CHAPTER 24 Vesicular Stomatitis
ETIOLOGY
Vesicular stomatitis viruses (VSVs) are members of the family Rhabdoviridae, which includes viruses that infect vertebrates, invertebrates, and many plant species.1 The viruses of this family that are known to infect mammals are in two genera, Lyssavirus and Vesiculovirus. Rabies is the most well characterized and most devastating virus of the Lyssavirus genus; VSVs are the prototype viruses of the Vesiculovirus genus. VSVs are bullet shaped and generally 180 nm long and 75 nm wide.2 The nucleocapsid, or ribonucleoprotein (RNP) core, and lipoprotein envelope surrounding the RNP core are the two major structural components of VSVs. Extending from the outer surface of the envelope are spikelike projections.1 The genome of VSVs consists of a single strand of negative-sense ribonucleic acid (RNA) and is composed of five genes, N, P, M, G, and L, representing the nucleocapsid protein, phosphoprotein (a component of the viral RNA polymerase), matrix protein, glycoprotein, and the large protein (a component of the viral RNA polymerase), respectively.1
Although there are many members of the Vesiculovirus genus, two are of particular interest in the United States, vesicular stomatitis virus–New Jersey (VSV-NJ) and vesicular stomatitis virus–Indiana (VSV-IN). These two viruses are similar in size and morphology but generate distinct neutralizing antibodies in infected animals. Thus, although considered distinct viruses, they are often distinguished only by terming one serotype “New Jersey” and the other serotype “Indiana.”3 Other members of the Vesiculovirus genus include Cocal, Jurona, Carajas, Maraba, Piry, Calchaqui, Yug Bogdanovac, Isfahan, Chandipura, Perinet, and Porton-S.1 Cocal and Alagoas are subtypes of VSV-IN and have been associated with disease in animals in South America. Piry, Chandipura, and Isfahan produced only mild lesions in experimentally infected animals.4 The remaining vesiculoviruses have been isolated from arthropods, mammals, or both but are not associated with disease.1
EPIDEMIOLOGY
Disease in United States
The first report of vesicular stomatitis (VS) in the United States was in 1916. However, anecdotal reports from the Civil War period leave little doubt that VS was occurring in horses during that time.5 In 1926 an extensive outbreak of VS occurred in New Jersey in which approximately 750 cattle on 33 farms were affected. The disease appeared in very few horses. The agent was isolated and determined to be distinct from the Indiana strain isolated in the previous year. This new strain of VS was termed “vesicular stomatitis New Jersey strain.”6 Over the next six decades, VS occurred sporadically throughout the United States. Only states in New England appear to have been spared incursions of VS.
In the 1990s, three outbreaks of VS occurred in the southwestern United States. On May 9, 1995, the first case of VS was confirmed in Las Cruces, New Mexico. A “case” was defined as an animal with positive virus isolation or serologic test results, in combination with clinical signs consistent with VS. Bridges et al.7 have provided an extensive review of this outbreak. Briefly, 1162 investigations were conducted in 42 states during the outbreak. VS was confirmed in six states, including Colorado (165 premises), New Mexico (186 premises), Utah (6 premises), Texas (1 premises), Arizona (1 premises), and Wyoming (8 premises). Overall, 78% of the positive premises housed horses that were positive for VS, 22% of positive premises housed cattle that were positive for VS, and there was one VS-positive llama. All cases where virus isolation was successful were caused by the VSV-NJ serotype.
McCluskey et al.8 have provided a detailed review of the 1997 outbreak. The index case for this outbreak in the United States was identified on May 27 in Yavapai County, Arizona, after a report of suspicious vesicular lesions in a horse by a private practitioner. During the 1997 outbreak, 689 investigations for suspect VS occurred in 40 states. There were 380 (55%) premises identified as housing animals positive for VS in four states: Arizona, Colorado, New Mexico, and Utah. Similar to the 1995 outbreak, clusters of cases occurred in the Albuquerque, New Mexico, and Grand Junction, Colorado, areas. However, unlike the 1995 outbreak, a large number of cases were identified in the counties east of the Continental Divide in Colorado, extending from Pueblo as far east as Brush, Colorado. Nationwide, horses comprised 704 of 802 (88%) of the examinations conducted for suspect VS, and 362 of 374 (97%) positive premises had horses positive for VS. Cattle comprised 78 of 802 (10%) of the examinations conducted, and 12 of 374 (3%) positive premises had positive cattle. No premises had both positive cattle and positive horses. Both VSV-NJ and VSV-IN were isolated from clinical cases.
VS is endemic on Ossabaw Island, Georgia, where cattle, raccoons, white-tailed deer, horses, and feral swine are seropositive to VSV-NJ.9,10 Serologic data indicate that transmission occurs annually, is seasonal, and is associated with maritime forest habitat.11 Clinical disease is rare and is only observed in feral swine.
VS is a disease of the Western Hemisphere. Although only one endemic focus of disease occurs in the United States, areas throughout South America, Central America, and Mexico are considered endemic for VS. There are reports of endemic VSV and other vesiculoviruses in Brazil,12,13 Argentina,14 Columbia,15 and other South American countries.12 Extensive research in Costa Rica has demonstrated the endemic nature of the virus and the disease.16–19 Work conducted by the author in El Salvador also indicated that the virus and disease are endemic in that country. A review of VS in Mexico revealed that cases occurred in every year between 1981 and 1995, with both serotypes identified in most years. VS has a national distribution in Mexico, although most cases occur in the southern states of Chiapas, Veracruz, and Tabasco. Disease is considered endemic in the central area of Mexico, but at a lower level than in southern states; viral activity in the northern area of Mexico is sporadic.
