Reaction norm for reproductive performance during Porcine Reproductive and Respiratory Syndrome (PRRS) and Porcine Epidemic Diarrhea (PED) outbreaks

PRRS and PED are two diseases with the largest economic impact in the swine industry. However, information regarding the relationship between host genetics and levels of disease impact has not been studied. The purpose of this study was to estimate reaction norms to evaluate the host genetic response in reproductive sows naturally infected with PRRS or PED.

Performance data and a five-generation pedigree were available from 10 commercial farms in North Carolina. A total of 21,060 farrow events from 5,448 crossbred (Large White x Landrace) multiparous sows were used for analyses. Traits included number of piglets born alive (NBA), of stillborn piglets (SB), of mummified piglets (MUM), born dead (NBD), and weaned (NW). Originally, PED and PRRS outbreaks were identified based on observations at the farms and confirmed by serological results. However, the dates of the PED and PRRS outbreak phases on each farm were determined based on data, using herd-year-week (HYW) estimates of the reproductive performance. A total of 8 and 15 outbreaks were identified for PRRS and PED, respectively. First-order reaction norm analyses included the fixed effects of HYW (covariate), season, disease phase, parity, year, and farm the random additive effect of intercept and slope (HYW). Separate analyses were performed for each disease: clean and PRRS phases, and clean and PED phases. The clean phase was defined as a time when reproductive performance returned to normal levels of production based on the HYW estimates. Traits with a large number of zeros (SB, MUM, and NBD) were analyzed as the natural log of the phenotype + 1. Analyses were done in ASReml4.

For PRRS, heritability estimates for plasticity (slope) were 0.24±0.04 (NBA), 0.20±0.03 (SB), 0.40±0.02 (MUM), 0.10±0.02 (NBD), and 0.83±0.01 (NW). For PED, these were 0.25±0.04, 0.19±0.02, 0.27±0.02, 0.21±0.03, and 0.81±0.01, respectively. The heritability of the intercept ranged from 0.05±0.01 (NW) to 0.16±0.01 (NBA) for PRRS. For PED, heritability of the intercept ranged from 0.03±0.01 (NW) to 0.15±0.01 (NBA). For PRRS genetic correlations between the intercept and slope were -0.45±0.07 (NBA), 0.59±0.07 (SB), 0.80±0.05 (MUM), 0.96±0.09 (NBD), and -0.84±0.02 (NW). For PED, these were -0.48±0.08, 0.63±0.07, 0.85±0.05, 0.52±0.08, and -0.82±0.03, respectively

These results show a clear genotype-by-environmental interaction for both diseases. The only trait with considerable re-ranking of animals was NBA for both diseases. In addition, the response to PRRS and PED was similar, which is advantageous for selection for improved performance in both disease environments simultaneously.