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Volume 32, Number 2—February 2026
Research Letter
Vesicular Disease Caused by Seneca Valley Virus in Pigs, England, 2022
Suggested citation for this article
Abstract
Vesicular disease caused by Seneca Valley virus infection occurred in pigs from 5 outdoor pig farms in England during June–September 2022. Clinical signs resembled notifiable vesicular diseases, such as foot-and-mouth disease. Full genome sequences shared a common ancestor with a virus circulating in the United States.
Researchers reported vesicular disease associated with Seneca Valley virus (SVV; Senecavirus valles, family Picornaviridae) in pigs imported into the United States from Canada in 2007 (1). Similar reports subsequently emerged from other countries, including Brazil, China, Thailand, Chile, India, Vietnam, Columbia, and Mexico (2–4). We describe cases of SVV infection in pigs from 5 pig breeding farms in eastern England during June–September 2022.
Farm staff initially observed signs of vesicular disease in recently inseminated sows at an outdoor breeding unit (SVV2022-01): lameness, reluctance to move, and lesions on the nose and feet, varying from discrete vesicles on the coronary band and interdigital space to deep erosions and heel horn separation. We collected blood and vesicular tissue samples as part of an official vesicular disease investigation; all samples tested negative by real-time reverse transcription PCR (rRT-PCR) for notifiable diseases (foot-and-mouth disease virus, swine vesicular disease virus, and vesicular stomatitis virus) (5). However, we observed cytopathic effect during virus isolation, and parallel rRT-PCR testing (6) generated positive results for SVV.
We subsequently identified vesicular disease in recently inseminated sows on 3 additional farms (SVV2022-02 [Figure 1], SVV2022-03 and SVV2022-05). Again, official veterinary investigations yielded negative results for notifiable diseases and confirmed the presence of SVV by rRT-PCR. Gilts, young boars, and weaners appeared clinically unaffected, despite evidence of SVV in rectal and nasal swab specimens. Retrospective tracing identified another farm (SVV2022-04) with confirmed SVV in a group of recently lame sows.
We collected samples including vesicular epithelium, vesicular fluid, rectal and nasal swabs, blood, and tonsils from dead pigs. We also collected samples from weaners derived from 4 of the 5 affected farms and from sows and postmortem pigs at farm SVV2022-03 for up to 4 months after the initial disease reports. In total, 461 (35.0%) of 1,319 samples tested positive for SVV by rRT-PCR from the 5 farms (Appendix Table). On farms SVV2022-01 and SVV2022-02, we initially collected blood samples, with 17 of 34 positive by rRT-PCR; however, because viremia is short-lived, that sampling matrix was not ideal for surveillance. Analysis revealed the highest viral loads in vesicular lesion and tonsil samples (strongest cycle threshold value 10.8). Rectal swabs were the most frequently collected sample type (n = 914) owing to ease of collection. Nasal swab specimens were useful in revealing acute stages of disease, but rectal swab specimens proved more useful in detecting SVV in recovering pigs, despite weaker rRT-PCR responses. That observation supports the use of rectal swab sampling in pigs of unknown SVV status, where resources or logistics limit sampling options. Our data also highlight the value of testing tonsils, illustrated by detection of SVV RNA in a tonsil from a dead piglet >35 days after the episode of clinical signs (farm SVV2022-02).
We conducted serologic investigations 5 weeks after the disease episode at farm SVV2022-04 and during the acute stage of disease at farm SVV2022-01. A total of 55 of 63 serum samples from farm SVV2022-01 and 10 of 10 samples from farm SVV2022-04 were positive for SVV-specific antibodies as determined by the virus neutralization test using SK6 cells.
Paired rectal and semen samples collected from boars supplying semen and historic batches of feed and soya bean meal samples supplied to affected farms all tested negative for SVV by rRT-PCR. We detected SVV RNA in 76 (56.7%) of 134 environmental samples (7) collected 3.5 weeks after the disease occurrence from farm SVV2022-01, where pigs no longer remained on the premises. Sample sites included walls, doors, feeders, drinkers, floors, gates, and a trailer. We also detected SVV RNA in 6 (10.2%) of 59 samples collected 6 weeks after the disease occurrence from farm SVV2022-04, where pigs remained (sites included loading area, drinker, ark, and trailer) (Appendix Figure). Our data highlight the importance of cleaning, disinfection, and stringent biosecurity to limit the spread of SVV.
We characterized SVV isolates using next-generation sequencing (8) and found they share a common ancestor with a virus isolated in the United States during 2020 (SVV/USA/TN/NADC6/2020; GenBank accession no. MZ733975) (Figure 2), predicted to have circulated around November 2020 (95% highest posterior density June 2020–March 2021). We assigned the SVV sequences into 2 sister clades differing at >50 nt sites, consistent with 2 possible epidemiologic scenarios: a single virus introduction, with the resulting diversity accruing from within-country transmissions and evolution; or independent introductions into England of viruses characterized by a slightly different genetic signature. Further epidemiologic investigation could determine the most important risk pathways for introduction, transmission routes between farms, and geographic spread of SVV infection in the United Kingdom.
