Hyperprolificacy in Modern Sow Genetics: A Review of the Neonatal, Immunological, and Welfare Costs of Increased Litter Size

Abstract

Over the past two decades, genetic selection has increased average total litter size in commercial sow herds from approximately 9–10 piglets to more than 14 piglets per farrowing, an achievement that has delivered clear economic benefit but has been accompanied by a parallel rise in pre-weaning mortality (PWM), which is now commonly reported in the range of 12–20% and, by some indicative estimates, is trending upward even in well-managed herds. This review synthesizes the veterinary and reproductive-physiology literature on hyperprolificacy in sows, examining its downstream consequences for individual piglet birth weight, farrowing duration, colostrum access, and passive immunoglobulin G (IgG) transfer. Attention is given to the biological mechanism by which litter size dilutes colostral IgG, including vaccine-induced maternally derived antibody (MDA) against porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2), and to the strength of the supporting evidence with regard to each pathogen, which differs considerably. This evidence is considerably stronger for PCV2, where maternal vaccination has a directly demonstrated effect on offspring antibody titres, than for PRRSV, where litter-size-specific dilution of maternally derived antibody has not yet been directly measured and remains an inferred, biologically plausible mechanism rather than a demonstrated one. The review further appraises management interventions including cross-fostering, split suckling, nurse sows, immunoglobulin supplementation, and structured neonatal triage, together with their documented trade-offs and considers the animal-welfare dimension of continued genetic selection for litter size. A dedicated section evaluates the current state of precision livestock farming (automated farrowing and crushing surveillance, computer-vision piglet weighing, and genomic selection for litter uniformity and robustness), concluding that these tools are promising but largely still at the research or early-adoption stage. We conclude that inadequate transfer of passive immunity behaves as an independent risk factor for mortality, separate from birth weight, and that management responses should be viewed as necessary complements to, rather than substitutes for, a re-balancing of genetic selection indices toward piglet survivability.