Quantifying the effect of lactogenic antibody on porcine epidemic diarrhea virus infection in neonatal piglets

•The objective of this experiment was to assess the role of lactogenic immunity in protecting piglets against the effects of PEDV by quantifying virus shedding in feces and piglet growth, thermoregulation, and survival in the presence (PEDV exposed sows) or absence (PEDV negative sows) of PEDV antibody in colostrum and milk.•The presence of lactogenic antibody markedly affected the outcome of PEDV infection in neonates, including less PEDV shedding in feces, better thermostability (p = 0.0001), higher rate of growth, and higher rate of survivability.•Therefore, maintenance of sufficient levels of lactogenic immunity will be the cornerstone for the prevention of PED in endemically-infected herds.

The contribution of lactogenic antibody to the protection of piglets against porcine epidemic diarrhea virus (PEDV) was evaluated. Pregnant multiparous sows and their litters were allocated to one of 3 treatment groups: Group 1-6 serum antibody-negative sows and a subset (n = 11) of their piglets. Group 2-8 serum antibody-positive sows and their 91 piglets. Piglets were orally inoculated with PEDV at 4 (Group 1) or 2 (Group 2) days of age. Group 3-2 PEDV serum antibody-negative sows and 22 piglets, provided a baseline for piglet survivability and growth rate. Piglets were monitored daily for clinical signs, body weight, and body temperature through day post-inoculation (DPI) 12 (Groups 2 and 3) or 14 (Group 1). Serum and mammary secretions were tested for PEDV IgG, IgA, and virus-neutralizing antibody. Feces were tested by PEDV real-time, reverse transcriptase PCR (rRT-PCR). Piglets on sows without (Group 1) or with (Group 2) anti-PEDV antibody showed significantly different responses to PEDV infection in virus shedding (p < 0.05), thermoregulation (p < 0.05), growth rate (p < 0.05), and survivability (p < 0.0001). Specifically, Group 1 piglets shed more virus on DPIs 1 to 5, were hypothermic at all sampling points except DPIs 9, 11, and 12, gained weight more slowly, and exhibited lower survivability than Group 2 piglets. Within Group 2 litters, significant differences were found in virus shedding (p < 0.05), and body temperature (p < 0.05), but not in piglet survival rate. The number of sows and litters in Group 2 was insufficient to derive the relationship between specific levels of lactogenic antibody (FFN, IgA, and IgG) and the amelioration of clinical effects. However, when combined with previous PEDV literature, it can be concluded that the optimal protection to piglets will be provided by dams able to deliver sufficient lactogenic immunity, both humoral and cellular, to their offspring.