Dexamethasone treatment did not exacerbate Seneca Valley virus infection in nursery-age pigs

Alexandra Buckley,Kelly Lager,Kyoung-Jin Yoon,Nestor Montiel,Vikas Kulshreshtha,Christopher Rademacher,Hai Hoang,Baoqing Guo,Albert Van Geelen

doi:10.1186/s12917-018-1693-8

Abstract

BackgroundSenecavirus A, commonly known as Seneca Valley virus (SVV), is a picornavirus that has been infrequently associated with porcine idiopathic vesicular disease (PIVD). In late 2014 there were multiple PIVD outbreaks in several states in Brazil and samples from those cases tested positive for SVV. Beginning in July of 2015, multiple cases of PIVD were reported in the United States in which a genetically similar SVV was also detected. These events suggested SVV could induce vesicular disease, which was recently demonstrated with contemporary US isolates that produced mild disease in pigs. It was hypothesized that stressful conditions may exacerbate the expression of clinical disease and the following experiment was performed. Two groups of 9-week-old pigs were given an intranasal SVV challenge with one group receiving an immunosuppressive dose of dexamethasone prior to challenge. After challenge animals were observed for the development of clinical signs and serum and swabs were collected to study viral shedding and antibody production. In addition, pigs were euthanized 2, 4, 6, 8, and 12 days post inoculation (dpi) to demonstrate tissue distribution of virus during acute infection.ResultsVesicular disease was experimentally induced in both groups with the duration and magnitude of clinical signs similar between groups. During acute infection [0–14 days post infection (dpi)], SVV was detected by PCR in serum, nasal swabs, rectal swabs, various tissues, and in swabs from ruptured vesicles. From 15 to 30 dpi, virus was less consistently detected in nasal and rectal swabs, and absent from most serum samples. Virus neutralizing antibody was detected by 5 dpi and lasted until the end of the study.ConclusionTreatment with an immunosuppressive dose of dexamethasone did not drastically alter the clinical disease course of SVV in experimentally infected nursery aged swine. A greater understanding of SVV pathogenesis and factors that could exacerbate disease can help the swine industry with control and prevention strategies directed against this virus.

Highlights

Senecavirus A, commonly known as Seneca Valley virus (SVV), is a picornavirus that has been infrequently associated with porcine idiopathic vesicular disease (PIVD)
Swabs of vesicular lesions may serve as the best sample to collect during clinical disease to reliably detect the presence of SVV due to the large quantities of virus found in that location
Dexamethasone administration in this study was based on previous studies that successfully induced recrudescence of wild-type and attenuated PRV vaccine [36], and presumably this dosing schedule would be a substitute for stress that would alter the immune system allowing for enhanced vesicular disease

Summary

Introduction

Senecavirus A, commonly known as Seneca Valley virus (SVV), is a picornavirus that has been infrequently associated with porcine idiopathic vesicular disease (PIVD). Beginning in July of 2015, multiple cases of PIVD were reported in the United States in which a genetically similar SVV was detected These events suggested SVV could induce vesicular disease, which was recently demonstrated with contemporary US isolates that produced mild disease in pigs. SVV was rarely detected in North America prior to the 2014/2015 unprecedented emergence of PIVD in Brazil and the United States, it has been detected many times since in the respective countries as well as recent novel case reports in Canada [21], China [22,23,24], Thailand [25], and Colombia [26] Viruses from these recent outbreaks are genetically similar sharing > 94% nucleotide identity at the full-length genomic level

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