vesicular stomatitis

Identity

Preferred Scientific Name

• vesicular stomatitis

International Common Names

• English: stomatitis, vesicular; vesicular stomatitis in large animals; VSV infection
• Spanish: estomatitis vesicular; la estomatitis vesicular

Local Common Names

• Mexico: mal de yerba
• USA: sore mouth

English acronym

• VS

Overview

Vesicular stomatitis (VS) is a viral disease of horses and cattle, and is reported to occur exclusively in the Western Hemisphere. On rare occasions, infection also occurs in pigs and humans. First determined to be of viral origin by Cotton (1927), VS was described clinically prior to that time (Mohler, 1918). The disease is caused by infection with one of two main serotypes of vesicular stomatitis virus (VSV), and is characterized by the appearance of vesicular lesions, especially on the tongue, oral and nasal mucosa, mammary glands, external genitalia and coronary bands.

Clinically, VS is indistinguishable from foot-and-mouth disease (FMD), and is therefore a critical consideration in FMD control programs worldwide. Although mortality associated with VSV infection is low, clinical manifestations such as weight loss, failure to gain, decreased milk production, and mastitis in affected animals can negatively impact production. In addition, VS is considered a zoonotic disease and has been documented to cause a flu-like disease in people working closely with infected animals (Reif et al., 1987).

Despite extensive epidemiological and laboratory research on VSV and the associated disease, questions and controversy remain. Several comprehensive reviews of the available data have been published (Hanson, 1952; Hanson, 1981; Webb and Holbrook, 1988; Letchworth, 1996; Letchworth et al., 1999; McCluskey and Mumford, 2000).

This data sheet mainly details the Indiana and New Jersey serotypes of VSV.

Hosts/Species Affected

Species clinically affected

Clinical VS has been reported in horses, cattle, swine, llamas, and humans (Acree et al., 1964; Jenney, 1967; Reif et al., 1987; Bridges et al., 1997). Reports of disease in these species are not comprehensive as to animal category, life stages, and husbandry type affected, although the nature of the disease does not preclude infection or clinical disease in any animals of susceptible species. In the USA, clinical cases of VS are infrequently reported in domestic swine although disease is endemic in feral swine inhabiting Ossabaw Island (Georgia, USA) (Stallknecht et al., 1985). The virus is also reported to cause clinical disease in sheep (Fenner et al., 1987). Humans are also clinically affected (see Zoonosis and Food Safety section).

Serological evidence of infection

Serum antibody titres have been detected in many other domestic and wild species including donkeys, goats, turkeys, ducks, dogs, coyotes, elk, deer, cotton rats, wood rats, deer mice, pronghorn antelope, and racoons (Jenney and Brown, 1972; Jenney et al., 1984; Webb et al., 1987a; Webb et al., 1987b), indicating past exposure to the virus.

Risk factors

Attack rates vary among affected premises (Webb et al., 1987b), suggesting that management and/or individual animal factors have a role in susceptibility to infection and development of clinical disease. Younger animals <1 year of age) are less likely to exhibit clinical signs of the disease although they become infected and do seroconvert (Letchworth et al., 1999). Reports vary as to associations between clinical disease and stage of lactation of dairy cattle (Alderink, 1984; Vanleeuwan et al., 1995).

Management factors which increase animals’ exposure to biting arthropods (such as housing on pasture) have been reported to increase the risk of clinical disease (Monath et al., 1986; Webb et al., 1987b; Hurd et al., 1997; Hurd et al., 1999). It remains unclear whether this increase is due to a difference in exposure to the virus or a difference in another risk factor, such as an increase in mucosal abrasions.

Distribution

VS is reported to be endemic in many tropical, subtropical and equatorial regions of the Americas, although original citations from some of these areas are not readily available. In the USA, outbreaks since 1985 have been restricted to states in the Southwest, although cases have been reported throughout much of the central and southern regions of the USA during the twentieth century. It is uncertain whether cases occurring in livestock outside the Southwest USA result from direct contact with the agent or from transport of infected animals into these regions (Jenney et al., 1984).

Other vesiculoviruses or subtypes of VSV that have been associated with clinical disease in humans, domestic animals, and/or rodents include Cocal in Brazil and Trinidad (Jonkers et al., 1964), Alagoas (also called Brazil) in Brazil and Colombia (Federer et al., 1967), Piry in Brazil (Theiler and Downs, 1973), Chandipura in India (Bhatt and Rodrigues, 1967), and Isfahan in Iran (Tesh et al., 1977).

Distribution Table

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Pathology

Histopathologically, VS lesions are typified by intercellular oedema of the Malpighian cell layer and epithelial cell necrosis, which may or may not incorporate the basal cells. Necrotic epithelial cells are strongly eosinophilic and contain pyknotic nuclei. Vesicular fluid is primarily seen separating cells at the basal cell level. In addition, non-specific signs of inflammation are evident, including granulocyte and monocyte infiltration, engorgement of the associated vasculature, and perivascular cuffing. These changes were reported to occur in infected bovine tongues whether or not gross lesions were present (Seibold and Sharp, 1960).

This disease is considered non-lethal. Deaths that do occur are generally due to secondary complications. In some cases, complications are sufficiently severe to warrant euthanasia. Gross pathological findings would reflect these secondary complications.

