OVERVIEW: What every clinician needs to know
Pathogen name and classification
Vesicular stomatitis virus (VSV) – A virus in the family Rhabdoviridae (like Rabies), genus Vesiculovirus. Of the numerous vesiculoviruses, at least six have been confirmed to cause animal or human disease. These are VS-New Jersey, VS-Indiana, VS-Alagoas, Chandipura, Isfahan, and Piry.
What is the best treatment?
There are no specific antiviral agents. Treatment consists of supportive care including the prevention or treatment of secondary infections. A mild antiseptic mouthwash may reduce the pain associated with oral lesions. Nutritional support is provided if eating is impaired.
How do patients contract this infection, and how do I prevent spread to other patients?
VSV is unable to penetrate intact skin and mucous membranes so the mechanism of transmission is somewhat unclear. Many potential insect vectors have been identified including mosquitos, sandflies, and black flies, but only the phlebotomine sandfly has been proven to be a vector in the United States.
In most areas, epizootic outbreaks generally begin in the spring and last until a heavy frost. In a few areas enzootic infections begin in the dry season (around November) and continue through spring.
Insects are a vector so the incidence depends on insect activity.
VSV outbreaks occur most frequently in the central and southwestern United States, Canada, and Mexico. Enzootic disease is seen in Central and South America. Up to 10% of animals on affected farms develop the disease. Humans living in enzootic areas have a high seroprevalence rate. 62–83% of people in an area of Columbia endemic for VS-Alagoas were seropositive. In an endemic area of Iran, 100% of people over age 5 years were seropositive for Isfahan, a related virus. Most seropositive people have not had clinical disease.
Infection control issues
In order to prevent the spread of VSV, the US Department of Agriculture recommends separating animals with lesions from healthy animals.
In an outbreak, insect control programs may be helpful.
Direct contact with active lesions should be avoided. Gloves should be worn if direct contact is necessary.
Recovery from VSV infection is not protective and no vaccination is recommended.
There is no effective anti-infective prophylaxis.
What host factors protect against this infection?
VSV-specific antibody production is correlated with recovery and CD4+ cells and interleukin-12 production may be beneficial.
The role of immunosuppression in this infection is unknown.
The histopathology of VSV infection depends on the site of innoculation. In animals infected naturally, there is intercellular edema and necrosis of keratinocytes. When injected intramuscularly, infection of the liver and kidney are seen with prominent focal necrosis of the tubular epithelium. When introduced intranasally in mice, inflammatory changes are seen in the central nervous system. Initially astrocytes and microglia are activated. Nitric oxide synthase (innate immunity) is induced, followed by infiltration of CD8+ and CD4+ T cells which corresponds to clearing of the virus. B cells appear later, after the virus is cleared and the animals are showing signs of recovery.
What are the clinical manifestations of infection with this organism?
In animals, VSV causes lesions that resemble the more dangerous foot and mouth disease, therefore identification is important. They can develop fever, excess salivation, and vesicular lesions in and around the mouth, nose, hooves, and teats. They may not eat and weight loss is common. In humans the disease is usually mild or subclinical, but can include fever, malaise, myalgias, emesis, pharyngitis, and oral vesicles.
What common complications are associated with infection with this pathogen?
The most common complications are lymphadenopathy and weight loss. Encephalitis and death are the most common complications from Chandipura, a related Vesiculovirus.
How should I identify the organism?
VSV has been a model for the life cycle of negative-stranded ribonucleic acid (RNA) viruses. The parasite life cycle is as follows: adsorption of the virus particle, penetration into the cell, uncoating the core ribonucleoprotein followed by transcription of the genome, translation of viral messenger RNAs, and modification of the viral proteins with assembly of new viral particles which then bud from the cell membrane.
Tissue samples taken directly from the lesions will provide the highest diagnostic yield.
Polymerase chain reaction (PCR), complement fixation, serum neutralization, enzyme-linked immunosorbent assay, and viral culture are the best diagnostic methods to use.
PCR is helpful but is available only at facilities approved by the US Department of Agriculture’s National Veterinary Services Laboratories.
How does this organism cause disease?
