Senecavirus

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Pablo Pineyro - One of the best experts on this subject based on the ideXlab platform.

  • Comprehensive review on immunopathogenesis, diagnostic and epidemiology of Senecavirus A.
    Virus research, 2020
    Co-Authors: Elizabeth Houston, Gun Temeeyasen, Pablo Pineyro
    Abstract:

    Senecavirus A (SVA), formerly known as Seneca Valley virus, is a single-strand, positive-sense RNA virus in the family Picornaviridae. This virus has been associated with recent outbreaks of vesicular disease (SVA-VD) and epidemic transient neonatal losses (ETNL) in several swine-producing countries. The clinical manifestation of and lesion caused by SVA are indistinguishable from other vesicular diseases. Pathogenicity studies indicate that SVA could regulate the host innate immune response to facilitate virus replication and the spread of the virus to bystander cells. SVA infection can induce specific humoral and cellular responses that can be detected within the first week of infection. However, SVA seems to produce persistent infection, and the virus can be shed in oral fluids for a month and detected in tissues for approximately two months after experimental infection. SVA transmission could be horizontal or vertical in infected herds of swine, while positive animals can also remain subclinical. In addition, mice seem to act as reservoirs, and the virus can persist in feed and feed ingredients, increasing the risk of introduction into naive farms. Besides the pathological effects in swine, SVA possesses cytolytic activity, especially in neoplastic cells. Thus, SVA has been evaluated in phase II clinical trials as a virotherapy for neuroendocrine tumors. The goal of this review is summarize the current SVA-related research in pathogenesis, immunity, epidemiology and advances in diagnosis as well as discuses current challenges with subclinical/persistent presentation.

  • Genetic diversity and evolution of the emerging picornavirus Senecavirus A.
    The Journal of general virology, 2019
    Co-Authors: Lok R. Joshi, Pablo Pineyro, Gerald F. Kutish, Kristin A. Mohr, Danielle Gava, Alaire S. Buysse, Fabio Vannucci, Beate Crossley, John Schiltz, Melinda Jenkins-moore
    Abstract:

    Senecavirus A (SVA) is an emerging picornavirus that causes vesicular disease (VD) in swine. The virus has been circulating in swine in the United Stated (USA) since at least 1988, however, since 2014 a marked increase in the number of SVA outbreaks has been observed in swine worldwide. The factors that led to the emergence of SVA remain unknown. Evolutionary changes that accumulated in the SVA genome over the years may have contributed to the recent increase in disease incidence. Here we compared full-genome sequences of historical SVA strains (identified before 2010) from the USA and global contemporary SVA strains (identified after 2011). The results from the genetic analysis revealed 6.32 % genetic divergence between historical and contemporary SVA isolates. Selection pressure analysis revealed that the SVA polyprotein is undergoing selection, with four amino acid (aa) residues located in the VP1 (aa 735), 2A (aa 941), 3C (aa 1547) and 3D (aa 1850) coding regions being under positive/diversifying selection. Several aa substitutions were observed in the structural proteins (VP1, VP2 and VP3) of contemporary SVA isolates when compared to historical SVA strains. Some of these aa substitutions led to changes in the surface electrostatic potential of the structural proteins. This work provides important insights into the molecular evolution and epidemiology of SVA.

  • seroprevalence of Senecavirus a in sows and grower finisher pigs in major swine producing states in the united states
    Preventive Veterinary Medicine, 2019
    Co-Authors: Elizabeth Houston, Ronaldo Magtoto, David H. Baum, Luis G Gimenezlirola, Juan Carlos Moradiaz, Pablo Pineyro
    Abstract:

