Swine vesicular disease (SVD) is typically a transient disease of pigs in which vesicular lesions appear on the feet and snout and in the mouth. It does not cause severe production losses, and recent outbreaks of infection have been mainly subclinical. However, infection is of major economic importance because it must be differentiated from foot-and-mouth disease, eradication is costly, and embargoes on export of pigs and pork products are often imposed on nations not free of SVD.
Although infection in laboratory workers has occurred, and the virus may be present in sheep or cattle, pigs are said to be the only natural host. The disease was first identified in Italy in 1966 and subsequently in Hong Kong, Japan, Taiwan, and 16 countries in Europe. Although SVD virus was eradicated from Japan in the mid-1970s and most European countries by the mid-1980s, it has remained endemic in Italy and caused sporadic outbreaks of disease in other European countries during the 1990s and in Portugal in 2003, 2004, and 2007.
The causal agent is an enterovirus of the family Picornaviridae. It belongs to the species Human enterovirus B and is thought to have evolved from the human pathogen coxsackievirus B5, with which it shares a close antigenic and genetic relationship. There is only 1 serotype of SVD virus, although isolates may be differentiated by antigenic or genetic typing and may differ in virulence. SVD virus is transmitted by direct or indirect contact or by feeding infected pork or pork products. Infection is via the oral route or through skin abrasions and can give rise to viremia, fecal viral shedding, and generalized vesicles that rupture to release large amounts of virus.
Clinical Findings and Lesions
The primary signs are fresh or healing vesicular lesions on the feet, especially the coronary band, and in other areas such as the mouth, lips, or snout. The lesions may be mild or inapparent, especially when pigs are kept on soft bedding. The lesions are similar to those of foot-and-mouth disease (see Foot-and-Mouth Disease), vesicular exanthema of swine (see Vesicular Exanthema of Swine), and vesicular stomatitis (see Vesicular Stomatitis); however, affected pigs do not lose condition, and the lesions heal rapidly. Nervous signs have been described but are rarely seen in the field.
Diagnosis is confirmed by laboratory tests on epithelial samples, feces, or serum. Virus detection is by antigen-detection ELISA, virus isolation, or reverse transcriptase-PCR. Serology is by antibody-detection ELISA or virus neutralization test.
Countries free of the disease can remain so by controlling the import of pigs and pork products or by ensuring that pork products are treated (heat or otherwise) to kill the virus. Feeding of garbage to pigs may be banned or regulated to ensure thorough cooking. Any suspected outbreak should be reported to the proper authorities. If disease does appear, control is by zoosanitary measures, including restrictions on pig movement. There are no commercially available vaccines. Extensive serosurveillance is necessary to detect subclinically infected herds, and seroreactor herds must be followed up by clinical inspection and fecal virus testing. The virus remains infective for long periods; thus, disinfection of premises, trucks, and equipment must be thorough. The most effective disinfectants are strong alkalis, although hypochlorites or acid-containing iodophors can be used when organic material is not present.
Last full review/revision March 2012 by Nick J. Knowles, MPhil; David J. Paton, MA, VetMB, PhD, MRCVS