plasma, 20% whey, and 10% added lactose. Experiment 3 used 150, 21-d-old pigs to compare the inclusion of skim milk, porcine plasma, porcine blood, bovine plasma, or meat extract in diets fed from 0 to 14 d postweaning. A common diet (the same as in Exp. 2) was fed from 14 to 35 d. Pigs fed porcine plasma had greater ADFI (P < .05) from 0 to 14 d than pigs fed other treatments. Also, pigs fed porcine plasma had greater ADG (P < .05) from 0 to 14 d than pigs fed all other diets except porcine blood. Pigs fed porcine blood had the largest ADFI (P < .05) from 14 to 35 d compared with pigs fed other diets. These experiments indicate that porcine plasma is a protein supplement superior to skim milk in diets of starting pigs and that porcine blood has a positive influence on subsequent growth performance.
Two experiments were conducted to evaluate the effect of dietary L-carnitine on growth performance and body composition of early-weaned pigs. In Exp. 1, 120 weanling pigs (initially 5.6 kg and 19 +/- 2 d of age) were allotted in a 3 x 2 factorial with four pigs per pen and five replications (pens) per treatment. Main effects from d 0 to 14 after weaning included dietary L-carnitine (0, 500, or 1,000 ppm) and soybean oil (0 to 10%). From d 14 to 35 after weaning, levels were reduced to 0, 250, or 500 ppm L-carnitine and 0 or 5% soybean oil. No L-carnitine x soybean oil interactions were observed (P > .10). From d 0 to 14, L-carnitine and soybean oil had no effect (P > .10) on pig performance. From d 14 to 35 and d 0 to 35, gain:feed ratio (G/F) improved (linear, P < .05) with increasing dietary L-carnitine; however, ADG and ADFI were not affected. Soybean oil improved ADG and G/F (P < .05) from d 14 to 35 and ADG from d 0 to 35. In Exp. 2, 180 weanling pigs (initially 6.0 kg and 22 +/- 2 d of age) were allotted in a 2 x 3 factorial. Pigs were fed either 0 or 1,000 ppm L-carnitine from d 0 to 14 after weaning and then pigs fed each of these diets were fed diets containing 0, 250, or 500 ppm L-carnitine from d 14 to 35. No interactions occurred between feeding L-carnitine from d 0 to 14 and performance observed from d 14 to 35. From d 0 to 14 after weaning, L-carnitine increased ADG (P < .08) and ADFI (P < .02). From d 14 to 35, ADFI decreased (linear, P < .05) and G/F increased (quadratic, P < .05) as dietary L-carnitine increased. Cumulative (d 0 to 35) ADFI decreased (linear, P < .05) and G/F increased (linear, P < .05) with increasing L-carnitine. On d 35, 14 pigs from each of four selected treatments (0 or 1,000 ppm L-carnitine from d 0 to 14 followed by either 0 or 500 ppm from d 14 to 35) were slaughtered, and carcass composition was recorded. Carcass moisture and CP percentages were not influenced (P > .10) by dietary L-carnitine. However, pigs fed 1,000 ppm L-carnitine from d 0 to 14 had less (P < .05) carcass lipid and daily lipid accretion on d 35 whether they were fed L-carnitine from d 14 to 35 or not. These results suggest that dietary L-carnitine improves G/F and reduces carcass lipid accretion in early-weaned pigs.
