Vesicular diseases in swine are identical clinically. They can be caused by infection with the viruses of foot-andmouth disease (FMD), vesicular stomatitis (VS), vesicular exanthema of swine (VES), and swine vesicular disease (SVD). FMD, VES, and SVD are exotic to the United States, while VS is enzootic. The importance of vesicular diseases in today's world-trade environment remains high. Because FMD is extremely contagious and has such a dramatic economic impact, vesicular diseases must be properly diagnosed, reported, and controlled.
In Italy in 1546, Fracastorius made what is probably the first report of a vesicular disease (Bulloch 1927). FMD was the first animal disease shown to be caused by a filterable agent (Loeffler and Frosch 1898). VS was recognized in horses and cattle in the United States during World War I (Cotton 1927), but infection in swine was not reported until 1943 (Schoening 1943). The first report of VES was in 1932 in California (Traum 1934), although it was initially thought to be FMD. A new vesicular disease, SVD, emerged in Italy in 1966 (Nardelli et al. 1968). San Miguel sea lion viruses (SMSVs), isolated from marine mammals, were shown to cause vesicular disease in inoculated swine (Smith et al. 1973; Berry et al. 1990). The history and distribution of these viruses are given in Table 25.1.
ETIOLOGY
The characteristics of the viruses that cause vesicular diseases are shown in Table 25.2.
SS RNA = single-stranded RNA.
Foot-and-Mouth Disease
FMD viruses (FMDVs) are in the family Picornaviridae and the genus Aphthovirus (Francki et al. 1991c). Aphtha is the Greek word for "vesicles in the mouth." These viruses are small (22-30 nm), nonenveloped, and labile below pH 7.0, and they have single-stranded positivesense RNA with approximately 8450 nucleotides that serve as messenger RNA. The high rate of nucleotide substitutions in the single-stranded RNA viruses accounts for their wide variation (Domingo et al. 1993; Vosloo et al. 1996). Perhaps one of the most important sites for substitutions is the GH loop (codons 133-158) of viral protein 1 (VP1) (Acharya et al. 1989), which is adjacent to the common aphthovirus receptor site RGD (Fox et al. 1989). There are four structural viral proteins, of which VP1 has been shown to elicit protective immunity in cattle (Bachrach 1977). Viral RNA polymerase, a nonstructural protein, has been termed "virus infection associated antigen" (VIAA) for diagnostic purposes but is more accurately termed "FMDV nonstructural protein 3D." One copy of 3D occurs in each viral particle (Newman et al. 1994). The FMDV nonstructural protein 2C is present in clarified FMD vaccines at levels insufficient to elicit an immune response (Lubroth et al. 1996).
There are seven serotypes of FMDV: A, O, C, Asia 1, and South African Territories (SAT) 1, 2, and 3. There is no cross-protection between the serotypes (Brooksby 1982). All serotypes have numerous subtypes, which may arise during acute or persistent infection (Gebauer et al. 1988; Vosloo et al. 1996). The serologic relatedness of subtypes is determined by "r-values," the ratio of antibody titers between new and reference viruses (Pereira 1977).
Swine Vesicular Disease
SVD virus (SVDV) is in the family Picornaviridae, genus Enterovirus (Francki et al. 1991c). The virions are small (22-30 nm), nonenveloped, and acid-stable. Each has a single-stranded positive-sense RNA and four structural viral proteins. There is one serotype of SVDV, whose closest relative is the human enterovirus Coxsackie B-5 (Graves 1973).
Vesicular Exanthema of Swine and San Miguel Sea Lion Viruses
The VESVs and SMSVs, members of the Caliciviridae family, are closely related caliciviruses (Smith et al. 1973), named from the Latin calices (cups) for the cupshaped depressions on the virion. The viruses are 35-39 nm in diameter, nonenveloped, moderately acid-stable, and contain single-stranded positive-sense RNA (Francki et al. 1991b). The capsomers are composed of one major polypeptide. There are 13 known serotypes of VESVs, which are sequentially designated (except for strains 1934B and 101) by a letter followed by the year of isolation (e.g., VESV A48).
There are at least 13 SMSV serotypes, which are numbered consecutively (with no SMSV 3, which does not exist) in order of discovery.