Gilt progeny have lighter weaning weights and greater postweaning medication and mortality rates compared with the progeny of older parity sows. Because weaning weight has been positively correlated with postweaning survival, this study aimed to determine whether the provision of supplemental milk preweaning could improve weaning weight and subsequent weights as well as postweaning survival of gilt progeny. The study was replicated in summer and winter as the effects of supplemental milk were expected to vary with season. The progeny of 80 gilts (parity 0) and 80 sows (parity 2 to 5) were allocated to both treatments: with or without supplemental milk in these 2 seasons with 5 sheds/season. Litter size was standardized (10 to 11 piglets) and each piglet was weighed at birth, d 21, weaning (4 wk), and 10 wk of age. Medications and mortalities were recorded both preweaning and postweaning. Pigs were housed within treatment groups postweaning, and ADFI and G:F were measured. Gilt progeny were 200 g lighter at birth in both replicates (P < 0.001) and were 500 g lighter at weaning in the winter replicate (P < 0.05) compared with sow progeny. The provision of supplemental milk improved weaning weight for both gilt and sow progeny by 800 g in summer (P < 0.05) and by 350 g in winter (P < 0.05). This improvement in weaning weight had no effect on the incidence of death or disease in milk-supplemented progeny of either gilts or sows (P > 0.05). Supplemental milk disappearance (the daily difference between the volume of milk provided and the residue left in the drinker) was greater in summer than winter (by 130 mL/piglet d(-1); P < 0.05) as were the associated weaning weight benefits. The weaning weights of supplemented gilt progeny reached or exceeded that of nonsupplemented sow progeny. Gilt progeny had greater postweaning mortality (2.6%) and medication rates (6.2%) than sow progeny (1 and 2.2%, respectively; both P < 0.05) in both seasons, but medication rates were greater in winter (7.2%) for both treatment groups than in summer (1.9%; P < 0.05). Gilt progeny also had less postweaning ADFI than sow progeny in winter (528 and 636 g, respectively; P < 0.05) with no dam parity effect on G:F (both P > 0.05). The hypothesis that supplemental milk provision did increase gilt progeny weaning weight was supported (especially in summer) but the supplementation had no effect on postweaning weights and survival. Efforts to improve gilt progeny postweaning growth and survival need to be aimed at improving health and immunity, not just weaning weight.

Gilt progeny have lower weaning weights and higher post-weaning medication and mortality rates, indicating greater disease susceptibility, than do sow progeny. The present study aimed to identify explanatory innate or adaptive immunity differences between gilt and sow progeny and potential pre- or post-natal influences. Sixty-four dams were vaccinated twice pre-farrowing with tetanus toxoid (TT). Serum (pre-vaccination) and colostrum and/or milk samples were collected to determine concentrations of TT-specific immunoglobulin G (IgG), by using an enzyme-linked immunosorbent assay (ELISA). Piglets were removed from their birth dam before suckling and fostered (not to their birth dam) to form 16 gilt and 16 sow litters, with five gilt-born and five sow-born piglets per litter. Piglets were vaccinated at weaning (4 weeks old) with either TT or saline (control). Sera and whole blood were collected from three gilt-born and three sow-born piglets per litter at 2, 4 and 7 weeks of age. Innate immunity was assessed indirectly on whole blood using an interferon gamma (IFN-γ) immune cell stimulation assay and a phagocytic assay. Piglets were weighed at birth, 4, 10, 17 and 22 weeks of age. There was no difference (P > 0.05) in the concentration of TT-specific IgG in colostrum and milk from gilts and older-parity sows, suggesting a similar ability to transfer IgG antibodies to a novel antigen. Birth dam parity did not affect piglets’ TT-specific IgG concentrations pre-weaning (P > 0.05) suggesting similar ability to absorb passively acquired IgG. Sow-reared piglets, however, had lower (P < 0.05) concentrations of TT-specific IgG than did gilt-reared piglets, possibly due to haemodilution in the faster-growing sow progeny. Gilt-born progeny had a reduced IgG response post-weaning to TT vaccination relative to sow-born progeny (P < 0.05), indicating adaptive immunity differences. Birth dam parity did not affect (P > 0.05) innate immunity (number/responsiveness of cells). Rearing dam parity influenced phagocytic activity pre- and post-weaning (gilt-reared > sow-reared; P < 0.05), possibly due to increased pathogen challenge. Birthweight was affected by birth dam parity (sow-born > gilt-born; P < 0.05) while rearing dam parity determined weaning weight (sow-reared > gilt-reared; P < 0.05), with no difference evident at 22 weeks. The results of the present study suggest that gilt-born progeny may be more susceptible to disease post-weaning than sow-born progeny due to their lower birthweight and reduced humoral immune responsiveness. The rearing dam may also affect disease susceptibility in progeny due to slower pre-weaning growth, lower weaning weights and increased pathogen challenge, both pre- and post-weaning.