    Senecavirus A (SVA) is a single-stranded RNA virus in the family Picornaviridae. Recently, SVA has been associated with idiopathic vesicular disease and increased neonate mortality outbreaks in the United States, Brazil, China, Colombia, and Thailand, with increasing incidence since 2014. Indirect detection by antibody detection methods, including indirect immunofluorescence assay (IFA), virus neutralization assay, and competitive or indirect enzyme-linked immunosorbent assays (ELISAs), have been reported in clinical and experimental trials. The objective of this study was to determine the seroprevalence of SVA in nonclinical affected herds in the United States. Individual samples were collected from 3654 and 2433 clinically healthy grower-finisher pigs and sows, respectively, from 219 unique commercial swine production sites. SVA seroprevalence was evaluated by SVA rVP1 ELISA and SVA IFA. The estimated seroprevalence for grower-finisher pigs and sows was 12.2% and 34.0%, respectively. The herd prevalence was 42.7% for grower-finisher farms and 75.8% for sow farms. The SVA rVP1 ELISA and SVA IFA exhibited a fair (sows) and moderate (grower-finisher) agreement at the herd level, while a fair agreement was observed at the individual level for both pig categories evaluated. The McNemar's test was significant at the individual and herd level (p <  0.05). In this study, we demonstrated the presence of SVA IgG antibodies in pigs from clinically healthy grower-finisher and sow herds. These results suggest that SVA is circulating subclinically in sow farms and grower-finisher pig farms in major swine producing-states in the United States.

  • Seroprevalence of Senecavirus A in sows and grower-finisher pigs in major swine producing-states in the United States.
    Preventive veterinary medicine, 2019
    Co-Authors: Elizabeth Houston, Luis G. Giménez-lirola, Ronaldo Magtoto, Juan Carlos Mora-díaz, David H. Baum, Pablo Pineyro
    Abstract:

    Senecavirus A (SVA) is a single-stranded RNA virus in the family Picornaviridae. Recently, SVA has been associated with idiopathic vesicular disease and increased neonate mortality outbreaks in the United States, Brazil, China, Colombia, and Thailand, with increasing incidence since 2014. Indirect detection by antibody detection methods, including indirect immunofluorescence assay (IFA), virus neutralization assay, and competitive or indirect enzyme-linked immunosorbent assays (ELISAs), have been reported in clinical and experimental trials. The objective of this study was to determine the seroprevalence of SVA in nonclinical affected herds in the United States. Individual samples were collected from 3654 and 2433 clinically healthy grower-finisher pigs and sows, respectively, from 219 unique commercial swine production sites. SVA seroprevalence was evaluated by SVA rVP1 ELISA and SVA IFA. The estimated seroprevalence for grower-finisher pigs and sows was 12.2% and 34.0%, respectively. The herd prevalence was 42.7% for grower-finisher farms and 75.8% for sow farms. The SVA rVP1 ELISA and SVA IFA exhibited a fair (sows) and moderate (grower-finisher) agreement at the herd level, while a fair agreement was observed at the individual level for both pig categories evaluated. The McNemar's test was significant at the individual and herd level (p 

  • serological and molecular detection of Senecavirus a associated with an outbreak of swine idiopathic vesicular disease and neonatal mortality
    Journal of Clinical Microbiology, 2016
    Co-Authors: Luis G Gimenezlirola, Christopher Rademacher, Daniel C. L. Linhares, David H. Baum, Karen M Harmon, Marisa Rotolo, Yaxuan Sun, Jeffrey J Zimmerman, Pablo Pineyro
    Abstract:

    We 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-and-mouth 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.

Douglas Marthaler - One of the best experts on this subject based on the ideXlab platform.

  • emergence and whole genome sequence of Senecavirus a in colombia
    Transboundary and Emerging Diseases, 2017
    Co-Authors: D. Sun, Fabio A. Vannucci, Todd P. Knutson, Cesar Corzo, Douglas Marthaler
    Abstract:

    In 2015 and 2016, Senecavirus A (SVA) emerged as an infectious disease in Brazil, China and the United States (US). In a Colombian commercial swine farm, vesicles on the snout and coronary bands were reported and tested negative for foot-and-mouth disease virus (FMDv), but positive for SVA. The whole-genome phylogenetic analysis indicates the Colombian strain clusters with the strains from the United States, not with the recent SVA strains from Brazil.

  • Longitudinal study of Senecavirus a shedding in sows and piglets on a single United States farm during an outbreak of vesicular disease
    BMC veterinary research, 2017
    Co-Authors: Steven J.p. Tousignant, Fabio A. Vannucci, Laura Bruner, Jake Schwartz, Stephanie Rossow, Douglas Marthaler
    Abstract:

    Background The study highlights the shedding pattern of Senecavirus A (SVA) during an outbreak of vesicular disease in a sow farm from the South-central Minnesota, USA. In this study, 34 individual, mixed parity sows with clinical signs of vesicular lesions and 30 individual piglets from 15 individual litters from sows with vesicular lesions were conveniently selected for individual, longitudinal sampling. Serum, tonsil, rectal, and vesicular swabs were collected on day1 post outbreak, and then again at 1, 2, 3, 4, 6, and 9 weeks post outbreak. Samples were tested at the University of Minnesota Veterinary Diagnostic Laboratory for SVA via Real Time Polymerase Chain Reaction (RT-PCR)