Transmission
Arthropod Vector Transmission
The evidence for arthropod transmission of VSV is most compelling for sandflies (Luzyomia shannoni) and black flies (Diptera: Simulidae). Other species of insects may also be competent biologic or mechanical vectors of VSV. Table 24-1 contains species of arthropods from which VSV have been isolated.
GENUS | COMMON NAME | TRANSMISSION |
---|---|---|
Tabanus | Horsefly | Yes |
Chrysops | Deerfly | Yes |
Aedes | Mosquito | Yes |
Culex | Mosquito | Yes |
Culicoides | Biting midge | Yes |
Musca | Housefly | No |
Hippelates | Eye gnats | No |
Simulium | Black fly | Yes |
Lutzyomia | Sandfly | Yes |
Stomoxys | Stable fly | Yes |
On Ossabaw Island, VSV-NJ has been isolated from sandflies, and virus activity, as measured by seroconversion in feral swine populations, corresponds to the seasonal appearance of sandflies.20,21 Sandflies feed on feral swine, white-tailed deer, and to a lesser extent, horses and raccoons in that environment,22 but neither swine nor white-tailed deer are competent amplifying hosts of VSV-NJ for sandflies.23,24
Black flies are competent experimental vectors for VSV-NJ, and this virus has been isolated from Simulidae trapped in the wild during outbreaks of VS.25,26 Simulium vittatum (black fly) females intrathoracically infected with virus transmit infectious virus in their saliva after 10 days.25 Efficient transmission of VSV-NJ occurs between infected and noninfected black flies co-feeding on nonviremic deer mice, suggesting that black flies could act as a transfer vector between nonviremic vertebrate hosts and domestic livestock.27,28 Clinical disease was detected in two of three horses when VSV-NJ–infected black flies fed on their lips and muzzle.29 Subclinical infection, as indicated by seroconversion, occurred in one horse when feeding was restricted to the thorax.
The flight range of potential VSV insect vectors vary, but none would be adequate to explain the often large distances observed between either individual or clusters of infected premises. Analysis of backward wind trajectories during the VS outbreaks in 1982 and 1985 suggest the feasibility of infected insects being transported for long distances on wind currents and subsequently landing on noninfected premises many miles away.30
Transport of Infected Animals
During the VS outbreak in 1983, disease entered California through transport of infected cattle purchased in Idaho.31 The only case of VSV infection identified in Texas during the 1995 outbreak was caused by movement of a horse from an area in New Mexico that was experiencing increased VSV activity into Texas. This horse apparently had become infected in New Mexico and subsequently exhibited clinical signs of VSV infection after being moved to Texas.
Direct-Contact Transmission
Transmission of VSV by direct contact with an infected animal was observed when pigs were experimentally inoculated with VSV-NJ.32 Seronegative pigs in contact with experimentally infected pigs were monitored daily for clinical disease, evidence of virus shedding, and seroconversion. Transmission occurred only when infected pigs had visible lesions. Resultant infections ranged from subclinical to clinical, with development of vesicular lesions. Seronegative pigs shed virus as early as 1 day after contact with infected pigs.
Reservoirs
Arboviruses generally use vertebrate hosts as reservoirs for transmission by arthropods. A vertebrate reservoir is normally infective for hematophagous insects when viremic. However, viremia has not been detected in livestock species that exhibit clinical signs of VS. Many vertebrate species have serologic evidence of exposure to VSV and may serve as reservoirs of infection. Table 24-2 lists select species from which antibodies to one or both VSV serotypes have been detected.
SPECIES | COMMON NAME |
---|---|
Alouatta villosa | Howler monkey |
Antilocapra americana | Pronghorn antelope |
Antilope cervicapra | Blackbuck |
Aotus trivirgatus | Night monkey |
Artibus spp. | Fruit bat |
Baiomys taylori | Pygmy mouse |
Bassaricyon gabii | Olingo |
Bradypus infuscatus | Sloth |
Canis latrans | Coyote |
Cervus elaphus | Elk |
Coendu rothschildi | Porcupine |
Dasypus novemcinctus | Armadillo |
Didelphis virgianus | Opossum |
Felis rufus | Bobcat |
Lepus californicus | Jackrabbit |
Lynx rufus | Lynx |
Meleagris gallopavo | Wild turkey |
Mus musculus | House mouse |
Mephitis mephitis | Skunk |
Myocastor coypu | Nutria |
Neotoma mexicana | Wood rat |
Odocoileus virginianus | White-tailed deer |
Odocoileus hemionus | Mule deer |
Ovis canadensis | Bighorn sheep |
Peromyscus maniculatus | Deer mouse |
Procyon lotor | Raccoon |
Saguinus geoffroyi | Marmoset |
Bats (Myotis lucifugus lucifugus) subcutaneously inoculated with Cocal VSV were viremic for 10 days when housed at 22° C (71.6° F) and for 16 days when maintained in hibernation conditions.33 These periods of viremia may be caused by active virus replication within the bats or may merely represent persistence of the original experimental inoculum. Virus is recoverable from spleen, liver, and brain homogenates for up to 8 months after experimental infection of immunocompetent Syrian hamsters with VSV-IN.34 In deer mice (Peromyscus maniculatus), a potential reservoir species in the southwestern United States, VSV-NJ can be demonstrated by immunohistochemistry in central nervous system tissues and the heart for up to 5 days after inoculation.35
Risk Factors
A case-control study of horses, cattle, and sheep on 395 premises in Colorado, New Mexico, Utah, and Arizona identified management factors affecting the risk of animals developing VS in the southwestern United States.36