The objectives of this experiment were to evaluate the effects of alternatives to antibiotic growth promoters (AGP), two group sizes, and their interaction on nursery pig performance to serve as a model for future AGP alternative studies. A 41-d experiment was conducted in a commercial wean-to-finish barn; 1,300 piglets weaned at 21 d of age (weaned 2 or 4 d prior to experiment; 6.14 ± 0.18 kg BW; PIC 1050 sows and multiple sire lines) were blocked by sire, sex, and weaning date, then assigned to eight treatments: four dietary treatments each evaluated across two group sizes. The four dietary treatments were: negative control (NC), positive control (PC; NC + in-feed antibiotics), zinc oxide plus a dietary acidifier (blend of fumaric, citric, lactic, and phosphoric acid) (ZA; NC + ZnO + acid), and a Bacillus-based direct-fed-microbial (DFM) plus resistant potato starch (RS) (DR; NC + DFM + RS). The two group sizes were 31 or 11 pigs/pen; floor space was modified so area/pig was equal between the group sizes (0.42 m2/pig). There were 7 pens/diet with 11 pigs/pen and 8 pens/diet with 31 pigs/pen. Data were analyzed as a randomized complete block design with pen as the experimental unit. Diagnostic assessment of oral fluids, serum, and tissue samples was used to characterize health status. Pigs experienced natural challenges of acute diarrhea and septicemia in week 1 and porcine reproductive and respiratory syndrome virus (PRRSV) in weeks 4–6. There was a significant interaction between diet and group size for ADG (P = 0.012). PC increased ADG in large and small groups (P < 0.05) and ZA increased ADG only in large groups (P < 0.05). Small groups had improved ADG compared to large groups when fed NC or DR diets (P < 0.05). Similarly, PC increased ADFI (P < 0.05). Compared to NC, ZA improved ADFI in large groups only (P < 0.05; diet × group size: P = 0.015). Pigs fed PC had greater G:F than NC (P < 0.05), and small groups had greater G:F than large groups (P < 0.05). There was no effect of ZA or DR on G:F. Pigs fed PC required fewer individual medical treatments than NC and pigs fed ZA were intermediate (P = 0.024). More pigs were removed from large than small groups (P = 0.049), and there was no effect of diet on removals (P > 0.10). In conclusion, careful study design, protocol implementation, sample collection, and recording of important information allowed us to characterize the health status of this group of pigs and determine treatment effects on growth performance and morbidity.
Previous research indicated that phytase may release less phosphorus (P) from phytate when it is evaluated using diets with P levels above requirement as compared with diets below requirement. The objectives of this experiment were to further test the hypothesis that the P release values determined for phytase are higher when pigs are fed diets that are deficient (DE) in P compared with when they are fed diets that are adequate (AD) in P, and that phytase will increase the digestibility of dry matter (DM), gross energy (GE), nitrogen (N), and calcium (Ca) independent of dietary P status. Twenty-four barrows (body weight: 23.2 ± 1.8 kg) were randomly assigned to one of eight dietary treatments and housed in individual pens for 21 d and then moved to metabolism crates for 9 d, with the collection of urine and feces occurring on the final 5 d. A basal corn–soybean meal diet (P-AD) was formulated at 0.36% standardized total tract digestible (STTD) P and total calcium:STTD P (Ca:STTD P) of 2:1. A P-DE diet was also formulated to maintain a constant Ca:STTD P of 2:1 in both basal diets. Phytase was added to AD and DE diets at 350, 600, 1,000 phytase units (FYT)/kg. Pig was the experimental unit; diet (P-AD or P-DE), phytase level, and replicate were fixed effects. Orthogonal polynomial contrasts were used to test linear and quadratic effects of phytase within P-AD and P-DE diets. Phytase improved apparent total tract digestibility (ATTD) and STTD of P in both P-AD (linear P < 0.001) and P-DE diets (quadratic P < 0.001). Estimates for STTD P release were 0.07%, 0.09%, and 0.09% for 350, 600, and 1,000 phytase units (FYT)/kg in P-DE diets, and 0.02%, 0.03%, and 0.05% in P-AD diets, respectively. In P-DE diets, phytase improved absorption and retention of P and increased urinary excretion of P (quadratic P < 0.001). In P-AD diets, phytase improved absorption of P (linear P = 0.066), tended to improve retention (linear P = 0.066), and increased urinary excretion of P (quadratic P = 0.021). Phytase improved ATTD of Ca in P-DE diets (quadratic P = 0.002) but not in P-AD diets (P > 0.1). In conclusion, the release of P by phytase is lower in diets that are AD in P than those which are DE. Phytase increased the availability of Ca only in the diets DE in P. Finally, phytase increased the ATTD of DM and tended to increase the ATTD of energy, independent of dietary P status.
