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Title: Vesicular disease in 9-week-old pigs experimentally infected with Senecavirus A

Author
item MONTIEL, NESTOR - Oak Ridge Institute For Science And Education (ORISE)
item BUCKLEY, ALEXANDRA - Oak Ridge Institute For Science And Education (ORISE)
item GUO, BAOQING - Iowa State University
item KULSHRESHTHA, VIKAS - Oak Ridge Institute For Science And Education (ORISE)
item VAN GEELEN, ALBERT - Oak Ridge Institute For Science And Education (ORISE)
item HOANG, HAI - Iowa State University
item RADEMACHER, CHRISTOPHER - Iowa State University
item YOON, KYOUNG-JIN - Iowa State University
item Lager, Kelly

Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/1/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Introduction: Senecavirus A (SVA), a picornavirus, has been infrequently associated with cases of idiopathic vesicular disease (IVD) in pigs in the US and Canada since 1988. In 2014 and 2015 there was surge of IVD cases in Brazil and US, respectively. SVA was identified in serum, vesicular fluid, and ruptured vesicles collected from affected pigs. Presumably, SVA was the cause of these recent epidemics; however, Koch’s postulates for this disease have not yet been fulfilled. Material and Methods: Nine-week-old pigs (n=29) received an intranasal inoculation of SVA15-41901SD isolate (5x107 pfu/pig) at 0 days-post-inoculation (dpi). Twelve pigs (Dex-SVA) were treated with an immunosuppressive dose of dexamethasone for 5 days prior to challenge. Serum and swab samples were collected at regular intervals and tested by PCR, SVA-antibody (serum) and virus isolation. A randomly selected SVA pig was euthanized and necropsied at 2, 4, 6, 8, and 10 dpi. Results: At 5 dpi, 24 of the remaining 27 infected pigs had intact or ruptured vesicular lesions on the coronary bands of toes and dewclaws and/or the interdigital cleft of one or more feet without causing severe lameness. A subset of animals developed erosions on the lower lip and snouts (after 10 dpi). Dex-SVA pigs developed slightly larger vesicular lesions than the untreated pigs and were observed around one day earlier. At 3 dpi SVA was detected in serum from each pig by PCR and in all swab samples collected from vesicular lesions at 5 dpi regardless of Dex treatment. All pigs seroconverted to SVA by 15 dpi as determined by indirect fluorescent antibody test. SVA was also isolated from vesicular fluid. Conclusions: Vesicular disease was experimentally induced in nursery-age pigs inoculated with SVA demonstrating for the first time a causal relationship between SVA infection and disease. This is important because SVA disease is clinically indistinguishable from foot-and-mouth disease, which is induced by a highly transmissible picornavirus that can cause devastating economic losses to the agricultural industry and human food supply. Therefore a better understanding of SVA pathogenesis and host response to infection should aid in the development of prevention and control measures and differentiation of this virus from other vesicular diseases.