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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.

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The objective of this study was to quantify the effect of heat stress during the life of a pig on its final weight, as a first step toward a genetic evaluation for heat tolerance. Data included carcass weights of 23,556 crossbred pigs [Duroc x (Landrace x Large White)] raised on 2 farms in North Carolina and slaughtered from May 2005 through December 2006. Weather data were available from a nearby weather station. Lifetime of a pig was assumed to be partitioned into 2 periods. During an initial period, the effect of heat stress was assumed to be negligible or compensated for later. During the second period ending in slaughtering, the ADG was assumed to be affected linearly by heat load. Weekly heat load was calculated as degrees of average temperature-humidity index in excess of a threshold (18 degrees C). The total heat load (H) was the sum of weekly heat loads during the second period. During the months of January to May H was 0; H reached a peak in September. The final BW during the peak of heat stress decreased about 6 kg compared with BW during months of non-heat stress. Weekly and monthly averages of carcass weight generally moved similarly to H. However, there were large fluctuations unrelated to H; the fluctuations were different on the 2 farms. The model included the effects of farm-year of slaughter, sex, age at slaughter, and H, where age at slaughter and H were linear regressions. In analyses, the threshold was varied from 16 to 20 degrees C, and the second period was varied from 8 to 16 wk. The greatest R(2) (10.4%) was at the threshold of temperature-humidity index = 18 degrees C for a period of 10 wk. Varying the threshold and the length of time reduced R(2) less than 1%. Least squares means of year-month and year-week of carcass weight were calculated using a model with the fixed effects farm-year-month or farm-year-week of slaughter, sex, and age at slaughter (linear covariate), and the random effect of birth litter. Changes in BW of finisher pigs due to heat stress can be quantified by H during the last 10 wk of the life of the pig.