One hundred pigs from the NE Index Line (NEI) and 100 Hampshire-Duroc cross pigs (HD) were inoculated intranasally with porcine respiratory and reproductive syndrome virus (PRRSV 97-7895 strain) at 26 d of age to determine whether genetic variation in response to PRRSV exists. An uninfected littermate to each infected pig served as a control. Pigs were from 163 dams and 83 sires. Body weight and rectal temperature were recorded, and blood samples were drawn from each pig on d 0 before inoculation and on d 4, 7, and 14 after inoculation. Pigs were sacrificed on d 14. Lung and bronchial lymph nodes were collected, placed in optimal cutting temperature compound, and frozen at -80 degrees C. The presence of PRRSV in serum and in lung tissue and bronchial lymph nodes was determined by isolation in cell culture. The presence of antibodies in serum collected on d 14 was determined by a commercial ELISA test. Lung tissue was examined microscopically and scored for incidence and severity of lesions (score of 1 to 3; 1 = no or few lesions, and 3 = severe interstitial pneumonia). Data were analyzed with a mixed model that included random sire and dam effects. The interaction of line x treatment was significant (P < 0.001) for weight change and rectal temperature. Un-infected HD pigs gained 0.67 kg more from d 0 to 14 and averaged 0.32 degrees C higher rectal temperature than uninfected NEI pigs (P < 0.001), whereas infected NEI pigs gained 0.34 kg more and had -0.54 degrees C lower temperature than infected HD pigs (P < 0.001). Viremic titer (cell culture infectious dose 50%/mL) was greater (P < 0.05) in HD than NEI at d 4 (10(4.52) vs. 10(4.22)), 7 (10(4.47) vs. 10(3.99)), and 14 (10(3.49) vs. 10(3.23)). Viral titer loads in lung (P = 0.11) and bronchial lymph nodes tended (P = 0.07) to be greater in HD than NEI pigs. Antibody signal-to-positive (S/P) ELISA ratios in infected pigs ranged from 0.18 to 3.38, and 88% had levels > or = 0.40, which is the positive threshold for this ELISA. The S/P range in uninfected pigs was 0 to 1.11, and 99% had levels < or = 0.40. Mean S/P ratio for infected pigs was 0.23 units higher in HD than in NEI (P < 0.001). The HD pigs had a greater incidence of interstitial pneumonia and 0.65 higher mean lesion scores than NEI pigs (P < 0.001). In summary, responses of pigs of the two lines to infection with PRRSV differed, indicating that underlying genetic variation existed.

ABSTRACT:One hundred Hampshire × Duroc crossbred pigs (HD) and 100 NE Index line (I) pigs were infected with porcine reproductive and respiratory syndrome (PRRS) virus and evaluated for resistance/susceptibility. Controls (100/line) were uninfected littermates to the infected pigs. Viremia, change in weight (WT⌬), and rectal temperature at 0, 4, 7, and 14 d postinfection were recorded. Lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 d postinfection). The first principal component from principal component analyses of all variables was used to rank the pigs for phenotypic response to PRRS virus. Low responders (low PRRS burden) had high WT⌬, low viremia, and few lung lesions; high responders (high PRRS burden) had low WT⌬, high viremia, and many lesions. The RNA was extracted from lung and BLN tissue of the 7 highest and 7 lowest responders per line

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Two experiments were conducted to evaluate the effects of adding combinations of wheat middlings (midds), distillers dried grains with solubles (DDGS), and choice white grease (CWG) to growing-finishing pig diets on growth, carcass traits, and carcass fat quality. In Exp. 1, 288 pigs (average initial BW = 46.6 kg) were used in an 84-d experiment with pens of pigs randomly allotted to 1 of 4 treatments with 8 pigs per pen and 9 pens per treatment. Treatments included a corn-soybean meal-based control, the control with 30% DDGS, the DDGS diet with 10% midds, or the DDGS diet with 20% midds. Diets were fed in 4 phases and formulated to constant standardized ileal digestible (SID) Lys:ME ratios within each phase. Overall (d 0 to 84), pigs fed diets containing increasing midds had decreased (linear, P ≤ 0.02) ADG and G:F, but ADFI was not affected. Feeding 30% DDGS did not influence growth. For carcass traits, increasing midds decreased (linear, P < 0.01) carcass yield and HCW but also decreased (quadratic, P = 0.02) backfat depth and increased (quadratic, P < 0.01) fat-free lean index (FFLI). Feeding 30% DDGS decreased (P = 0.03) carcass yield and backfat depth (P < 0.01) but increased FFLI (P = 0.02) and jowl fat iodine value (P < 0.01). In Exp. 2, 288 pigs (initial BW = 42.3 kg) were used in an 87-d experiment with pens of pigs randomly allotted to 1 of 6 dietary treatments with 8 pigs per pen and 6 pens per treatment. Treatments were arranged in a 2 × 3 factorial with 2 amounts of midds (0 or 20%) and 3 amounts of CWG (0, 2.5, or 5.0%). All diets contained 15% DDGS. Diets were fed in 4 phases and formulated to constant SID Lys:ME ratios in each phase. No CWG × midds interactions were observed. Overall (d 0 to 87), feeding 20% midds decreased (P < 0.01) ADG and G:F. Pigs increasing CWG had improved ADG (quadratic, P = 0.03) and G:F (linear, P < 0.01). Dietary midds or CWG did not affect ADFI. For carcass traits, feeding 20% midds decreased (P < 0.05) carcass yield, HCW, backfat depth, and loin depth but increased (P < 0.01) jowl fat iodine value. Pigs fed CWG had decreased (linear, P < 0.05) FFLI and increased (linear, P < 0.01) jowl fat iodine value. In conclusion, feeding midds reduced pig growth performance, carcass yield, and increased jowl fat iodine value. Although increasing diet energy with CWG can help mitigate negative effects on live performance, CWG did not eliminate negative impacts of midds on carcass yield, HCW, and jowl fat iodine value.

Differences in gene expression were compared between RNAs from lungs of high (HR) and low (LR) porcine reproductive and respiratory syndrome virus (PRRSV) burden pigs using the swine protein-annotated long oligonucleotide microarray, the Pigoligoarray. Pathway analyses were carried out to determine biological processes, pathways and networks that differ between the LR and HR responses. Differences existed between HR and LR pigs for 16 signalling pathways [P < 0.01/-log (P-value) >1.96]. Top canonical pathways included acute phase response signalling, crosstalk between dendritic cells and natural killer cells and tight junction signalling, with numerous immune response genes that were upregulated (SOCS1, SOD2, RBP4, HLA-B, HLA-G, PPP2R1A and TAP1) or downregulated (IL18, TF, C4BPA, C1QA, C1QB and TYROBP). One mechanism, regulation of complement activation, may have been blocked in HR (PRRSV-susceptible) pigs and could account for the poor clearance of PRRSV by infected macrophages. Multiple inhibiting signals may have prevented effective immune responses in susceptible HR pigs, although some protective genes were upregulated in these pigs. It is likely that in HR pigs, expression of genes associated with protection was delayed, so that the immune response was not stimulated early; thus, PRRSV infection prevented protective immune responses.