Serological and Molecular Detection of Senecavirus A Associated with an Outbreak of Swine Idiopathic Vesicular Disease and Neonatal Mortality

Abstract

bWe performed a longitudinal field study in a swine breeding herd that presented with an outbreak of vesicular disease (VD) that was associated with an increase in neonatal mortality. Initially, a USDA Foreign Animal Disease (FAD) investigation confirmed the presence of Senecavirus A (SVA) and ruled out the presence of exotic agents that produce vesicular lesions, e.g., foot-andmouth disease virus and others. Subsequently, serum samples, tonsil swabs, and feces were collected from sows (n ‫؍‬ 22) and their piglets (n ‫؍‬ 33) beginning 1 week after the onset of the clinical outbreak and weekly for 6 weeks. The presence of SVA RNA was evaluated in all specimens collected by reverse transcriptase quantitative PCR (RT-qPCR) targeting a conserved region of the 5= untranslated region (5=-UTR). The serological response (IgG) to SVA was evaluated by the weekly testing of sow and piglet serum samples on a SVA VP1 recombinant protein (rVP1) indirect enzyme-linked immunosorbent assay (ELISA). The rVP1 ELISA detected seroconversion against SVA in clinically affected and non-clinically affected sows at early stages of the outbreak as well as maternal SVA antibodies in offspring. Overall, the absence of vesicles (gross lesions) in SVA-infected animals and the variability of RT-qPCR results among specimen type demonstrated that a diagnostic algorithm based on the combination of clinical observations, RT-qPCR in multiple diagnostic specimens, and serology are essential to ensure an accurate diagnosis of SVA. S enecavirus A (SVA), formerly Seneca Valley virus (SVV), is a nonenveloped, single-stranded, positive-sense RNA virus that belongs to the genus Senecavirus in the family Picornaviridae (1). The virus was first described as a contaminant of a PER C6 cell line (2). The virus encodes one polyprotein that is posttranslationally processed by virus-encoded proteases into 4 structural (VP1 to VP4) and 7 nonstructural (2A to 2C and 3A to 3D) proteins (2, 3). The pathogenic role of these SVA proteins is unknown, but VP1 is considered to be the most immunogenic protein in viruses of the Picornaviridae family (4, 5).Idiopathic vesicular disease (IVD), a sporadic and transient condition affecting swine, has been reported in pigs in Australia, New Zealand, and the United States (6-8). It was not until 2007 that the presence of SVA was linked with IVD outbreaks in Canada (9). Most recently, SVA was detected in sporadic and transient outbreaks of IVD in the United States, Brazil, and China (10-13). Lesions observed in cases of IVD associated with SVA infection are characterized by vesicle formations and epidermal erosions that progress to ulcers of the coronary band, oral cavity, and nasal planum. Affected animals present transient fever and lameness. Vesicular lesions in pigs resemble those in other foreign vesicular diseases, such as foot-and-mouth disease (FMD), vesicular stomatitis (VS), swine vesicular disease (SVD), and vesicular exanthema of swine (VES). In addition, numerous reports associate the presence of SVA with increased ne...

An indirect enzyme-linked immunosorbent assay for the identification of antibodies to Senecavirus A in swine

“…The kinetics of the antibody response to SVA have been recently examined. In a naturally infected farm ELISA-positive antibodies (anti-SVA VP1) were observed in pig serum at 1 week post-clinical signs in less than 15% of animals [11]. However, at 3 weeks post-clinical signs over 70% of animals were seropositive and by 6 weeks over 90% of animals were seropositive [11].…”

“…In a naturally infected farm ELISA-positive antibodies (anti-SVA VP1) were observed in pig serum at 1 week post-clinical signs in less than 15% of animals [11]. However, at 3 weeks post-clinical signs over 70% of animals were seropositive and by 6 weeks over 90% of animals were seropositive [11]. Experimental SVA infection of 9 week old pigs showed that all animals seroconverted by 15 days post-infection as determined by an indirect fluorescent antibody test [10].…”

“…The SVA ELISA was first evaluated using samples from a farm showing clinical signs, starting at the day clinical signs were first observed (Day 0) and sampled up to 60 days post-break ( Days 4,11,18,25,39,60). Comparison of antibody reactivity to VP1, VP2, or VP3 showed that VP2 was significantly different than VP1 and VP3 (p < 0.0001) giving the largest range of OD values and the biggest difference between positive and negative sample values (Fig.…”

“…An indirect ELISA only requires a purified antigen and so is not susceptible to mutations that change reactivity of the monoclonal antibody-binding epitope. An SVA VP1 ELISA has recently been used to examine antibody presence in sows and piglets naturally infected with SVA, however a comprehensive validation of this assay was not shown [11]. Although numerous ELISA kits used for the detection of viral antibodies are commercially available, an indirect ELISA kit is not yet commercially available for the detection of anti-SVA antibodies in pigs.…”

Identification and genomic characterization of the emerging Senecavirus A in southeast China, 2017

“…Senecavirus A (SVA), also known as Seneca Valley virus, is an emerging causative agent linked to swine idiopathic vesicular disease (SIVD) and epidemic transient neonatal losses (ETNL) (Canning et al., ; Gimenez‐Lirola et al., ; Guo et al., ). SIVD is a vesicular disease syndrome with obvious clinical signs, including vesicular lesions and coalescing erosions on the snout and coronary bands, which are indistinguishable from the infections of swine vesicular disease virus (SVDV), foot‐and‐mouth disease virus (FMDV) and vesicular stomatitis virus (VSV).…”