  • Emergence and whole‐genome sequence of Senecavirus A in Colombia
    Transboundary and emerging diseases, 2017
    Co-Authors: D. Sun, Fabio A. Vannucci, Todd P. Knutson, Cesar Corzo, Douglas Marthaler
    Abstract:

    In 2015 and 2016, Senecavirus A (SVA) emerged as an infectious disease in Brazil, China and the United States (US). In a Colombian commercial swine farm, vesicles on the snout and coronary bands were reported and tested negative for foot-and-mouth disease virus (FMDv), but positive for SVA. The whole-genome phylogenetic analysis indicates the Colombian strain clusters with the strains from the United States, not with the recent SVA strains from Brazil.

  • Senecavirus a an emerging pathogen causing vesicular disease and mortality in pigs
    Veterinary Pathology, 2017
    Co-Authors: Joaquim Segales, D E S N De Barcellos, A Alfieri, Eric R Burrough, Douglas Marthaler
    Abstract:

    Senecavirus A (SVA) is the only member of the genus Senecavirus within the family Picornaviridae. This virus was discovered as a serendipitous finding in 2002 (and named Seneca Valley virus 001 [SV...

  • Senecavirus A: An Emerging Pathogen Causing Vesicular Disease and Mortality in Pigs?
    Veterinary pathology, 2016
    Co-Authors: Joaquim Segales, D E S N De Barcellos, A Alfieri, Eric R Burrough, Douglas Marthaler
    Abstract:

    Senecavirus A (SVA) is the only member of the genus Senecavirus within the family Picornaviridae. This virus was discovered as a serendipitous finding in 2002 (and named Seneca Valley virus 001 [SVV-001]) while cultivating viral vectors in cell culture and has been proposed for use as an oncolytic virus to treat different types of human neoplasia. SVA was found in lesions in pigs affected by porcine idiopathic vesicular disease in Canada and the USA in 2008 and 2012, respectively. In 2014 and 2015, SVA infection was associated with outbreaks of vesicular disease in sows as well as neonatal pig mortality in Brazil and the USA. Phylogenetic analysis of the SVA VP1 indicates the existence of 3 clades of the virus. Clade I contains the historical strain SVV-001, clade II contains USA SVA strains identified between 1988 and 1997, and clade III contains global SVA strains from Brazil, Canada, China, and the USA identified between 2001 and 2015. The aim of this review is to draw the attention of veterinarians and researchers to a recently described infectious clinical-pathologic condition caused by a previously known agent (SVA). Apart from the intrinsic interest in a novel virus infecting pigs and causing economic losses, the major current concern is the similarity of the clinical picture to that of other swine diseases, because one of them-foot and mouth disease-is a World Organization for Animal Health-listed disease. Because the potential association of SVA with disease is rather new, there are still many questions to be resolved.

Charles Nfon - One of the best experts on this subject based on the ideXlab platform.

  • Vesicular disease in pigs inoculated with a recent Canadian isolate of Senecavirus A.
    Canadian journal of veterinary research = Revue canadienne de recherche veterinaire, 2019
    Co-Authors: Kate Hole, Thanuja Ambagala, Charles Nfon
    Abstract:

    The objective of this study was to investigate whether a virulent Canadian isolate of Senecavirus A (SVA) causes idiopathic vesicular disease (IVD) in pigs. Senecavirus A, which was first isolated in the United States in 2002 as Seneca Valley Virus, was linked to cases of porcine idiopathic vesicular disease in Canada in 2007 and in the United States in 2010. Since 2014, SVA outbreaks in Brazil, the US, Canada, China, Thailand, and Colombia point to an expanding global distribution and the need to study the pathogenicity of the virus. Unlike the prototype virus, recent US isolates of SVA have been shown to cause vesicular disease in pigs. We report vesicular disease in pigs following experimental inoculation with a 2016 Canadian isolate of SVA. All inoculated pigs developed vesicular lesions regardless of route of inoculation. Virus was detected in blood and oral fluids as well as on oral and fecal swabs. In addition, all pigs seroconverted to SVA by 6 days post-inoculation (DPI). This study confirms that recent Canadian isolates of SVA cause vesicular disease in pigs and highlights the importance of monitoring SVA for increased virulence.

