Senecavirus A infection in market weight gilts, sows and neonates with subsequent protective immunity

Authors: BUCKLEY, A - Oak Ridge Institute For Science And Education (ORISE); GUO, B - Iowa State University; MONTIEL, N - Oak Ridge Institute For Science And Education (ORISE); KULSHRESHTHA, V - Oak Ridge Institute For Science And Education (ORISE); VAN GEELEN, A - Oak Ridge Institute For Science And Education (ORISE); YOON, K - Iowa State University; Lager, Kelly

Submitted to: North American Porcine Reproductive and Respiratory Syndrome (NA-PRRS) Symposium
Publication Type: Abstract Only
Publication Acceptance Date: 11/1/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Objective: The objectives of this study were to 1) characterize SVA infection in market weight pigs, late-gestation sows, and neonates and 2) examine protective immunity in late-gestation gilts Materials and Methods: For Part 1 of the study 15 gilts were inoculated with SVA, bled regularly for 2 weeks, and clinical observations were made daily. In addition 10 sows were split into 2 groups. Group A was inoculated at various times pre-farrow (-17, -12, -10, -4, -3) and Group B was inoculated various times post-farrow (2, 3, 7, 7, 14) with their piglets. All animals were bled and swabbed at 0, 7, and 14 days post inoculation (dpi). In addition piglets were bled pre-colostrum intake. For Part 2 of the study, 12 of the 15 gilts inoculated in Part 1 were bred and challenged again in late gestation. Serum samples were collected from the gilts and piglets along with milk samples. Serum and swab samples were tested for SVA by PCR and a virus neutralization assay was used for serum antibody testing Results: During Part 1, all market weight gilts developed coronary band vesicles by 5 dpi. Snout lesions appeared 2 days after the first coronary band lesions and only developed in 40% of the gilts. Viremia lasted about a week in most gilts. Lameness was apparent starting on 2 dpi and lasted around 1 week, though feed intake was not affected. On the contrary, of the ten sows inoculated, only one sow developed a vesicle on the snout, though all had evidence of viral replication by PCR. Piglets born to sows infected on -17 and -12 were negative for SVA. Piglets born to the sow infected at -10 were positive for SVA before suckling and in subsequent sampling. Finally, piglets born to sows infected at -4 and -3 were negative at pre-suckle sampling, but positive by PCR in subsequent samplings. Two litters developed a yellow diarrhea often seen with enteric colibacillosis just after birth, but recovered completely in 2-3 days. All sows and piglets infected post-farrowing showed evidence of viral replication, but did not develop any clinical signs. All gilts and sows had increased antibody titers post exposure to SVA. During Part 2, there was no evidence of viral replication in any of the gilts or their piglets. In addition, all milk samples were negative for SVA. Conclusions: Market weight gilts experimentally infected with SVA developed a clinical picture similar to reports from the field. On the other hand, we were not able to experimentally reproduce clinical signs observed in sow farms naturally infected with SVA, namely neonatal mortality. We did show evidence of infection and viral replication in neonates, but we did not observe increased pre-weaning mortality. Gilts were challenged 5 months after initial exposure in late gestation and we were able to demonstrate protective immunity. Continued experimental studies with SVA will improve understanding of the pathogenesis of SVA and help shape control and prevention measures in the swine industry.