The etiologic agent, vesicular stomatitis virus (VSV), is a rhabdovirus. There are 2 serotypes of VSV, New Jersey and Indiana. Infection with one serotype is not cross-protective for the second serotype.
VSV versus the other vesicular disease viruses of livestock:
Vesicular stomatitis virus infection resembles foot-and-mouth disease when it occurs in cattle, and the other viral vesicular diseases when it occurs in pigs. However, VSV is the only one of the "Big 4" viral vesicular diseases of livestock (foot and mouth disease virus [FMDV], swine vesicular disease virus [SVDV], vesicular exanthema of swine virus [VESV] and VSV) that infects horses (inoculation of a horse's tongue was historically used to differentiate VSV from the others). VSV is also the most important of these 4 viruses as a zoonotic agent for humans.
Most experts agree that humans can harbor FMDV in their pharynx for 24-36 hours, and possibly as long as 5 days. In addition, there are a very small number of documented cases (40 cases between 1921-1969) of actual human infection with FMDV, associated with mild flu-like illness and mild vesicular lesions. Infected people may shed virus for up to 14 days and may serve as a source for infection of other animals, but the risk of such biological transmission is considered "negligible" by the USDA.
FMD is NOT the same as hand, foot, and mouth disease in human children. Hand, foot, and mouth disease is, like FMD, caused by infection with a picornaviruses, but picornaviruses distinct from FMDV (such as the Coxsackie viruses and enterovirus 71).
SVDV can cause a mild flu-like illness in humans.
VESV and related viruses from marine mammals have been reported to cause vesicular lesions on the hands and feet in humans.
Vesicular stomatitis virus is primarily viewed as an arbovirus.
Phlebotomine sandflies are confirmed biological vectors of VSV.
The virus has also been found to replicate in Culicoides midges and Simulium blackflies.
However, VSV can also be spread by direct contact among infected pigs. (See Stallknecht et al. 1999)
Although often treated as an "exotic" disease to the U.S., there is one enzootic focus of VSV in the country (Ossabaw Island just off the Georgia coast), and outbreaks of VSV infection occur periodically in the western U.S.
Outbreaks in the U.S. are thought to originate with the movement of animals and/or insect vectors from Mexico.
Major outbreaks have occurred repeatedly in the U.S. over ~10 year cycles, with disease occurring for 2-3 years and then disappearing again for ~10 years.
In 1995, 367 VSV (+) premises were reported in the southwestern U.S. and there were cases of VSV infection in horses in the southwestern U.S. again in 1997 and 1998.
VS in horses, cattle and swine:
fever 24-48 hours after infection
oral vesicles and inflammatory lesions at the coronary band
Rupture of the oral vesicles leads to pain, excessive salivation and inappetance.
The coronary band lesions lead to lameness.
Diagnosis in livestock:
virus isolation from vesicular fluid
serology
Control of outbreaks is dependent upon rapid recognition of initial cases, quarantine and restriction of movement of infected and in-contact animals, and insect control. There are no commercially-available VSV vaccines in the U.S., but an autologous vaccine was made in 1995 to help control that outbreak. Several inactivated vaccines containing both the Indiana and New Jersey serotypes are used in Central and South America.