  • Genome wide analysis of the evolution of Senecavirus A from swine clinical material and assembly yard environmental samples.
    PloS one, 2017
    Co-Authors: Kate Hole, Melissa Goolia, Bradley Pickering, Tim Salo, Oliver Lung, Charles Nfon
    Abstract:

    Senecavirus A (SVA), previously known as Seneca Valley virus, was first isolated in the United States in 2002. SVA was associated with porcine idiopathic vesicular disease in Canada and the USA in 2007 and 2012, respectively. Recent increase in SVA outbreaks resulting in neonatal mortality of piglets and/or vesicular lesions in sows in Brazil, the USA and Canada point to the necessity to study the pathogenicity and molecular epidemiology of the virus. Here, we report the analysis of the complete coding sequences of SVA from 2 clinical cases and 9 assembly yard environmental samples collected in 2015 in Canada, along with 22 previously released complete genomes in the GenBank. With this combined data set, the evolution of the SVA over a 12-month period in 2015/2016 was evaluated. These SVA isolates were characterized by a rapid accumulation of genetic variations driven mainly by a high nucleotide substitution rate and purifying selection. The SVA sequences clustered in clearly defined geographical areas with reported cases of SVA infection. No transmission links were identified between assembly yards, suggesting that point source introductions may have occurred. In addition, 25 fixed non-synonymous mutations were identified across all analyzed strains when compared to the prototype SVA strain (SVV-001). This study highlights the importance of monitoring SVA mutations for their role in increased virulence and impact on SVA diagnostics.

  • efficacy of accelerated hydrogen peroxide disinfectant on foot and mouth disease virus swine vesicular disease virus and Senecavirus a
    Journal of Applied Microbiology, 2017
    Co-Authors: Kate Hole, Faraz Ahmadpour, Jay Krishnan, Carol Stansfield, John Copps, Charles Nfon
    Abstract:

    Aims In a laboratory, disinfectants used to inactivate pathogens on contaminated surfaces and to prevent spread of diseases often have adverse side effects on personnel and the environment. It is, therefore, essential to find safer, fast-acting and yet effective disinfectants. The objective of this study was to evaluate an accelerated hydrogen peroxide® (AHP®)-based disinfectant against high consequence foreign animal disease pathogens such as foot-and-mouth disease virus (FMDV) and swine vesicular disease virus (SVDV), as well as Senecavirus A (SVA), which causes similar lesions as FMDV and SVDV. Methods and Results We tested varying dilutions and contact times of AHP against FMDV, SVDV and SVA by the standard US EPA and modified methods. AHP was effective against all three viruses, albeit at a higher concentration and double the manufacturer recommended contact time when testing wet films of SVDV. Conclusions AHP is an effective disinfectant against FMDV, SVDV and SVA. Significance and Impact of the Study AHP-based disinfectant can, therefore, be used in high containment laboratories working with FMDV, SVDV and related pathogens.

  • Efficacy of accelerated hydrogen peroxide® disinfectant on foot-and-mouth disease virus, swine vesicular disease virus and Senecavirus A.
    Journal of applied microbiology, 2017
    Co-Authors: Kate Hole, Faraz Ahmadpour, Jay Krishnan, Carol Stansfield, John Copps, Charles Nfon
    Abstract:

    In a laboratory, disinfectants used to inactivate pathogens on contaminated surfaces and to prevent spread of diseases often have adverse side effects on personnel and the environment. It is, therefore, essential to find safer, fast-acting and yet effective disinfectants. The objective of this study was to evaluate an accelerated hydrogen peroxide® (AHP® )-based disinfectant against high consequence foreign animal disease pathogens such as foot-and-mouth disease virus (FMDV) and swine vesicular disease virus (SVDV), as well as Senecavirus A (SVA), which causes similar lesions as FMDV and SVDV. We tested varying dilutions and contact times of AHP against FMDV, SVDV and SVA by the standard US EPA and modified methods. AHP was effective against all three viruses, albeit at a higher concentration and double the manufacturer recommended contact time when testing wet films of SVDV. AHP is an effective disinfectant against FMDV, SVDV and SVA. AHP-based disinfectant can, therefore, be used in high containment laboratories working with FMDV, SVDV and related pathogens. © 2016 The Canadian Food Inspection Agency. Journal of Applied Microbiology published by John Wiley & Sons Ltd on behalf of The Society for Applied Microbiology.

