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J Anim Sci. 2009 Mar;87(3):876-84. doi: 10.2527/jas.2008-0892. Epub 2008 Oct 24.

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

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  • 1The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Midlothian, United Kingdom.


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 method based on veterinary diagnosis and a threshold/threshold method based on trends in underlying performance data, creating the DTD and TTD data sets, respectively. The threshold/threshold method was more stringent in defining periods when PRRS was likely to be having an impact on reproductive performance, resulting in a data set (TTD) that was slightly smaller (1,977 litters from 1,526 sows) than that from the date/threshold 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 less (mummified piglets = 0.03 +/- 0.01, matings per conception = 0.04 +/- 0.01) than during the PRRSV outbreak (TTD data set; 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 data set. Genetic correlations between reproductive traits measured in the healthy phase and TTD data set 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 because effective control measures remain elusive.

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