Claire Stenhouse
Pre-weaning mortality remains a major constraint to productivity and animal welfare in modern swine production and has not declined proportionally with improvements in genetics, nutrition, and housing. Mortality is commonly attributed to crushing, starvation, or impaired temperature regulation. However, accumulating evidence indicates that these outcomes frequently represent the final manifestations of compromised neonatal viability rather than independent primary causes. Selection for increased litter size has altered the intrauterine environment, such that uterine capacity and placental development limit fetal growth. Resulting variation in fetal development produces neonates with differing physiological reserves at birth, including reduced energy stores and impaired thermoregulatory capacity in vulnerable individuals. Parturition imposes an additional hypoxic and metabolic challenge. Prolonged farrowing and increased birth intervals due to large litter sizes expose fetuses to intermittent reductions in oxygen supply, and tolerance to this stress depends on developmental condition. Piglets that recover rapidly establish thermoregulation, locomotor activity, and adequate colostrum intake whereas compromised piglets exhibit delayed standing, poor suckling, and reduced vigor. These impairments initiate a cascade of impaired temperature regulation, inadequate energy intake, and inactivity that predisposes affected piglets to the commonly recorded causes of death. This review integrates evidence from fetal development, placental biology, parturition physiology, and neonatal adaptation to propose a unified model of pre-weaning mortality. Early mortality in pigs is best interpreted as a consequence of neonatal viability at birth, shaped by prenatal and perinatal processes, rather than solely a failure of postnatal management. Improving survival will therefore require strategies that enhance utero-placental function and neonatal resilience in addition to farrowing management.