In conclusion, the clinical similarity of the SVV disease outbreaks we describe to notifiable vesicular diseases highlights the value of passive surveillance and the legal requirement for pig keepers and veterinarians to report vesicular lesions promptly. Cases of SVV infection were transient, and pigs recovered quickly, with minimal productivity losses. We alerted regional veterinarians and farmers of the need to remain vigilant for vesicular disease, and there have been no further clinical cases of SVV in England since September 2022.
Dr Armson is a postdoctoral scientist at The Pirbright Institute. Her research interests include the epidemiology, diagnostics, and control of viral diseases of livestock.
Acknowledgments
The authors are grateful to the pig farmers, their staff, and veterinary surgeons for their cooperation with official veterinary investigations. We also recognize the contribution of a wide number of staff from the Animal and Plant Health Agency and The Pirbright Institute as part of their routine work.
This study was funded by a combination of UK Department for Environment, Food and Rural Affairs–funded projects at the Animal and Plant Health Agency: Scanning surveillance for Diseases in Pigs (ED1200) and The Pirbright Institute (SE2722, SE2945, SE2947, SE0573, SE0579 and SE1131). The Pirbright Institute also receives grant-aided support from the Biotechnology and Biological Sciences Research Council of the United Kingdom (projects BBS/E/I/00007037, BBS/E/PI/230001 A, BBS/E/PI/230002 C, and BBS/E/PI/23NB0004).
We submitted the 14 full genome sequences associated with this study to GenBank and received the corresponding accession numbers: PV845105 (UKG/26/2022), PV845106 (UKG/36/2022), PV845107 (UKG/52/2022), PV845108 (UKG/53/2022), PV845109 (UKG/58/2022), PV845110 (UKG/208/2022), PV845111 (UKG/212/2022), PV845112 (UKG/230/2022), PV845113 (UKG/231/2022), PV845114 (UKG/1864/2022), PV845115 (UKG/1866/2022), PV845116 (UKG/1868/2022), PV845117 (UKG/2199/2022), and PV845118 (UKG/2811/2022).
References
- Pasma T, Davidson S, Shaw SL. Idiopathic vesicular disease in swine in Manitoba. Can Vet J. 2008;49:84–5.PubMedGoogle Scholar
- Bennett B, Urzúa-Encina C, Pardo-Roa C, Ariyama N, Lecocq C, Rivera C, et al. First report and genetic characterization of Seneca Valley virus (SVV) in Chile. Transbound Emerg Dis. 2022;69:e3462–8. DOIPubMedGoogle Scholar
- Maan S, Batra K, Chaudhary D, Punia M, Kadian V, Joshi VG, et al. Detection and genomic characterization of Senecavirus from Indian pigs. Indian J Anim Res. 2023;57:1344–50.
- Navarro-López R, Perez-De la Rosa JD, Rocha-Martínez MK, Hernández GG, Villarreal-Silva M, Solís-Hernández M, et al. First detection and genetic characterization of Senecavirus A in pigs from Mexico. J Swine Health Prod. 2023;31:289–94. DOIGoogle Scholar
- Reid SM, Grierson SS, Ferris NP, Hutchings GH, Alexandersen S. Evaluation of automated RT-PCR to accelerate the laboratory diagnosis of foot-and-mouth disease virus. J Virol Methods. 2003;107:129–39. DOIPubMedGoogle Scholar
- Fowler VL, Ransburgh RH, Poulsen EG, Wadsworth J, King DP, Mioulet V, et al. Development of a novel real-time RT-PCR assay to detect Seneca Valley virus-1 associated with emerging cases of vesicular disease in pigs. J Virol Methods. 2017;239:34–7. DOIPubMedGoogle Scholar
- Colenutt C, Brown E, Nelson N, Wadsworth J, Maud J, Adhikari B, et al. Environmental sampling as a low-technology method for surveillance of foot-and-mouth disease virus in an area of endemicity. Appl Environ Microbiol. 2018;84:e00686–18. DOIPubMedGoogle Scholar
- Logan G, Freimanis GL, King DJ, Valdazo-González B, Bachanek-Bankowska K, Sanderson ND, et al. A universal protocol to generate consensus level genome sequences for foot-and-mouth disease virus and other positive-sense polyadenylated RNA viruses using the Illumina MiSeq. BMC Genomics. 2014;15:828. DOIPubMedGoogle Scholar
- Tamura K, Nei M. Estimation of the number of nucleotide substitutions in the control region of mitochondrial DNA in humans and chimpanzees. Mol Biol Evol. 1993;10:512–26.PubMedGoogle Scholar
- Tamura K, Stecher G, Kumar S. MEGA11: Molecular evolutionary genetics analysis version 11. Mol Biol Evol. 2021;38:3022–7. DOIPubMedGoogle Scholar
Figures
Suggested citation for this article: Armson B, Mioulet V, Wood BA, Di Nardo A, Knowles NJ, Wadsworth J, et al. Vesicular disease caused by Seneca Valley virus in pigs, England, 2022. Emerg Infect Dis. 2026 Feb [date cited]. https://doi.org/10.3201/eid3202.251194
Original Publication Date: February 15, 2026
Table of Contents – Volume 32, Number 2—February 2026
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Please use the form below to submit correspondence to the authors or contact them at the following address:
Bryony Armson, The Pirbright Institute, Ash Road, Woking, Surrey GU24 0NF, UK
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