More Efficient Pigs Are More Resistant to PRRS Virus

Contrary to expectations, the growth of the more efficient pigs was less affected by experimental infection with the Porcine Reproductive and Respiratory Syndrome (PRRS) virus than the inefficient line, according to research published in the Iowa State University Animal Industry Report 2014.

16 April 2014

4 minute read

By: Jackie Linden

Summary and Implications

Analyses of average daily gain and viral load suggest that selection for increased feed efficiency based on residual feed intake does not increase the impact of PRRS infection on these two traits, according to Jenelle Dunkelberger and others at Iowa State University.

In fact, the results show that growth of the more efficient pigs was less affected by PRRS infection than that of the inefficient line.

These findings provide commercial farmers with additional incentives to invest in feed-efficient pigs.

Introduction

Feed efficiency is of great importance to the swine industry, yet little research has been performed to evaluate the robustness of pigs selected for increased feed efficiency to disease, they said.

Feed efficiency measured using RFI is defined as the difference between observed versus expected feed intake based on growth and backfat. Pigs that eat less than expected (i.e. negative residual feed intake) are more efficient.

Recent theories suggest that more efficient animals may be more susceptible to disease as a result of having less available energy to mount an immune response.

Since PRRS is the most economically devastating disease to the US swine industry, the objective of this study was to analyse the effect of PRRS on lines of pigs divergently selected for low versus high residual feed intake.

The hypothesis was that efficient low residual feed intake pigs would have a greater reduction in average daily gain and greater viral load upon infection with the PRRS virus compared to pigs selected for high residual feed intake (reduced feed efficiency).

Materials and Methods

Two hundred piglets from generation 8 of the ISU high- and low-residual feed intake selection lines (HRFI and LRFI, respectively), were shipped to Kansas State University upon weaning and received an intranasal/oral dose of the NVSL 97-7985 PRRS strain one week post-arrival.

Blood samples were collected on zero, four, seven, 11 and 14 days post-infection and weekly thereafter.

Viral load was calculated as area under the curve for 0-21 days post-infection of the log of PCR-based serum viraemia. Bodyweights were collected weekly and used to calculate average daily gain.

For comparison, bodyweights for average daily gain were also collected on 489 non-challenged full-siblings and half-siblings in the nursery at the Iowa State Lauren Christian Swine Research Center.

Results

For the PRRS challenged pigs, viral load tended to be slightly lower (p=0.12) and average daily gain slightly higher (p=0.10) for the more efficient LRFI line.

In contrast, for the non-challenged pigs, average daily gain was slightly lower for the LRFI line but again not significantly (p=0.20).

A joint analysis of challenged and non-challenged pigs demonstrated that growth of the LRFI line was less reduced by PRRS-challenge than growth of the HRFI line (p=0.04).

Discussion

The initial hypothesis was that LRFI pigs would experience a greater reduction in average daily gain and greater viral load upon infection with PRRS virus compared to HRFI pigs. However, results of analyses for viral load and average daily gain did not support this hypothesis.

Instead, results demonstrate that selection for increased feed efficiency based on residual feed intake does not increase the impact of PRRS infection on viral load or average daily gain. In fact, growth of the more efficient pigs was less affected by PRRS infection than that of the inefficient line.

The authors of this paper were Jenelle Dunkelberger (Graduate Student, ISU), Nicholas Boddicker (Research Geneticist, Genesus), Jennifer Young (Post-doctoral Research Associate, ISU), Dinesh Thekkoot (Graduate Student, ISU), Bob Rowland (Professor, Department of Diagnostic Medicine and Pathobiology, KSU) and Jack Dekkers (Professor, Department of Animal Science, ISU).

Acknowledgements: The authors would like to thank Dr Nick Serão for assistance with analyses and Dr Bob Rowland’s lab for conducting the PRRS trails.
The work presented here was supported by USDA ARS and NIFA Awards 2012-38420-19286 and 2011-68004-30336 and the breeding companies of the PRRS Host Genetics Consortium.