Genetic parameters for performance traits in commercial sows estimated before and after an outbreak of porcine reproductive and respiratory syndrome1

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 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.

Genetic analysis of tolerance to infections using random regressions: a simulation study

“…Pathogen infections can indeed change heritabilities of performance traits, which then impact genetic responses to selection (e.g. Vehvila¨inen et al, 2008;Lewis et al, 2009). In contrast to pathogen-induced changes, changes in heritabilities due to other biotic (e.g.…”

Evidence for a major QTL associated with host response to Porcine Reproductive and Respiratory Syndrome Virus challenge1

“…In general, heritability of disease resistance in livestock is low (e.g., Salmonella resistance as measured by survival time in broilers at 0.06; Janss and Bolder, 2000), bovine respiratory disease in beef cattle at 0.08 (Snowder et al, 2006), and PRRS resistance in swine at 0.10 ( Lewis et al, 2009b;Lunney and Chen, 2010). However, in a study that evaluated performance traits of sows during non-diseased and PRRS-diseased states, heritability of total weaned increased from 0.02 during the non-diseased state to 0.15 during the diseased state (Lewis et al, 2009b).…”

“…Estimates of heritability of PRRS resistance are scarce, but estimates for number born alive, number stillborn, and number of mummies in sows infected with PRRSV ranged from 0.12 to 0.15 (Lewis et al, 2009b). The PRRS Host Genetics Consortium was established to investigate the genetic basis of host response to PRRSV infection in experimentally infected commercial crossbred pigs (Lunney et al, 2011).…”

An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

“…Breed differences have been reported (Halbur et al, 1998;Petry et al, 2005 andVincent et al, 2005 andAit-Ali et al, 2007) as summarised by Lewis et al (2007), within-breed variation in apparent tolerance of this disease is now becoming available (Lewis et al, 2008). From a research perspective, PRRS has some advantages.…”

“…Secondly, indicators of the impacts of infection are relatively easily collected in herds undergoing outbreaks, e.g. the numbers of mummified piglets, and these indicators will enable genetic effects to be relatively easily quantified (see Lewis et al, 2008). Although this is a disease that still requires much more fundamental research, it is rapidly becoming an interesting target for an OG approach.…”