African swine fever virus (ASFV) is a contagious, rapidly spreading, transboundary animal disease and a major threat to pork production globally. Although plant-based feed has been identified as a potential route for virus introduction onto swine farms, little is known about the risks for ASFV transmission in feed. We aimed to determine the minimum and median infectious doses of the Georgia 2007 strain of ASFV through oral exposure during natural drinking and feeding behaviors. The minimum infectious dose of ASFV in liquid was 10 0 50% tissue culture infectious dose (TCID 50 ), compared with 10 4 TCID 50 in feed. The median infectious dose was 10 1.0 TCID 50 for liquid and 10 6.8 TCID 50 for feed. Our findings demonstrate that ASFV Georgia 2007 can easily be transmitted orally, although higher doses are required for infection in plant-based feed. These data provide important information that can be incorporated into risk models for ASFV transmission.

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.

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.

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.

This study evaluated responses of the systemic endocrine stress (cortisol) and growth (IGF-I, GH) axes, as well as those of inflammatory mediators (prostaglandin E2 [PGE2] and tumor necrosis factor alpha [TNFalpha]), to active infection with Salmonella typhimurium. Eighteen crossbred barrows were penned individually with ad libitum access to feed and water. After an acclimation period, jugular catheters were placed in all animals. Control pigs received sterile broth orally (CON, n = 7), whereas the treated pigs (S.TYP, n = 11) received 3 x 10(9) cfu of S. typhimurium orally. Plasma was collected at 6-h intervals from -48 to 120 h. Body weights, feed intake, and rectal temperatures also were monitored. Rectal temperatures were elevated in S.TYP pigs (P < .01) relative to CON pigs by 12 h, peaked at 42 h (P < .001), and remained elevated throughout the remainder of the study. Feed intake was reduced maximally in S.TYP pigs at 48 h (P < .001) and remained reduced through 120 h after the challenge. Daily body weight gain also was reduced during the 2 wk following infection (P < .001). Plasma cortisol concentrations increased (P < .05) at 18 h after the challenge in S.TYP pigs and remained elevated generally until 60 h after infection. A marked suppression of plasma IGF-I occurred in S.TYP pigs beginning at 30 h after infection (P < .001), and it remained lower through 108 h. Plasma GH was not affected consistently by treatment, nor did infection alter plasma TNFalpha and PGE2. Taken together, the results reveal that infectious processes produce profound alterations in the endocrine stress and the somatotropic axis, and this may occur in the absence of significant changes in systemic proinflammatory mediators.

The objective of this research was to provide an integrated look at systemic adrenal, somatotropic, and immune responses of growing pigs to challenge with lipopolysaccharide (LPS). Weaned pigs were challenged intraperitoneally with 100 microg/kg BW of LPS or sterile saline, and rectal temperature and blood data were collected for 72 h. Daily feed intake also was monitored. Plasma was analyzed for concentrations of cortisol, tumor necrosis factor alpha (TNFalpha), the acute phase protein haptoglobin, growth hormone (GH), insulin-like growth factor I (IGF-I), and prostaglandin E2 (PGE2). As expected, LPS decreased feed intake, stimulated a febrile response, and activated the hypothalamic-pituitary-adrenal (HPA) axis as demonstrated by increased cortisol levels. Cortisol reached maximum elevation 2 h after treatment (P < .001) and remained elevated through 12 h (P < .001). Circulating TNFalpha was increased by LPS at 2 and 4 h after treatment (P < .001), and an apparent (not statistically significant) increase in haptoglobin also occurred in challenged animals. The LPS injection suppressed IGF-I by 2 h following treatment (P < .01), and circulating IGF-I remained reduced relative to controls through 44 h. Overall, GH was increased in LPS-treated pigs (P < .05), although the treatment x time interaction was not significant. Plasma PGE2 was increased transiently at 2 h (P < .05) and then subsequently suppressed at 4, 8, and 12 h following LPS (P < .05). This study provides a comprehensive view of systemic effects of LPS on components of the HPA, growth, and immune axes. In addition, these are the first data to document changes in circulating PGE2 in unrestrained animals during the early hours of the acute phase response to LPS.

The objective of this study was to determine the effects of diets containing crude glycerol on pellet mill production efficiency and nursery pig growth performance. In a pilot study, increasing crude glycerol (0, 3, 6, 9, 12, and 15%) in a corn-soybean meal diet was evaluated for pellet mill production efficiency. All diets were steam conditioned to 65.5 degrees C and pelleted through a pellet mill equipped with a die that had an effective thickness of 31.8 mm and holes 3.96 mm in diameter. Each diet was replicated by manufacturing a new batch of feed 3 times. Increasing crude glycerol increased both the standard (linear and quadratic, P < 0.01) and modified (linear, P < 0.01; quadratic, P

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