Vesicular Stomatitis

1 - Introduction 2 - Rift Valley Fever Virus 3 - Bluetongue Virus 4 - Vesicular Stomatitis 5 - Vocabulary 6 - Web Links 7 - Outside Reports

Introduction. Vesicular stomatitis virus (VSV) is a rhabdovirus which causes re-emerging disease in cattle, horses and swine.  For the past two decades, VSV has caused disease outbreaks in the western US every 2-9 years ('82-83, '85-86, '95, '97-98, '04-'06).  Economic impact results in direct loss from decreased animal production (Ellis and Kendall 1964), as well as serious economic losses associated with cancellation of livestock events and quarantines which are lifted 21 days after the last clinical sign has abated.  Additional concerns arise from the fact that VS is clinically indistinguishable from foot-and-mouth disease, one of the most devastating exotic diseases in livestock that was eradicated from the US in 1929. 

Two antigenically distinct serotypes of VSV, VSV-New Jersey (VSV-NJ) and VSV-Indiana (VSV-IN) cause hundreds to thousands of vesicular disease outbreaks annually in southern Mexico, Central America and in northern South America (Anonymous 1990, Barrera 1992).  Outbreaks sweep northward with the movement of animals and/or insect vectors from Mexico through the southwestern US, sometimes reaching as far north as Canada (Rodriguez et al. 2000, Rodriguez 2002, Rainwater-Lovett et al. 2007).  VSV infects such a broad variety of hosts that it is not clear that any animal is naturally resistant to infection.  Clinical signs are well documented (Tesh et al. 1975) and abate within two weeks if there are no complications such as secondary infections.  The disease is rarely fatal, but mastitis, anorexia, dehydration, and weight loss result in significant production losses. 

Human infection during epizootics is relatively common and is related to direct contact with infected animals (Fields and Hawkins 1967, Clewley and Bishop 1979, Reif et al. 1987).  In the US, human infections are rare (Hanson et al. 1950, Patterson et al. 1958), but typically result from handling infected animals (Brody et al. 1967) or through laboratory infections (Johnson et al. 1966a).  To date, there are no reported cases of human infection resulting from the bite of an infected insect. 

Recent VS outbreaks.  Surveillance is conducted primarily by the State Departments of Agriculture, who report to USDA, APHIS, Veterinary Services.  Veterinarians examine all animals for events and for interstate or international movement.  Veterinarians and livestock owners must immediately contact State or Federal animal health authorities if a case of VSV is suspected.  If virus isolation and serology confirm a VSV diagnosis, animal health officials and the attending veterinarian are notified and a quarantine is placed on the premises.  The most recent outbreak (VSV-NJ) occurred from 2004 to 2006 resulting in a total of 13 states, 114 counties, 748 premises, and 1,276 affected animals.

Mechanisms of pathogenesis and infection.  Morbidity rates vary greatly, but can be as high as 90%.  VS spreads through a herd by direct contact 1-5 days after the initial animal infection (Arbelaez and Valbuena 1987, Howerth et al. 1997, Stallknecht et al. 1999).  Virus is shed from oral lesions into saliva (Patterson et al. 1955, Thurmond et al. 1987), contaminating feed, water troughs and other fomites for up to 3-4 days (Hanson 1952, Leder et al. 1983).  VSV is infectious by the oral route (Stallknecht et al. 1999) and can be transmitted by blood-feeding insects (Tesh et al. 1975).  VSV-NJ has been isolated from potential insect vector species during VS outbreaks, including sand flies, black flies, biting midges, eye gnats, and muscoid flies (Letchworth et al. 1999).  Experimentally infected sand flies, black flies, and Culicoides midges have been shown to be competent vectors and transmit virus by feeding on animals (Tesh et al. 1971, Cupp and Cupp 1997, Mead et al. 1997, Mead et al. 1999, Mead et al. 2004, Drolet et al. 2005, Perez De Leon et al. 2006, Perez de Leon and Tabachnick 2006).  Interestingly, VSV does not circulate in blood at levels required to infect blood feeding insects (Carbrey, Johnson et al. 1969, Yuill and Steele 1981, Arbelaez 1983, Arbelaez and Valbuena 1987, Orrego et al. 1987, Thurmond et al. 1987, Comer et al. 1995), thus, it is believed that insects become infected while feeding near VS lesions which contain as much as 109 PFU/ml of virus and contaminate the surrounding skin (Patterson et al. 1955, Thurmond et al. 1987).

