VESICULAR STOMATITIS VIRUS (VSV)
LEVELS: Likely to occur: Effective control measures not fully understood; Occupational exposure risk: Non-foodborne transmission pathway(s) that are strongly associated with occupational exposure and can lead to human infection; Unlikely to be effective: One or more pathways of farm-to-farm transmission exist that cannot be controlled by on-farm biosecurity; Moderate: Clinical signs not unique but existing tests available at local/regional laboratory(s); Moderate: Manageable losses related to endemic (population) or chronic (individual) occurrence; Temporary disruption: Measureable negative effect on demand for less than a month when disease occurs on one or more farms; Minimal risk: Agent inherently unlikely to develop clinically important resistance to antibacterial or antiviral treatments; Minimal risk: Antibacterial or antiviral treatments rarely occur, or are typically limited to short-course individual animal therapy; No availability: Effective treatments not currently available in the US (or have not been developed); No availability: Effective vaccines not currently available in the US (or have not been developed); Not feasible: Eradication extremely unlikely
OVERVIEW
Vesicular stomatitis (VS) is a vesicular disease of livestock caused by Vesicular Stomatitis Virus (VSV), a member of the genus Vesiculovirus in the family Rhabdoviridae. VSV affects domestic livestock including horses, cattle, and pigs throughout the Americas, from northern South America through Central America to North America. Two VSV species are recognized: Vesiculovirus newjersey (VSNJV) and Vesiculovirus indiana (including VSIV1, VSIV2, VSIV3). VSNJV and VSIV1 are distributed from northern South America to North America, while VSIV2 and VSIV3 occur only in Brazil and Argentina. In pigs, VS is clinically indistinguishable from foot-and-mouth disease (FMD), swine vesicular disease (SVD), vesicular exanthema of swine (VESV), and Seneca Valley virus (SVV) infection—laboratory testing is mandatory to differentiate these diseases. Clinical signs include fever, lethargy, lameness, and vesicular lesions on the lips, tongue, gums, snout, coronary bands, and teats. VSNJV is more virulent than VSIV in pigs based on experimental studies. Transmission occurs through direct animal-to-animal contact and via insect vectors (black flies, biting midges). The virus can be transmitted from both clinically and subclinically infected pigs through saliva and feces. Morbidity during outbreaks can reach 90%, but mortality is low and the disease is typically self-limiting with recovery in 2-3 weeks. In the United States, sporadic VS outbreaks occur in the western states at 5-10 year intervals, primarily affecting horses and cattle. Naturally occurring VSV in domestic swine has not been reported in the US since 1968. Economic losses include direct production impacts and indirect effects from movement restrictions placed on affected premises during diagnostic investigation to rule out FMD.
FOODBORNE ZOONOTIC TRANSMISSION POTENTIAL
Level: Likely to occur: Effective control measures not fully understood
The chapter explicitly states: "VSV is a zoonotic agent and humans can become infected by direct contact with lesioned animals or in laboratory settings by aerosolization of virus." While foodborne transmission is not the primary route, the documented zoonotic capacity of VSV through contact with infected animals indicates that handling or processing infected pig tissues could potentially result in human infection. People living in endemic areas show serological evidence of infection without reporting severe symptoms, "suggesting they likely had natural exposure to lower doses of virus (e.g. by insect bite)." The presence of high virus titers in vesicular fluid and infected tissues means that butchering or processing infected animals could theoretically pose a risk, though this specific route is not documented.
NON-FOODBORNE ZOONOTIC TRANSMISSION POTENTIAL
Level: Occupational exposure risk: Non-foodborne transmission pathway(s) that are strongly associated with occupational exposure and can lead to human infection
Human VSV infection is well documented through multiple routes. The chapter states that "humans can become infected by direct contact with lesioned animals or in laboratory settings by aerosolization of virus." Clinical signs in infected humans include "flu-like symptoms, fever, photophobia, and in rare cases, blister-like lesions appearing 1-2 days after exposure." The disease is typically self-limiting in humans. Seroprevalence studies in endemic areas demonstrate that human infection occurs through natural exposure, likely via insect bites or occupational contact. Laboratory-acquired infections through aerosol exposure are documented, indicating the virus's capacity for respiratory transmission under certain conditions.
