Poor weaning transition average daily gain in pigs is not correlated with pathological or immunological markers of enteric disease during a porcine reproductive and respiratory syndrome virus outbreak1

Previous research suggests that enteric disease and poor gut health interact to decrease pig performance. Our objective was to determine if light birth weight pigs or those from the bottom 10th percentile of transition ADG (tADG) have a higher incidence of pathogen presence or enteric lesions than heavier or faster-growing contemporaries. A total of 1,500 pigs were weighed at birth and divided into 5 birth weight (BRW) categories: <1, 1 to 1.25, 1.26 to 1.5, 1.51 to 1.75, and >1.76 kg. At weaning, 1,054 random pigs were moved to a commercial wean-to-finish barn. Pigs were weighed individually at 0 and 3 wk postweaning. Transition ADG was calculated as the ADG between wk 0 and 3 postweaning. One pig from each of the 10th, 30th, and 70th percentiles of tADG was used to create 1 set of 3 pigs with the same litter size and from the same parity sow. Forty pigs from each of the 3 tADG percentiles were matched for sex, litter size, and sow parity but not BRW to create 20 matched sets of 60 pigs. This allowed for the main effects of BRW and tADG to be studied as a 5 × 3 factorial design. At 3 and 22 wk postweaning, pigs were euthanized for organ system tissue evaluation. Lung, lymph node, and digesta were analyzed for presence of pathogens and for severity of microscopic lesions (0 = not present, 1 = present, with slight erosion, 2 = present, with moderate erosion, and 3 = present and severe erosion). Data were analyzed using PROC GENMOD and GLIMMIX, where pig served as the experimental unit. The fixed effects were BRW and tADG and the random effects were pen and set. There were no BRW × tADG interactions (P = 0.16). There was no correlation (P = 0.12) between tADG and pathogen presence at either 3 or 22 wk postweaning. Incidence and severity of microscopic lesions in the large intestine at 3 wk postweaning decreased linearly with increasing tADG (P = 0.01). Lesion incidence and severity were also affected (P < 0.04) by tADG at 22 wk postweaning, with greater stomach incidence in the 10th percentile. Birth weight affected (P = 0.02) haemolytic Escherichia coli and Salmonella spp. B (includes Salmonella typhimurium) isolation at 3 wk postweaning as well as Brachyspira spp. isolation at 22 wk postweaning (P = 0.05) but in mixed directions. There were no effects (P = 0.21) of BRW or tADG on serum or ileum mucosa immune markers. In summary, it is apparent from this research that neither BRW nor tADG are likely causes of pathogen or lesion incidence.