Two trials were conducted to determine the effects of weaning age on pig performance in a multisite production system. The second trial also evaluated the effects of modifying the nursery feeding program according to weaning age. In Trial 1 (2,272 pigs), treatments included weaning litters at 12, 15, 18, or 21 d of age. In Trial 2 (3,456 pigs), litters were weaned at 15, 16, 18, 19, 21, or 22 d of age and categorized into three treatments (15.5, 18.5, or 21.5 d of age). In Trial 2, pigs in each age group were fed one of two nursery feeding programs. Nursery feeding programs varied in both diet formulation and in the quantity of diets fed containing increased levels of whey and spray-dried animal plasma. Each trial was conducted as a randomized complete block design with four blocks of nursery and finishing sites. All weaning-age treatments were weaned from a 7,300-sow farm on the same day into the same nursery. Each block remained intact as pigs moved from nursery to finishing site. Increasing weaning age (12, 15, 18, or 21 d in Trials 1; and 15.5, 18.5, or 21.5 d in Trial 2) increased (linear, P < 0.001) ADG (299, 368, 409, 474 +/- 7 g/d; 435, 482, 525 +/- 13 g/d) and tended to decrease (linear, P < 0.09) mortality (5.25, 2.82, 2.11, 0.54 +/- 0.76%; 2.17, 1.56, 1.30 +/- 0.36%) in the initial 42 d after weaning. Finishing ADG (722, 728, 736, 768 +/- 11 g/d; 783, 790, 805 +/- 11 g/d) also improved (linear, P < 0.01) with increasing weaning age. Overall, increasing weaning age increased (linear, P < 0.001) wean-to-finish ADG (580, 616, 637, 687 +/- 8 g/d; 676, 697, 722 +/- 6 g/d), weight sold per pig weaned (94.1, 100.5, 104.4, 113.1 +/- 1.3 kg; 107.6, 111.6, 116.2 +/- 1.1 kg), and decreased (linear, P < 0.03) mortality rate (9.4, 7.9, 6.8, 3.6 +/- 0.95%; 3.9, 3.4, 2.5 +/- 0.5%). Altering the nursery feeding program did not affect wean-to-finish growth performance. In this multisite production system, increasing weaning age from 12 to 21.5 d of age increased weight sold per pig weaned by 1.80 +/- 0.12 kg for each day increase in weaning age. These studies suggest increasing weaning age up to 21.5 d can be an effective management strategy to improve wean-to-finish growth performance in multisite pig production.
Our objective was to determine an optimum Lys:calorie ratio (g of total dietary Lys/Mcal of ME) for 35- to 120-kg barrows and gilts (Pig Improvement Company, L337 x C22) in a commercial finishing environment. Seven (3 barrow and 4 gilt) trials were conducted using randomized complete block designs (42 pens per trial, a total of 7,801 pigs). Six treatments with increasing Lys:calorie ratio were used in each study. Diets were corn-soybean meal-based with 6% choice white grease. Lysine:calorie ratios were attained by adjusting the amount of corn and soybean meal. No crystalline Lys was used. In barrow trial 1 (43 to 70 kg), increasing the Lys:calorie ratio (2.21, 2.55, 2.89, 3.23, 3.57, and 3.91) increased (quadratic, P < 0.01) ADG, G:F, income over feed costs (IOMFC), and feed cost per kilogram of gain, and decreased (linear, P < 0.01) backfat. In barrow trial 2 (69 to 93 kg), increasing the Lys:calorie ratio (1.53, 1.78, 2.03, 2.28, 2.53, and 2.78) improved (linear, P < 0.01) ADG, G:F, and IOMFC, and decreased (quadratic, P < 0.01) backfat. In barrow trial 3 (102 to 120 kg), increasing the Lys:calorie ratio (1.40, 1.60, 1.80, 2.00, 2.20, and 2.40) increased (linear, P < 0.03) ADG and G:F, and numerically improved (linear, P = 0.12) IOMFC. In gilt trials 1 (35 to 60 kg), 2 (60 to 85 kg), and 3 (78 to 103 kg), increasing the Lys:calorie ratio (2.55, 2.89, 3.23, 3.57, 3.91, and 4.25; 1.96, 2.24, 2.52, 2.80, 3.08, and 3.36; and 1.53, 1.78, 2.03, 2.28, 2.53, and 2.78, respectively) improved (quadratic, P < 0.04) ADG, G:F, IOMFC, and feed cost per kilogram of gain, and decreased (linear, P < 0.01) backfat. In gilt trial 4 (100 to 120 kg), increasing the Lys:calorie ratio (1.40, 1.60, 1.80, 2.00, 2.20, and 2.40) improved (linear, P < 0.02) ADG, G:F, LM depth, IOMFC, and (quadratic, P < 0.06) feed cost per kilogram of gain. These studies suggest that feed cost per kilogram of gain decreases, and reductions in biological performance and IOMFC are rather modest when feeding marginally Lys-deficient diets early (35 to 70 kg) in the grower-finishing period compared with the more severe penalties in growth and economic performance of feeding marginally deficient diets in the late finishing period (70 kg to slaughter). The equations (Lys:calorie ratio = -0.0133 x BW, kg, + 3.6944 and = -0.0164 x BW, kg, + 4.004, for barrows and gilts, respectively) best describe our interpretation of the Lys:calorie ratio that met biological requirements and optimized IOMFC on these pigs (PIC, L337 x C22; 35 to 120 kg) in this commercial finishing environment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.