Paul L. Hallenbeck - One of the best experts on this subject based on the ideXlab platform.

  • Structure of Seneca Valley Virus-001: an oncolytic picornavirus representing a new genus
    Structure (London England : 1993), 2008
    Co-Authors: Sangita Venkataraman, Seshidhar P. Reddy, Jackie Loo, Neeraja Idamakanti, Paul L. Hallenbeck, Vijay S. Reddy
    Abstract:

    The crystal structure of Seneca Valley Virus-001 (SVV-001), the representative member of a new genus, Senecavirus, is reported at 2.3A resolution. SVV-001 is the first naturally occurring nonpathogenic picornavirus shown to mediate selective cytotoxicity towards tumor cells with neuroendocrine cancer features. The nonsegmented (+) ssRNA genome of SVV-001 shares closest sequence similarity with the genomes of the members of Cardiovirus. The overall tertiary structure of VP1-VP4 subunits is conserved with the exception of loops, especially those of VP1 that show large deviations relative to the members of the cardioviruses. The surface loops of VP1 and VP2 are predicted to mediate cell tropism of SVV-001. In addition, the organization of the packaged nucleic acid density indicates that certain regions of VP2 and VP4 interact closely with the packaged nucleic acid.

  • complete genome sequence analysis of seneca valley virus 001 a novel oncolytic picornavirus
    Journal of General Virology, 2008
    Co-Authors: Laura M Hales, Seshidhar P. Reddy, Nick J Knowles, Carl Hay, Paul L. Hallenbeck
    Abstract:

    The complete genome sequence of Seneca Valley virus-001 (SVV-001), a small RNA virus, was determined and was shown to have typical picornavirus features. The 7280 nt long genome was predicted to contain a 5′ untranslated region (UTR) of 666 nt, followed by a single long open reading frame consisting of 6543 nt, which encodes a 2181 aa polyprotein. This polyprotein could potentially be cleaved into 12 polypeptides in the standard picornavirus L-4-3-4 layout. A 3′ UTR of 71 nt was followed by a poly(A) tail of unknown length. Comparisons with other picornaviruses showed that the P1, 2C, 3C and 3D polypeptides of SVV-001 were related most closely to those of the cardioviruses, although they were not related as closely to those of encephalomyocarditis virus and Theiler's murine encephalomyelitis virus as the latter were to each other. Most other regions of the polyprotein differed considerably from those of all other known picornaviruses. SVV-001 contains elements of an internal ribosome entry site reminiscent of that found in hepatitis C virus and a number of genetically diverse picornaviruses. SVV-001 is a novel picornavirus and it is proposed that it be classified as the prototype species in a novel genus named ‘Senecavirus’.

  • Crystallization and preliminary X-ray diffraction studies of Seneca Valley virus-001, a new member of the Picornaviridae family.
    Acta Crystallographica Section F Structural Biology and Crystallization Communications, 2008
    Co-Authors: Sangita Venkataraman, Seshidhar P. Reddy, Jackie Loo, Neeraja Idamakanti, Paul L. Hallenbeck, Vijay S. Reddy
    Abstract:

    Seneca Valley Virus-001 (SVV-001) is a newly found species in the Picornaviridae family. SVV-001 is the first naturally occurring nonpathogenic picornavirus observed to mediate selective cytotoxicity towards tumor cells with neuroendocrine cancer features. The nonsegmented (+)ssRNA genome of SVV-001 shares closest sequence similarity to the genomes of the members of the Cardiovirus genus. However, based on the distinct characteristics of the genome organization and other biochemical properties, it has been suggested that SVV-001 represents a new genus, namely 'Senecavirus', in the Picornaviridae family. In order to understand the oncolytic properties of SVV-001, the native virus was crystallized using the hanging-drop vapour-diffusion method. The crystals belonged to space group R3, with unit-cell parameters (in the hexagonal setting) a = b = 311.5, c = 1526.4 A. Although the SVV crystals diffracted to better than 2.3 A resolution, the data quality is acceptable [I/sigma(I) > 2.0] to 2.6 A resolution. The unit-cell volume and the locked rotation-function analysis suggest that six particles could be accommodated in the unit cell, with two distinct sets of one third of a particle, each containing 20 protomers, occupying the crystallographic asymmetric unit. (ClinicalTrials.gov identifier NCT00314925)

