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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #336369
Title: Senecavirus A infection in sows, neonates, and market weight gilts with subsequent protective immunity

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

Submitted to: Conference Research Workers Disease Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 11/4/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Objective: The objectives of this study were to 1) characterize SVA infection late-gestation sows, neonates, and market weight gilts and 2) examine protective immunity in late-gestation gilts Methods: For Part 1, 15 market weight gilts were inoculated with SVA, bled regularly, 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 various times post-farrow (2, 3, 7, 7, 14) with their piglets. All animals were bled and swabbed at 0, 7, and 14 dpi. For Part 2, 12 of the 15 gilts inoculated in Part 1 were bred and challenged again in late gestation. Serum was collected from gilts and piglets along with milk samples. Serum and swab samples were tested for SVA by PCR and a VN assay was used for serum antibody testing. Results: During Part 1, all market weight gilts developed coronary band vesicles by 5 dpi. Snout lesions only developed in 40% of the gilts. Viremia and visible lameness lasted about a week in most gilts, 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 days were negative for SVA. Piglets born to sows infected at -10, -4, and -3 days were positive on at least one sampling time point. All piglets infected post-farrow 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. Gilts challenged 5 months after initial exposure demonstrated protective immunity. Continued experimental studies with SVA will improve understanding of the pathogenesis of SVA and help shape control measures in the swine industry.