Diagnosis.  VS is diagnosed in suspected animals by virus isolation from vesicular fluid or epithelium, detection of viral antigen by capture ELISA (Alonso et al. 1991, Hernandez De Anda et al. 1992) and immunohistochemistry (Stallknecht et al. 1999), detection of nucleic acid through PCR (Rodriguez et al. 1993, Callens and De Clercq 1999), and detection of virus-specific antibodies with ELISA (Vernon and Webb 1985, Zhou et al. 2001), complement fixation, and virus neutralization (Johnson et al. 1966b). 

Treatment, Vaccines, Control.  There is no specific treatment or cure for VS.  Supportive care (soft feeds, fresh, clean water and electrolyte replacement therapy) can be helpful.  Mild antiseptic mouthwashes and antibiotics are often used to treat or prevent secondary infections.  Neutralizing antibodies can last eight years in exposed cattle (Sorenson et al. 1958). This protection, however, is questionable as most cattle in VS endemic areas have antibodies capable of neutralizing the virus strain causing their clinical disease (Rodriguez et al. 1990, Vernon et al. 1990, Vanleeuwen et al. 1995), but can be reinfected with that strain as early as 30-60 days (Brandly et al. 1951, Hanson 1952, Vernon et al. 1990, Vanleeuwen et al. 1995).  Reinfection, in the presence of strain-specific neutralizing antibodies, makes effective vaccination strategies difficult, thus, more molecular targets to interrupt transmission and infection are needed.  Recombinant (Martinez et al. 2004), and inactivated (House et al. 2003) virus vaccines have been experimentally tested, but are not yet available commercially.  Several inactivated vaccines are used in Central and South America for animals, but no human vaccines are available.  Control of outbreaks is dependent upon rapid recognition of initial cases, quarantine of animals, rigorous disinfection practices (personnel materials, instruments, equipment, vehicles, shared equipment, feed bunks, and water sources) and insect control.

REFERENCES

Alonso, A., M. A. Martins, P. Gomes Mda, R. Allende, and M. S. Sondahl. 1991. Development and evaluation of an enzyme-linked immunosorbent assay for detection, typing, and subtyping of vesicular stomatitis virus. J Vet Diagn Invest 3: 287-92.

Anonymous. 1990. Situation of the foot-and-mouth disease control programs in South America. Pan American Health Organization, Washington, D.C.

Arbelaez, G. 1983. Respuesta de dos bovinos adultos inoculados con dos cepas de virus de estomatitis vesicular New Jersey. Revista ICA 18: 491-500.

Arbelaez, G., and R. M. Valbuena. 1987. La instilacion nasal como via de infeccion experimental de estomatitis vesicular tipo Indiana, en bovinos. Revista ICA 22: 59-64.

Barrera, J. C. 1992. Persistence of Vesicular Stomatitis New Jersey RNA in Convalescent Animals, Ph.D. Thesis, University of Wisconsin-Madison.

Brandly, C. A., R. P. Hanson, and T. L. Chow. 1951. Vesicular stomatitis with particular reference to the 1949 Wisconsin Epizo•tic. Proc. Amer. Vet. Med. Assoc.: 61-67.

Brody, J. A., G. F. Fischer, and P. H. Peralta. 1967. Vesicular stomatitis virus in Panama. Human serologic patterns in a cattle raising area. Am J Epidemiol 86: 158-61.

Callens, M., and K. De Clercq. 1999. Highly sensitive detection of swine vesicular disease virus based on a single tube RT-PCR system and DIG-ELISA detection. J Virol Methods 77: 87-99.

Carbrey, E. A. Focus on vesicular stomatitis. Its cause, characteristics, and diagnosis. Foreign Animal Disease Reports: 8-11.

Clewley, J. P., and D. H. Bishop. 1979. Assignment of the large oligonucleotides of vesicular stomatitis virus to the N, NS, M, G, and L genes and oligonucleotide gene ordering within the L gene. J. Virol. 30: 116-123.

Comer, J. A., D. E. Stallknecht, and V. F. Nettles. 1995. Incompetence of white-tailed deer as amplifying hosts of vesicular stomatitis virus for Lutzomyia shannoni (Diptera: Psychodidae). J. Med. Entomol. 32: 738-40.

Cupp, E. W., and M. S. Cupp. 1997. Black fly (Diptera: Simuliidae) salivary secretions: Importance in vector competence and disease. J. Med. Entomol. 34: 87-94.

Drolet, B. S., C. L. Campbell, M. A. Stuart, and W. C. Wilson. 2005. Vector competence of Culicoides sonorensis (Diptera: Ceratopogonidae) for vesicular stomatitis virus. J Med Entomol 42: 409-418.

