Disease from endemic respiratory and enteric pathogen agents such as Mycoplasma hyopneumoniae (Mh) and Lawsonia intracellularis (LI) is common in swine herds worldwide and reduces profits at all production stages. However, the metabolic mechanisms behind these reductions in growth performance and tissue accretion have not been fully explained. Additionally, to minimize feed costs, producers place heavy emphasis on selection for production traits such as enhanced feed efficiency (FE), but genetic selection for higher FE has been touted to have negative consequences on a pig’s ability to respond to disease. Therefore, the overall objective of this thesis was to characterize how a Mycoplasma hyopneumoniae and Lawsonia intracellularis dual challenge (MhLI) alters pig performance and metabolism, using pigs divergently selected for residual feed intake (RFI) as a model for divergence in feed efficiency. Pigs selected for low RFI (LRFI, high feed efficiency) pigs are considered more FE compared to their high RFI (HRFI, low feed efficiency) selected counterparts.

To address the overall thesis objective, two research chapters were conducted using grow-finish pigs (Chapter 2 and 3). In Chapter 2, the longitudinal impact of MhLI on growth performance, feed efficiency, and tissue accretion of pigs divergent in RFI was assessed in a 42 day challenge study. We initially hypothesized that MhLI dual challenge would reduce growth performance, protein accretion, and feed efficiency. In Chapter 3, a subset of pigs was randomly selected from the larger cohort used in Chapter 2 for necropsy and tissue collection at 21 days post inoculation (dpi). This subset of pigs was utilized to examine effects of MhLI, RFI line, and their interaction on markers of oxidative stress, skeletal muscle metabolism and proteolysis, and liver gluconeogenesis. We hypothesized that MhLI would alter metabolism to reallocate nutrients toward the immune system, which would be evident by increased skeletal muscle proteolysis and increased liver gluconeogenesis.

The challenge model utilized resulted in sub-clinical disease in the lungs and intestinal tract of infected pigs. Overall, the results of this work suggest that genetic selection for enhanced FE (i.e. low RFI) does not alter the ability of pigs to respond to and resolve pathogen challenges due to the hypothesized inability to allocate energy and nutrients to the immune response. This was evident as there were no MhLI x line interactions for any performance (Chapter 2) or post-absorptive metabolism (Chapter 3) parameters assessed. However, this thesis indicates that MhLI dual challenge reduces average daily gain, feed intake, feed efficiency, and lean tissue accretion in growing pigs (Chapter 2). Additionally, MhLI dual challenge alters the post-absorptive skeletal muscle and liver metabolism of grow-finish pigs. The challenged pigs had increased reactive oxygen species (ROS) production in the Longissimus dorsi (LM) and liver, and greater hexokinase to citrate synthase activity ratios, but did not have increased skeletal muscle protein carbonyls or enhanced skeletal muscle proteolysis (Chapter 3). Additionally, gluconeogenesis was not upregulated in the liver due to MhLI dual challenge (Chapter 3).

Collectively, this line of investigation demonstrated that a dual respiratory and enteric pathogen challenge in grow-finish pigs resulted in reduced growth performance (17%) and feed efficiency (7%) compared to the non-challenged control pigs, regardless of RFI line. These performance reductions are comparable to the previous body of literature utilizing these two pathogens. The MhLI dual challenge also results in increased mitochondrial ROS production and causes pigs to favor glycolytic energy generation. However, contrary to the initial hypothesis, skeletal muscle proteolysis and liver gluconeogenesis are not upregulated during MhLI challenge. These data suggest that during mild disease stress such as what was observed under this MhLI dual challenge, the pig can meet energy demands without reliance on nutrient mobilization and gluconeogenesis.