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This Article Full Text (PDF) All Versions of this Article: jas.2008-0892v1 87/3/876    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lewis, C.R.G. Articles by Bishop, S.C. Search for Related Content PubMed PubMed Citation Articles by Lewis, C.R.G. Articles by Bishop, S.C.

Genetic parameters for performance traits in commercial sows estimated before and after an outbreak of porcine reproductive and respiratory syndrome (PRRS)

C.R.G. Lewis^*, M. Torremorell, L. Galina-Pantoja and S.C. Bishop^*

^* The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Midlothian, EH25 9PS, United Kingdom PIC / Genus plc, Hendersonville, TN, 37075, USA

craig.lewis{at}roslin.ed.ac.uk

Abstract

Porcine reproductive and respiratory syndrome (PRRS), caused by the PRRS virus (PRRSV), is globally the most economically important disease in commercial pigs, and novel control strategies are sought. This paper explores the potential to use host genetics to decrease the impact of PRRS on reproductive sows. Commercial pig data (7,542 phenotypic records) from a farm undergoing an outbreak of PRRSV were analyzed to assess the impact of PRRS on reproductive traits and the inheritance of such traits. First, differing methodologies were used to partition the data into time periods when the farm was disease free and when the farm was experiencing PRRSV outbreaks. The methods were a date/threshold (DT) method based on veterinary diagnosis and a threshold/threshold (TT) method based on trends in underlying performance data, creating the DTD and TTD datasets, respectively. The TT method was more stringent in defining periods when PRRS was likely to be having an impact on reproductive performance, resulting in a dataset (TTD) that was slightly smaller (1,977 litters from 1,526 sows) than that from the DT method (3,164 litters and 1,662 sows), and it showed more pronounced impacts of PRRS on performance. Impacts on performance included significant increases in mean values of mummified and stillborn piglets (0.04 to 1.13 and 0.63 to 1.02 respectively) with a significant decrease in total born alive (10.3 to 9.08). Estimated heritabilities during the healthy phase were generally lower (mummified piglets = 0.03 ± 0.01, matings per conception = 0.04 ± 0.01) than during the PRRSV outbreak (TTD dataset) (mummified piglets = 0.10 ± 0.03, matings per conception = 0.46 ± 0.04). These results imply genetic variation for host resistance to, or tolerance of, PRRSV, particularly with the TTD dataset. Genetic correlations between reproductive traits measured in the healthy phase and TTD dataset varied from effectively zero for traits describing numbers of mummified or dead piglets to strongly positive for litter size traits. This indicates genetic variation in piglet losses during PRRSV outbreaks is independent of genetic variation in the same traits in healthy herds. In summary, our findings show that there is within-breed genetic variation for commercially relevant traits that could be exploited in future breeding programs against PRRSV infection. Selection for increased PRRS resistance would be desirable to the industry as effective control measures remain elusive.

Key Words: genetic parameters • pigs • PRRS • resistance