Ellis, E. M., and H. E. Kendall. 1964. The public health and economic effects of vesicular stomatitis in a herd of dairy cattle. J. Am. Vet. Med. Assoc. 144: 377-380.

Fields, B. N., and K. Hawkins. 1967. Human infection with the virus of vesicular stomatitis during an epizootic. N. Engl. J. Med. 277: 989-994.

Hanson, R. P. 1952. The natural history of vesicular stomatitis. Bacteriol. Rev. 16: 179-204.

Hanson, R. P., A. F. Rasmussen, C. A. Brandly, and J. A. Brown. 1950. Human infection with the virus of vesicular stomatitis. J. Lab. Clin. Med. 36: 754-758.

Hernandez De Anda, J., M. D. Salman, P. A. Webb, T. J. Keefe, A. Arregin Arevalo, and J. Mason. 1992. Evaluation of an enzyme-linked immunosorbent assay for detection of antibodies to vesicular stomatitis virus in cattle in an enzootic region of Mexico. Am J Vet Res 53: 440-3.

House, J. A., C. House, P. Dubourget, and M. Lombard. 2003. Protective immunity in cattle vaccinated with a commercial scale, inactivated, bivalent vesicular stomatitis vaccine. Vaccine 21: 1932-7.

Howerth, E. W., D. E. Stallknecht, M. Dorminy, T. Pisell, and G. R. Clarke. 1997. Experimental vesicular stomatitis in swine: effects of route of inoculation and steroid treatment. J. Vet. Diagn. Invest. 9: 136-42.

Johnson, K. M., J. E. Vogel, and P. H. Peralta. 1966a. Clinical and serological response to laboratory-acquired human infection by Indiana type vesicular stomatitis virus (VSV). Am J Trop Med Hyg 15: 244-6.

Johnson, K. M., J. E. Vogel, and P. H. Peralta. 1966b. Clinical and serological response to laboratory-acquired human infection by Indiana type vesicular stomatitis virus (VSV). Am. J. Trop. Med. Hyg. 15: 244-246.

Johnson, K. M., R. B. Tesh, and P. H. Peralta. 1969. Epidemiology of vesicular stomatitis virus: some new data and a hypothesis for transmission of the Indian serotype. J. Am. Vet. Med. Assoc. 155: 2133-40.

Leder, R. R., J. Maas, V. M. Lane, and J. F. Evermann. 1983. Epidemiologic investigation of vesicular stomatitis virus in a dairy and its economic impact. Bov. Practitioner 18: 45-49.

Letchworth, G. J., L. L. Rodriguez, and J. Del cbarrera. 1999. Vesicular stomatitis. Vet. J. 157: 239-260.

Martinez, I., C. Barrera Jd Jdel, L. L. Rodriguez, and G. W. Wertz. 2004. Recombinant vesicular stomatitis (Indiana) virus expressing New Jersey and Indiana glycoproteins induces neutralizing antibodies to each serotype in swine, a natural host. Vaccine 22: 4035-43.

Mead, D. G., C. J. Mare, and E. W. Cupp. 1997. Vector competence of select black fly species for vesicular stomatitis virus (New Jersey serotype). Am. J. Trop. Med. Hyg. 57: 42-48.

Mead, D. G., C. J. Mare, and F. B. Ramberg. 1999. Bite transmission of vesicular stomatitis virus (New Jersey serotype) to laboratory mice by Simulium vittatum (Diptera: Simuliidae). J. Med. Entomol. 36: 410-413.

Mead, D. G., E. W. Gray, R. Noblet, M. D. Murphy, E. W. Howerth, and D. E. Stallknecht. 2004. Biological transmission of vesicular stomatitis virus (New Jersey serotype) by Simulium vittatum (Diptera: Simuliidae) to domestic swine (Sus scrofa). J Med Entomol 41: 78-82.

Orrego, U. A., G. R. Arbbelaez, and R. J. Rocha. 1987. Avances en las investigaciones sobre la estomatitis vesicular en Colombia. Instituto Colombiano Agropecuario 1-56.

Patterson, W. C., E. W. Jenny, and A. A. Holbrook. 1955. Experimental infections with vesicular stomatitis in swine. I. Transmission by direct contact and feeding infected meat scraps. U. S. Livestock Sanit. Assoc. Proc. 59: 368-378.

Patterson, W. C., L. O. Mott, and E. W. Jenney. 1958. Study of vesicular stomatitis in man. J. Am. Vet. Assoc. 133: 57-66.

Perez de Leon, A. A., and W. J. Tabachnick. 2006. Transmission of vesicular stomatitis New Jersey virus to cattle by the biting midge Culicoides sonorensis (Diptera: Ceratopogonidae). J Med Entomol 43: 323-329.