Functional corpora lutea (CL) are required for pregnancy establishment and gestational maintenance in swine. Manganese (Mn) could be critical in regulating CL function since it is a cofactor for the enzyme Mn superoxide dismutase (Mn-SOD) as well as enzymes involved in progesterone (P4) synthesis. We hypothesized a more bioavailable dietary Mn source would increase CL Mn content thereby influencing luteal function during the mid-luteal phase of the estrous cycle. Post-pubertal gilts (n = 32) were assigned to one of four gestation diets. The control diet (CON) met or exceeded NRC requirements and was formulated to contain 20 ppm added Mn in the form of Mn sulfate. Three additional diets included 20 (TRT1), 40 (TRT2) or 60 (TRT3) ppm Mn from a Mn-amino acid complex (Availa-Mn; Zinpro Corporation) in place of Mn sulfate. Dietary treatment began at estrus synchronization onset and continued through D12 of the ensuing estrous cycle when gilts were euthanized. Mn content increased (P ≤ 0.06) 19, 21 and 24% in CLs of gilts fed TRT1, TRT2, and TRT3, respectively, and luteal P4 concentration decreased (P ≤ 0.03) 25, 26, and 32% in gilts fed TRT1, TRT2, and TRT3, respectively, compared to CON. Total CL protein was extracted and liquid chromatography with tandem mass spectrometry (LC-MS/MS) was performed to assess global protein abundance. Compared to CON, 29, 105, and 118 proteins were differentially abundant (P < 0.01) in TRT1, TRT2, and TRT3, respectively. KEGG pathway analysis revealed proteins involved in P4 signaling (membrane-associated P4 receptor component 2) and cholesterol synthesis and transport (mevalonate kinase, diphosphomevalonate decarboxylase, low density lipoprotein receptor) were downregulated in response to Availa-Mn. Collectively, these data support the posit that dietary Mn source affects Mn accumulation and P4 concentration in CL tissue and influences protein abundance which may affect CL function.
An experiment was conducted to determine the optimal dietary concentration of standardized total tract digestible (STTD) Ca for growth and feed efficiency of nursery pigs. A total of 2,185 pigs (initial BW =11.2 ± 1.4 kg) were blocked according to BW and randomly allotted to 1 of 6 dietary treatments, with STTD Ca formulated to 0.38, 0.46, 0.54, 0.62, 0.70, or 0.78% by increasing dietary limestone at the expense of corn. Each treatment had 16 replicate pens with 23 pigs per pen. Corn and soybean-based diets were formulated to contain 0.36% STTD P, which exceeds NRC 2012 (+9%). This resulted in STTD Ca: STTD P ranging from 1.1 to 2.2. To minimize variation, 2 basal diets were produced (0.38 and 0.78% Ca diets), and then blended on site to produce the intermediary levels. Data were analyzed using the MIXED procedure of SAS (Cary, NC) with fixed effect of diet and random effect of block. Prediction equations were generated using the FITTED GROUP of JMP with goodness of fit techniques to optimize the R2 value and RMSE. Feed conversion ratio (FCR) declined linearly (P = 0.011) with increasing levels of STTD Ca in the diet, and is described by: FCR = [1.456 + (0.115 x STTD Ca)] (R2 = 0.698, RMSE = 0.013). Final pig weight tended to increase (quadratic, P = 0.110) as dietary STTD Ca increased, and is described by: BW = [22.77 – (0.55 x STTD Ca) – (7.72 x (STTD Ca – 0.58)2] (R2 = 0.696, RMSE = 0.135). Exceeding 0.70% STTD Ca (2.0:1.0 STTD Ca: STTD P) reduced pig growth, FCR, and profitability. Adequate STTD Ca levels ranged from 0.46 to 0.62% (STTD Ca:STTD P, 1.3 to 1.8), but growth and profit were optimized at 0.54% (1.5:1.0 STTD Ca: STTD P).
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