  • The family Picornaviridae currently comprises nine genera:
    2008
    Co-Authors: Carl Hay, Paul L. Hallenbeck
    Abstract:

    The complete genome sequence of Seneca Valley virus-001 (SVV-001), a small RNA virus, was determined and was shown to have typical picornavirus features. The 7280 nt long genome was predicted to contain a 59 untranslated region (UTR) of 666 nt, followed by a single long open reading frame consisting of 6543 nt, which encodes a 2181 aa polyprotein. This polyprotein could potentially be cleaved into 12 polypeptides in the standard picornavirus L-4-3-4 layout. A 39 UTR of 71 nt was followed by a poly(A) tail of unknown length. Comparisons with other picornaviruses showed that the P1, 2C, 3C and 3D polypeptides of SVV-001 were related most closely to those of the cardioviruses, although they were not related as closely to those of encephalo-myocarditis virus and Theiler’s murine encephalomyelitis virus as the latter were to each other. Most other regions of the polyprotein differed considerably from those of all other known picornaviruses. SVV-001 contains elements of an internal ribosome entry site reminiscent of that found in hepatitis C virus and a number of genetically diverse picornaviruses. SVV-001 is a novel picornavirus and it is proposed that it be classified as the prototype species in a novel genus named ‘Senecavirus

Paisley Canning - One of the best experts on this subject based on the ideXlab platform.

  • novel Senecavirus a in swine with vesicular disease united states july 2015
    Emerging Infectious Diseases, 2016
    Co-Authors: Baoqing Guo, Hai Hoang, Christopher Rademacher, Pablo Pineyro, Ying Zheng, Darin M Madson, Phillip C Gauger, Jian Yuan, Kent J Schwartz, Paisley Canning
    Abstract:

    To the Editor: Senecavirus A (SVA; formerly known as Seneca Valley virus [SVV] belongs to the genus Senecavirus, family Picornaviridae (1,2). SVA was first isolated in 2001 as a contaminant of the PER.C6 cell line and designated as SVV-001 (1,3). Since its discovery, SVA has been infrequently detected in swine with idiopathic vesicular disease (IVD) (4–6), which clinically resembles foot-and-mouth disease, swine vesicular disease, vesicular exanthema of swine, and vesicular stomatitis. The virus has also been retrospectively detected in previous cases with various clinical conditions in the United States during 1988–2001 (7). However, the clinical significance of SVA in swine could not be determined (7,8).

  • Neonatal Mortality, Vesicular Lesions and Lameness Associated with Senecavirus A in a U.S. Sow Farm.
    Transboundary and emerging diseases, 2016
    Co-Authors: Paisley Canning, Christopher Rademacher, Kyoung-jin Yoon, Pablo Pineyro, Kent J Schwartz, A. Canon, Jessica L. Bates, K. Gerardy, Daniel Linhares, Derald Holtkamp
    Abstract:

    A 300-sow farrow-to-finish swine operation in the United States experienced a sudden and severe increase in mortality in neonatal piglets with high morbidity followed by vesicular lesions on the snout and feet of adult females and males. Affected live piglets were submitted for diagnostic investigation. Samples tested polymerase chain reaction (PCR) negative for foot-and-mouth disease virus, porcine delta coronavirus, porcine epidemic diarrhoea virus, porcine rotavirus types A, B and C, transmissible gastroenteritis virus, and porcine reproductive and respiratory syndrome virus. Senecavirus A (SV-A) formerly known as Seneca Valley virus was detected by real-time reverse-transcription polymerase chain reaction (rRT-PCR) from serum, skin and faeces of piglets and from serum and faeces of sows. SV-A was isolated in cell culture from piglet samples. SV-A VP1 gene region sequencing from piglet tissues was also successful. A biosecurity and disease entry evaluation was conducted and identified potential biosecurity risks factors for the entry of new pathogens into the operation. This is the first case report in the United States associating SV-A with a clinical course of severe but transient neonatal morbidity and mortality followed by vesicular lesions in breeding stock animals. Veterinarians and animal caretakers must remain vigilant for vesicular foreign animal diseases and report suspicious clinical signs and lesions to state animal health authorities for diagnostic testing and further investigation.