EFFECTIVENESS OF ON-FARM BIOSECURITY IN PREVENTING FARM-TO-FARM TRANSMISSION
Level: Unlikely to be effective: One or more pathways of farm-to-farm transmission exist that cannot be controlled by on-farm biosecurity
VSV transmission involves multiple pathways that can partially bypass standard biosecurity: (1) Insect vector transmission: "Two main groups of biological vectors, black flies (Simulium spp.) and biting midges (Culicoides spp.), seem to play pivotal roles during VS epidemics in the United States"; infected insects can transmit virus through co-feeding even on uninfected hosts; (2) Environmental persistence: VSV "can remain viable in contaminated saliva on pails or food buckets for 3-4 days" and "can be recovered from plant surfaces up to 24 hours after surface inoculation at room temperature"; (3) Subclinical transmission: "Transmission by direct contact has been observed from both clinically and subclinically infected pigs." However, the virus is susceptible to common disinfectants (lipid solvents, bleach, formalin, detergents), heat treatment (56°C), and UV irradiation. Standard biosecurity combined with insect control measures can significantly reduce transmission risk. The chapter notes that "housing animals indoors during peak insect feeding times" and "insect repellants" are effective preventive measures.
DIFFICULTY OF DETECTING AND CONFIRMING INFECTION
Level: Moderate: Clinical signs not unique but existing tests available at local/regional laboratory(s)
Clinical detection is complicated by the indistinguishable vesicular lesions from FMD, SVD, VESV, and SVV—"it is imperative to collect and submit diagnostic samples for laboratory testing." However, once VSV is suspected, laboratory confirmation is straightforward with multiple established methods: (1) Real-time PCR: "highly sensitive and rapid tests that can identify VSV serotype and rule out other vesicular agents"; (2) Virus isolation: in Vero or BHK-21 cells with CPE detectable in <24 hours at high titers; (3) Antigen detection: complement fixation and antigen-capture ELISA; (4) Serology: virus neutralization, complement fixation, and ELISA for antibody detection; neutralizing antibodies detectable as early as 5 days post-infection in pigs. Preferred specimens include vesicular fluid, tissue tags from ruptured vesicles, and lesion swabs. The main diagnostic challenge is recognizing that vesicular disease is present and initiating the mandatory laboratory investigation to rule out FMD.
FINANCIAL IMPACT ON FARM'S COST OF PRODUCTION
Level: Moderate: Manageable losses related to endemic (population) or chronic (individual) occurrence
VSV causes significant but manageable production losses: (1) Direct disease effects: fever, lethargy, anorexia from painful oral lesions, lameness from foot lesions, weight loss; in severe cases tongue epithelium may slough and claws may separate; (2) Morbidity/mortality: "Morbidity rates during an outbreak can be as high as 90%, especially among animals in direct contact" but "mortality due to VSV infection is low"; (3) Recovery: "VS is usually a self-limiting disease in pigs and animals typically recover in 2-3 weeks, if there are no complications from secondary bacterial infections"; (4) Outbreak patterns: in endemic areas, "outbreaks in free-range and small-scale open pig farms can be severe." The economic impact includes both direct production losses and indirect costs from quarantine/movement restrictions during diagnostic investigation. However, the self-limiting nature of disease, low mortality, and relatively rapid recovery mean losses are manageable rather than catastrophic. Naturally occurring VSV in US domestic swine has not been reported since 1968.
EFFECT ON DOMESTIC OR EXPORT MARKETS
Level: Temporary disruption: Measureable negative effect on demand for less than a month when disease occurs on one or more farms
VSV detection triggers significant regulatory response due to its clinical similarity to FMD: "During VS outbreaks, affected premises are quarantined and diagnostic samples submitted to rule out these diseases." Market impacts include: (1) Movement restrictions: "the economic losses associated with VS include both the direct impact of clinical disease on production and the indirect effect of movement restrictions placed on affected premises"; (2) Regulatory investigation: every vesicular disease case requires laboratory confirmation to exclude FMD, causing delays in animal movements; (3) Geographic scope: VS is endemic in parts of the Americas but does not trigger the catastrophic trade consequences of FMD detection because once VSV is confirmed (rather than FMD), restrictions are limited to affected premises rather than national-level embargoes. The chapter notes that "except for historical reports of VS in horses sent to France during World War I, vesicular stomatitis is not known to occur outside of the Americas"—this geographic limitation means international trade impacts are primarily relevant for intra-Americas trade.
