Swine vesicular disease (SVD) is a viral vesicular disease of pigs caused by an enterovirus that most likely was a recombination of human coxsackievirus B5 and coxsackievirus A9. It is generally a mild disease that causes vesicular lesions on the feet and in the mouth of pigs. It was endemic in Italy, where the last clinical case occurred in 2015 — the last reported clinical case worldwide. Its importance was as a differential diagnosis for foot-and-mouth disease, from which it is clinically indistinguishable. Killing and destroying susceptible animals in SVD-infected herds has been the method of control used in Europe.
Swine vesicular disease (SVD) is a transient disease of pigs in which vesicular lesions appear on the feet and snout and in the mouth. SVD is usually mild in nature and can infect pigs subclinically. However, the disease had some economic importance in that it needed to be differentiated from foot-and-mouth disease (FMD). Current molecular diagnostic techniques (RT-PCR assay) make differentiation much quicker; therefore, SVD is no longer listed by the World Organisation for Animal Health.
Domestic and wild pig are considered the only natural host of the SVD virus. However, it can infect sheep in close contact with infected pigs. SVD has been reported only in Europe and Asia, having first been identified in Italy in 1966 and subsequently in Hong Kong (1970), Japan (1973), Taiwan (1997–2000), and 17 countries in Europe (1). Although SVD virus was eradicated from Japan in the mid-1970s and most European countries by the mid-1980s, it had remained endemic in Italy and caused sporadic outbreaks of disease in the Netherlands, Belgium, and Spain during the 1990s and in Portugal in 2003, 2004, and 2007. The last reported clinical case was in 2015 in Italy (2).
Etiology of Swine Vesicular Disease
The causative agent of swine vesicular disease is an enterovirus of the family Picornaviridae. It belongs to the species Enterovirus betacoxsackie (formerly Enterovirus B) and is thought to have evolved from the human pathogens coxsackievirus B5 and coxsackievirus A9 (3). SVD virus shares a close antigenic relationship with coxsackievirus B5, from which the sequence of the capsid proteins was derived.
There is only one serotype of SVD virus. However, isolates can be differentiated by antigenic or genetic typing and can differ in virulence. SVD virus is transmitted by direct or indirect contact or by ingestion of infected pork or pork products. Infection is via the oral route or through skin abrasions, and it can cause viremia, fecal viral shedding, and generalized vesicles that rupture to release large amounts of virus. It is considered a pen disease, as transmission to other pens is often limited (4).
Clinical Findings and Lesions of Swine Vesicular Disease
The primary clinical signs of swine vesicular disease are fresh or healing vesicular lesions on the feet, especially the coronary band, often extending to the bulb of the heel, and less often other areas, such as the mouth, lips, teats, or snout (see , and , images). The lesions can be mild or inapparent, especially when pigs are kept on soft bedding. The lesions are similar to those of foot-and-mouth disease, vesicular exanthema of swine, Seneca Valley virus, and vesicular stomatitis; however, affected pigs usually do not lose condition, and the lesions heal rapidly.
An extensive nasal lesion on a sow during an SVD outbreak in the Netherlands in 1992.
Courtesy of WBVR-Lelystad.
Vesicular lesion at the coronary band (red arrow). Note the lesion erupting from the area adjacent to the bulb of the heel.
Courtesy of WBVR-Lelystad.
Neurological signs related to SVD have been described; however, they are rarely observed in the field. The World Organisation for Animal Health recommends that any outbreaks of vesicular disease in pigs should be assumed to be FMD until proven otherwise by means of laboratory testing, which can be performed within a day.
Pearls & Pitfalls
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Diagnosis of Swine Vesicular Disease
Laboratory testing of samples of epithelium, feces, or serum
Real-time reverse-transcription PCR assay
Virus isolation with antigen detection for confirmation
Serological testing (ELISA or virus neutralization test)
Diagnosis of swine vesicular disease is confirmed by laboratory testing of samples of epithelium, feces, or serum from affected animals. Virus detection is initially performed by real-time RT-PCR assay (5). This test is more sensitive and quicker than virus isolation, which is only performed for confirmation of positive results. Serological diagnosis is done by antibody-detection ELISA or virus neutralization; however, low specificity can be a concern. In clinical cases, the preferred specimens are lesion material. Subclinical infection can be detected by testing pen-floor fecal samples using RT-PCR assay or virus isolation.
SVD is no longer a listed disease with the World Organisation for Animal Health because of its mild clinical signs and ease of differentiation from foot-and-mouth disease via laboratory testing. However, it remains a notifiable disease in some countries.
Control of Swine Vesicular Disease
Controlling the import of pigs and pork products
Appropriate methods of treating pork products to kill the virus
Banning or regulating feeding of food remains to pigs
Control of swine vesicular disease is not relevant currently, as it has not been detected since 2015. Countries that were free of SVD remained so by controlling the import of pigs and pork products or by ensuring that pork products were treated (by heat or otherwise) to kill the virus. Feeding of food remains to pigs was banned or regulated to ensure thorough cooking of raw animal products. Any suspected outbreak should be reported to the appropriate authorities, as the clinical signs of disease cannot be clinically differentiated from foot-and-mouth disease.
There are no commercially available vaccines for SVD, so killing and destroying susceptible animals in SVD-infected herds and hygiene are the only control tools. Italy controlled the circulation of SVD by extensive serosurveillance to detect subclinically infected herds, and herds with seropositive pigs were followed up by clinical inspection and fecal virus testing.
SVD virus is extremely resistant in the environment and is stable over a wide pH range (2.5–12); thus, disinfection of premises, trucks, and equipment must be thorough. The most effective disinfectants are strong alkalis. Many other products work; however, often only in a higher concentration than is recommended and only after a lengthy contact time.
Key Points
Swine vesicular disease is a mild viral disease that causes vesicular lesions of the coronary band, snout, and mouth.
SVD is indistinguishable from foot-and-mouth disease.
The last case of clinical SVD was reported in 2015 (in Italy).
The virus that causes SVD is extremely resistant and can survive for months in the environment and in poorly cooked meat products.
For More Information
WOHA Technical Disease Card: Swine Vesicular Disease
DisConTools SVD information: Swine Vesicular Disease
References
Dekker A, Knowles NJ, Belsham GJ, et al. Picornaviruses. In: Zimmerman JJ, Burrough ER, Karriker LA, Schwartz KJ, Zhang J, eds. Diseases of Swine. 12th ed. Wiley; 2025:723-768. doi:10.1002/9781394179466.ch36
Tamba M, Plasmati F, Brocchi E, and Ruocco L. Eradication of Swine Vesicular Disease in Italy. Viruses. 2020;12(11):1269. doi:10.3390/v12111269
Bruhn CAW, Nielsen SCA, Samaniego JA, Wadsworth J, Knowles NJ, Gilbert MTP. Viral meningitis epidemics and a single, recent, recombinant and anthroponotic origin of swine vesicular disease virus. Evol Med Public Health. 2015;2015(1):289-303. doi: 10.1093/emph/eov026
Dekker A, van Hemert-Kluitenberg F, Baars C, Terpstra C. Isotype specific ELISAs to detect antibodies against swine vesicular disease virus and their use in epidemiology. Epidemiol Infect. 2002;128(2):277-284. doi:10.1017/s0950268801006458
van Rijn PA, Wellenberg GJ, Hakze-van der Honing R, Jacobs L, Moonen P, Feitsma H. Detection of economically important viruses in boar semen by quantitative RealTime PCR technology. J Virol Methods. 2004;120(2):151-60. doi: 10.1016/j.jviromet.2004.04.014
