Effects of increasing omega-3 fatty acids on growth performance, immune response, and mortality in nursery pigs.

Three experiments evaluated omega-3 fatty acids, provided by O3 trial feed, on nursery pig growth performance, mortality, and response to an LPS immune challenge or natural Porcine reproductive and respiratory virus (PRRSV) outbreak. In experiment 1, 350 pigs (241 × 600, DNA; initially 5.8 kg) were used. Pens of pigs were randomly assigned to one of the five dietary treatments containing increasing omega-3 fatty acids (0%, 1%, 2%, 3%, and 4% O3 trial feed) with 14 replications per treatment. On day 25, two pigs per pen were injected intramuscularly with 20 μg LPS per kg BW and one pig per pen was injected with saline as a control. Body temperature was taken from all three pigs prior to and 2, 4, 6, and 12 h post-LPS challenge. Serum IL-1β and TNF-α concentrations were determined in LPS-challenged pigs 24 h prior and 4 h post-LPS challenge. There was no interaction between treatment and time for change in body temperature ( > 0.10). Overall, increasing the O3 trial feed did not affect ( > 0.10) ADG, ADFI, G:F, IL-1β, or TNF-α. In experiment 2, 1,056 pigs (PIC TR4 × [Fast LW × PIC L02] initially 7.3 kg) were used. Pens of pigs were randomly assigned to one of the four dietary treatments containing increasing omega-3 fatty acids (0%, 0.75%, 1.5%, and 3% O3 trial feed) with 12 replications per treatment. Oral fluids tested negative on days 7 and 14, but then positive for North American PRRSV virus via PCR on days 21, 28, 35, and 42. Overall, increasing O3 trial feed increased (linear,  < 0.001) ADG, ADFI, and G:F and decreased (linear,  = 0.027) total removals and mortality. In experiment 3, 91,140 pigs (DNA 600 × PIC 1050; initially 5.1 kg), originating from PRRSV-positive sow farms, were used across eight nursery sites. Each site contained five barns with two rooms per barn and ~1,100 pigs per room. Rooms of pigs were blocked by nursery site and allocated within sow source to one of the two dietary treatments (control or 3% O3 trial feed) with 40 replications per treatment. Oral fluids from 61 of the 80 rooms tested positive for North American PRRSV virus 1 wk postweaning and 78 of the 80 rooms tested positive 3 wk after weaning. Overall, O3 trial feed did not affect ADG, ADFI, or G:F but increased ( < 0.001) total removals and mortalities. In summary, increasing omega-3 fatty acids, sourced by O3 trial feed, did not improve growth performance or immune response in healthy pigs given an LPS challenge. However, it appears that if omega-3 fatty acids are fed prior to a natural PRRSV break (as in experiment 2), growth performance may be improved, and mortality reduced.