Perez De Leon, A. A., D. O'Toole, and W. J. Tabachnick. 2006. Infection of guinea pigs with vesicular stomatitis New Jersey virus Transmitted by Culicoides sonorensis (Diptera: Ceratopogonidae). J Med Entomol 43: 568-73.

Rainwater-Lovett, K., S. J. Pauszek, W. N. Kelley, and L. L. Rodriguez. 2007. Molecular epidemiology of vesicular stomatitis New Jersey virus from the 2004-2005 US outbreak indicates a common origin with Mexican strains. J Gen Virol 88: 2042-51.

Reif, J. S., P. A. Webb, T. P. Monath, J. K. Emerson, J. D. Poland, G. E. Kemp, and G. Cholas. 1987. Epizootic vesicular stomatitis in Colorado, 1982: infection in occupational risk groups. Am. J. Trop. Med. Hyg. 36: 177-182.

Rodriguez, L. L. 2002. Emergence and re-emergence of vesicular stomatitis in the United States. Virus Res 85: 211-9.

Rodriguez, L. L., S. Vernon, A. I. Morales, and G. J. Letchworth. 1990. Serological monitoring of vesicular stomatitis New Jersey virus in enzootic regions of Costa Rica. Am. J. Trop. Med. Hyg. 42: 272-281.

Rodriguez, L. L., G. J. Letchworth, C. F. Spiropoulou, and S. T. Nichol. 1993. Rapid detection of vesicular stomatitis virus New Jersey serotype in clinical samples by using polymerase chain reaction. J Clin Microbiol 31: 2016-20.

Rodriguez, L. L., T. A. Bunch, M. Fraire, and Z. N. Llewellyn. 2000. Re-emergence of vesicular stomatitis in the western United States is associated with distinct viral genetic lineages. Virology 271: 171-81.

Sorenson, D. K., T. L. Chow, T. Kowalczyk, R. P. Hanson, and C. A. Brandly. 1958. Persistence in cattle of serum-neutralizing antibodies of vesicular stomatitis virus. Am. J. Vet. Res. 19: 74-77.

Stallknecht, D. E., E. W. Howerth, C. L. Reeves, and B. S. Seal. 1999. Potential for contact and mechanical vector transmission of vesicular stomatitis virus New Jersey in pigs. Am. J. Vet. Res. 60: 43-48.

Tesh, R. B., B. N. Chaniotis, and K. M. Johnson. 1971. Vesicular stomatitis virus, Indiana serotype: multiplication in and transmission by experimentally infected phlebotomine sandflies (Lutzomyia trapidoi). Am J Epidemiol 93: 491-495.

Tesh, R. B., K. M. Johnson, W. T. Hubbert, W. F. McCulloch, and P. R. Schnurrenberger. 1975. Vesicular Stomatitis, pp. 897-910, Vesicular Stomatitis. Charles C. Thomas, Springfield, Ill.

Thurmond, M. C., A. A. Ardans, J. P. Picanso, T. McDowell, B. Reynolds, and J. Saito. 1987. Vesicular stomatitis virus (New Jersey strain) infection in two California dairy herds: an epidemiologic study. J. Am. Vet. Med. Assoc. 191: 965-970.

Vanleeuwen, J. A., L. L. Rodriguez, and D. Waltner-Toews. 1995. Cow, farm, and ecologic risk factors of clinical vesicular stomatitis on Costa Rican dairy farms. Am. J. Trop. Med. Hyg. 53: 342-350.

Vernon, S. D., and P. A. Webb. 1985. Recent vesicular stomatitis virus infection detected by immunoglobulin M antibody capture enzyme-linked immunosorbent assay. J Clin Microbiol 22: 582-6.

Vernon, S. D., L. L. Rodriguez, and G. J. Letchworth. 1990. Vesicular stomatitis New Jersey virus glycoprotein gene sequence and neutralizing epitope stability in an enzootic focus. Virology 177: 209-215.

Yuill, T. M., and J. H. Steele. 1981. Vesicular Stomatitis, pp. 125-142, Vesicular Stomatitis. CRC Press, Inc, Boca Raton.

Zhou, E. M., J. Riva, and A. Clavijo. 2001. Development of an immunoglobulin M (IgM) capture enzyme-linked immunosorbent assay for detection of equine and swine IgM antibodies to vesicular stomatitis virus. Clin Diagn Lab Immunol 8: 475-81.

 

<< Previous 1 2 3 [4] 5 6 7 Next >>