Vesicular Exanthema of Swine (San Miguel Sea Lion Viral Disease)
In swine, an acute, contagious disease caused by a Calicivirus and characterized by vesicles on the feet, snout, mucous membranes of the mouth and tongue, and non-haired skin. The disease in sea lions causes vesicles on the flippers.
Of the domestic animals, vesicular exanthema (VE) occurs only in swine. The disease has only occurred in the US; in swine shipped from the United States to Hawaii, and in swine fed raw garbage from a US military post in Iceland. The disease has never been reported from any other country. Vesicular exanthema has not recurred in domestic swine since it was eradicated in 1956.
San Miguel sea lion viral disease (SMSL) occurs in sea lions, fur seals, elephant seals, opal-eye fish and several other marine animals of the western coast of the United States.
Beginning in 1932, a vesicular disease, now believed to have been VE, occurred repeatedly in California. The lesions closely resembled those of foot-and-mouth disease (FMD). Outbreaks were contained by slaughtering the infected herds. In 1951, uncooked garbage from a train originating in California was fed to swine in Wyoming. Those swine developed vesicular exanthema. The disease spread throughout many states. Eradication required five years. In 1959, VE was declared to be an exotic disease.
Beginning in 1973, caliciviruses indistinguishable from the virus that causes vesicular exanthema were isolated from sea lions, northern elephant seals, fur seals and certain kinds of fish. Each of the viruses can produce lesions in swine and certain sea mammals.
The calicivirus that causes VE and SMSL is believed to be the same. However, spontaneous outbreaks of VE in swine caused by SMSL virus have not been substantiated. Caliciviruses have a cup-shaped morphology from which they are named. The calicivirus that causes VE is sensitive to many common disinfectants including 2% sodium hydroxide.
Antibodies to several other closely related caliciviruses have been detected in both marine and terrestrial animals. The latter include swine, cattle, donkeys, foxes and buffalo. The taxonomy and exact relationship between these various caliciviruses have yet to be agreed upon.
The opal-eye fish (Girella nigricans) now is believed to be the primary host of the calicivirus that may be passed to pinnipeds and swine. The method of spread of the virus among sea lions and other sea mammals is speculative. It could be through ingestion of infected fish or small marine life, by coastal contamination, or direct contact.
Swine usually are exposed to the VE calicivirus by eating uncooked garbage containing infectious meat scraps from swine or certain fish. Although unproven, some marine origin feed supplements for swine may contain calicivirus. Vesicular exanthema is quite contagious among swine and spreads by direct contact and fomites. Neither long-term carriers nor aerosol spread have been demonstrated.
In swine, the VE calicivirus is ingested in uncooked garbage. Virus enters the epithelium through abrasions and multiplies in the basal layer of the epidermis. Intracellular and intercellular edema and coalescence of disintegrating cells leads to vesicle formation. Virus spreads cell to cell as lesions develop. A low-grade viremia occurs and leads to secondary lesions at other sites. Extensive lymphocyte destruction occurs in regional lymph nodes. Since much of the basal layer of epidermis survives, regeneration of epithelium in swine usually occurs within one to two weeks. Lesions in sea lions closely resemble those seen in swine.
Experimentally, it requires much more virus by oral exposure to produce VE than is required by intradermal injection. This suggests that the virus can be spread more readily through abrasions on the skin.
Most swine with VE probably would recover if allowed to do so. However, it is required that they be destroyed as a precaution to prevent the surreptitious entry of foot-and-mouth disease.