Upon VSV infection, host cytoplasmic RNA helicase/translocase retinoic acid inducible-gene I (RIG-1) recognizes the viral double-stranded RNA and activates the production of interferons, but the VSV matrix (M) protein blocks host cell polymerase functions and messenger RNA nuclear export thus rapidly cutting off host gene expression and allowing rapid viral replication.
These virulence factors lead to severe cytopathic effects.
WHAT’S THE EVIDENCE for specific management and treatment recommendations?
Bridges, VE, McCluskey, BJ, Salman, MD, Hurd, HS, Dick, J. “Review of the 1995 vesicular stomatitis outbreak in the western United States”. J Am Vet Med Assoc. vol. 211. 1997. pp. 556-60. (Documents the extent of a 1995 outbreak of VSV on farms in the United States.)
Vanleeuwen, JA, Rodriguez, LL, Waltner-Toews, D. “Cow, farm, and ecologic risk factors of clinical vesicular stomatitis on Costa Rican dairy farms”. Am J Trop Med Hyg. vol. 53. 1995. pp. 342-50. (A review of epidemic VSV on dairy farms during an outbreak in Costa Rica.)
Rodriguez, LL, Vernon, S, Morales, AI, Letchworth, GJ. “Serological monitoring of vesicular stomatitis New Jersey virus in enzootic regions of Costa Rica”. Am J Trop Med Hyg. vol. 42. 1990. pp. 272-81. (A review of serology showing that asymptomatic VSV infections in people occur at high rates when they are in contact with infected animals.)
Quiroz, E, Moreno, N, Peralta, PH, Tesh, RB. “A human case of encephalitis associated with vesicular stomatitis virus (Indiana serotype) infection”. Am J Trop Med Hyg. vol. 39. 1988. pp. 312-14. (Case report describing a human case of encephalitis due to VSV.)
Reif, JS, Webb, PA, Monath, TP. “Epizootic vesicular stomatitis in Colorado, 1982: infection in occupational risk groups”. Am J Trop Med Hyg. vol. 36. 1987. pp. 177-82. (A description of human infections with VSV associated with an outbreak of animal disease.)
Bhatt, PN, Rodrigues, FM. “Chandipura: a new Arbovirus isolated in India from patients with febrile illness”. Indian J Med Res. vol. 55. 1967. pp. 1295-305. (Early description of the isolation of the Chandipura virus.)
Rao, BL, Basu, A, Wairagkar, NS. “A large outbreak of acute encephalitis with high fatality rate in children in Andhra Pradesh, India, in 2003, associated with Chandipura virus”. Lancet. vol. 364. 2004. pp. 869-74. (Early reports of an outbreak of encephalitis associated with the Chandipura virus.)
Chadha, MS, Arankalle, VA, Jadi, RS. “An outbreak of Chandipura virus encephalitis in the eastern districts of Gujarat state, India”. AM J Trop Med Hyg. vol. 73. 2005. pp. 566-70. (Epidemiologic and clinical descriptions of an outbreak of encephalitis believed to be due to the Chandipura virus.)
Basak, S, Mondal, A, Polley, S, Mukhopadhyay, S, Chattopadhyay, D. “Reviewing Chandipura: a vesiculovirus in human epidemics”. Biosci Rep. vol. 27. 2007. pp. 275-98. (A review of Chandipura as an emerging infectious disease and of the recent outbreaks described in India.)
“Vesicular stomatitis”. 17 May 2012. (US Department of Agriculture description of VSV disease and control measures.)
“Vesicular stomatitis factsheet”. 17 May 2012. (US Department of Agriculture description of VSV epidemics and recommended testing and control measures.)
(Facilities approved by the US Department of Agriculture to provide PCR.)
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- OVERVIEW: What every clinician needs to know
- Pathogen name and classification
- What is the best treatment?
- How do patients contract this infection, and how do I prevent spread to other patients?
- What host factors protect against this infection?
- What are the clinical manifestations of infection with this organism?
- What common complications are associated with infection with this pathogen?
- How should I identify the organism?
- How does this organism cause disease?
- WHAT’S THE EVIDENCE for specific management and treatment recommendations?