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

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.

Persistent Infection and Transmission of Senecavirus A from Carrier Sows to Contact Piglets

“…Interestingly, many natural cases of SVA have been reported following stressful conditions, such as transportation (3,4) and parturition (7,17,18). Thus, it has been hypothesized that stress and/or immunosuppression may contribute to SVA-induced VD (4,19). Previously we developed an SVA infection model in which animals were inoculated upon arrival at the animal facility after a 2-h trip from the farm (14).…”

“…Interestingly, the sows inoculated with SVA in the present study displayed clinical signs and developed vesicular lesions earlier than nursery (36) or finishing pigs used in previous SVA pathogenesis studies (14,20,21), suggesting that age, sex, and/or weight may potentially contribute to disease onset and severity in pigs. A recent study conducted to evaluate the effect of immunosuppression on acute SVA-induced VD concluded that immunosuppressive doses of Dx had no significant effect on disease onset and severity or on the levels of viremia and virus shedding (19). Results here, showing early lesion development and enlarged lesions following transportation stress, suggest that while stressors are not required for SVA-induced VD in pigs, exposure of animals to stressful conditions may contribute to or accelerate the development of vesicular lesions following infection with SVA.…”

“…Clinically, SVA-induced VD is indistinguishable from foot-and-mouth disease (FMD) (14,15), a highly contagious VD caused by the related picornavirus, foot-and-mouth disease virus (FMDV) (16). Interestingly, several cases of natural SVA infection have been reported following common swine production stressors, such as transportation (3,4) and parturition (7,17,18), suggesting that stressors may contribute to SVA-induced VD (19).…”

Pathogenesis and control of Senecavirus A in swine

“…Lesions can begin with erythematous areas or blanched areas of the skin progressing to vesicles with varying levels of fluid that rupture leaving an erosion on the skin that crusts over and resolves (72). Histologically, areas of separation between the dermis and epidermis with clefts are noted containing edema, fibrin, necrotic debris, and inflammatory infiltrates (neutrophils, lymphocytes, and plasma cells) (72,118). Development of vesicular lesions on the coronary bands have been observed in as little as 48 hours in market-weight animals, but most animals develop vesicular lesions 3-6 days after experimental challenge and heal within 7-14 days (41,71,72,119,120).…”

“…In addition, some studies have reported seeing less snout lesions compared to coronary band lesions (118,122). Other clinical signs that have been reported intermittently in pigs inoculated with SVA include fever, lameness, lethargy, and decreased feed intake (26,106).…”