PATHOGEN'S ABILITY TO DEVELOP AND SPREAD RESISTANCE
Level: Minimal risk: Agent inherently unlikely to develop clinically important resistance to antibacterial or antiviral treatments
VSV is a viral pathogen (negative-sense single-stranded RNA rhabdovirus) that does not carry, acquire, or transmit antimicrobial resistance genes. The virus poses no AMR concerns. VSV exists as multiple serotypes and strains with varying virulence, and genetic diversity exists within and between serotypes, but this represents viral evolution rather than antimicrobial resistance. The chapter notes that "VSNJV has been placed into six different genetic phylogenetic clades which correspond to their geographical distribution."
AMR DEVELOPMENT DRIVEN BY DISEASE MANAGEMENT
Level: Minimal risk: Antibacterial or antiviral treatments rarely occur, or are typically limited to short-course individual animal therapy
No antiviral treatments exist for VSV. Management is supportive: "treatment of VSV-infected animals is focused on alleviating pain, fever, and distress. Palliative care includes feeding soft feed and providing padding for hard surfaces." The chapter notes that "antibiotics may be useful to prevent or treat secondary bacterial infections" and "treatment of vesicular lesions with topical antiseptics may promote faster healing and reduce the risk of secondary infections." Antimicrobial use is limited to individual animals with secondary bacterial complications rather than routine population-wide treatment. The self-limiting nature of disease (2-3 week recovery) further limits treatment duration.
AVAILABILITY OF EFFECTIVE TREATMENT OPTIONS
Level: No availability: Effective treatments not currently available in the US (or have not been developed)
No specific antiviral treatments exist for VSV infection. Management is entirely supportive: pain relief, fever management, soft feed, padded surfaces for animals with foot lesions, and topical antiseptics for lesions. The chapter states treatment is "focused on alleviating pain, fever, and distress." Antibiotics are used only for secondary bacterial infections. Infected pigs must clear the infection through their own immune response over 2-3 weeks.
AVAILABILITY OF EFFECTIVE VACCINES OR BACTERINS
Level: No availability: Effective vaccines not currently available in the US (or have not been developed)
The chapter explicitly states: "There are no commercially available vaccines in North America to prevent VS." However, "inactivated vaccines are commercially available and are used to protect pigs against clinical VS in South American countries where VSV is endemic." For the US context relevant to this assessment, no licensed vaccines are available. Prevention relies on: biosecurity measures to avoid introduction; insect control and repellents; housing animals indoors during peak insect feeding times; and isolation of affected animals. The lack of commercial vaccines in North America reflects both the sporadic nature of outbreaks and the self-limiting nature of disease.
FEASIBILITY OF ERADICATING THE DISEASE FROM THE US
Level: Not feasible: Eradication extremely unlikely
VSV eradication from the US is not feasible because: (1) Wildlife reservoirs: "although reports of naturally occurring clinical disease in wildlife are rare, antibodies to VSV have been found in a variety of wild animals" including deer and feral swine in the southeastern US; during the 2023 VS outbreak in California, VSV caused severe vesicular disease in Asian and African rhinoceros in a safari park; (2) Insect vectors: black flies (Simulium spp.) and biting midges (Culicoides spp.) serve as biological vectors; "hematophagous insects can become infected with VSNJV when they feed on or near virus-rich vesicular lesions and the virus can be horizontally transmitted from infected to uninfected black flies during the process of co-feeding on the same vertebrate host, regardless of whether the host is infected"; (3) Endemic regions: VSV "occurs in endemic cycles in southern Mexico, Central America, and the countries of northern South America" with periodic incursions into the western US; (4) Subclinical infection: pigs can shed virus and transmit infection while subclinically infected; "transmission by direct contact has been observed from both clinically and subclinically infected pigs"; (5) Environmental persistence: virus "can remain viable in contaminated saliva on pails or food buckets for 3-4 days" and "can be recovered from plant surfaces up to 24 hours after surface inoculation." The historical pattern shows that despite the absence of clinical cases in US domestic swine since 1968, VSV continues to cause sporadic epidemics in horses and cattle in western states at 5-10 year intervals, demonstrating ongoing virus circulation. Control rather than eradication is the practical approach.