Diagnosis

Because of the extreme variability in clinical manifestations, VS cannot be definitively diagnosed clinically. Differential diagnoses include foot and mouth disease (FMD), swine vesicular disease, vesicular exanthema of swine, infectious bovine rhinotracheitis, bluetongue, Balclutha horse syndrome, trauma, contact with or ingestion of toxins or irritants, dermatological conditions (including auto-immune disease), and photosensitizations (Mohler, 1918; McCosker and Keenan, 1983; Fenner et al., 1987; Schmitz and Reagor, 1987; Campagnolo et al., 1995; Schlipf, 1997; Barrendeguy, 1999). As well, outbreaks of vesicular disease in horses for which no etiologic agent is determined have been reported (Kim et al., 1999; McCluskey and Mumford, 2000).

Definitive diagnosis of VSV infection must be laboratory-based. Virus isolation may be attempted on biological samples from clinically affected animals. Appropriate samples of lesions may include nasal/oral swabs, epithelial tags, skin scrapings, or biopsies. As infective virus is only present in active lesions, virus isolation is unrewarding once lesions have begun to resolve. PCR has been used as a research tool to detect viral RNA in VS lesions (Rodriguez et al., 1993). As this technique detects only RNA and does not require active virus to be present, it is potentially a more sensitive test. PCR is not currently being used on a routine basis for clinical diagnosis of VS.

Serology is routinely used to diagnose VSV infection. These tests are serotype-specific and little cross-reactivity between antibody to VS-NJ and VS-IN occurs. Typically, a competitive ELISA (cELISA) is used as a screening test. This test is rapid and relatively easy to perform. It detects both IgM and IgG antibodies. Serum neutralisation (SN) and complement fixation (CF) tests are also commonly used. The SN detects IgG and the CF detects primarily IgM and some IgG. Antibody can be detected in the serum 5-9 days post-infection.

Because both the cELISA and SN tests detect serum IgG, animals may maintain a detectable antibody titre in their serum for 1-3 years, making the interpretation of titres in a single serum sample difficult (Geleta and Holbrook, 1961; Mumford et al., 1998; Mumford et al., 2000). An elevated CF titre in a single serum sample is more diagnostic for recent infection as CF titres tend to become undetectable by 110 days post-infection, but the CF test may be affected by high concentrations of IgG (Geleta and Holbrook, 1961; Katz et al., 1997). A rising SN or CF titre is therefore required to definitively diagnose recent VSV infection in outbreak index case or non-outbreak situations. Currently, an ELISA test to specifically detect serum IgM is being evaluated at the USDA’s National Veterinary Services Laboratories (NVSL; Ames, IA) (Katz et al., 1997). This test would improve the ability to differentiate active VS infections from past exposure.

Specific immune responses in infected natural host species have not been evaluated. Although animals infected with VSV do develop an immune response as indicated by detectable specific antibody in the serum, it is unclear whether this serological response is protective. Vaccine has been shown to induce antibody production, and an anemnestic antibody response is detected when animals with serum antibody are vaccinated (Gearhart et al., 1987). However, serologically positive animals may be susceptible to re-infection (Geleta and Holbrook, 1961; Rodriguez et al., 1990; Katz et al., 1997), perhaps as a result of ineffective protection afforded by circulating antibody to viral infection of the epidermal and mucosal layers.

List of Symptoms/Signs

Disease Course

Clinical signs of VS appear approximately 1-3 days after exposure. Pyrexia is typically present at this time. Initially, blanched macules appear on the oral or nasal mucosa, gums, mammary glands, external genitalia, or coronary bands due to intercellular oedema and to rapid cytoplasmic replication and cytopathogenicity of VSV in infected cells (Ribelin, 1958; Seibold and Sharp, 1960; Fenner et al., 1987). These areas then develop into vesicular lesions that progress to ulcers and erosions within 24-48 hours. Body temperature is typically within normal limits by this time. Vesicular fluid contains large concentrations of infective virus. Further intercellular spread results in coalescing of lesions and often results in extensive epithelial or mucosal necrosis and sloughing, especially of the dorsum of the tongue in horses. The lips and nares may be involved, and swelling of these areas is common (Acree, 1964). Virus shedding from active lesions has been reported to cease 6-7 days post-exposure (Katz et al., 1997). Lesions resolve within 10-14 days, unless complicated by secondary bacterial infections. Other secondary complications may include mastitis, weight loss or failure to gain, and hoof wall or claw deformities secondary to coronary band lesions (Alderink, 1984). Depigmentation of the affected epithelium may occur after the lesions have healed (Knight and Messer, 1983). Clinical manifestations and disease severity are variable among affected animals (Webb et al., 1987b), and subclinical infection has been shown to occur commonly during outbreaks of VS (Monath et al., 1986; Mumford et al., 1998).

The mechanism of VSV entry into susceptible hosts has not been completely elucidated. It is suspected that the virus gains entry through breaks in the epidermal or mucosal barrier either through direct transmission from infected animals or via the bite of an infected arthropod vector (see Epidemiology section).

Virus multiplication in the infected host appears to remain localised in the skin or mucous membrane, and there are no reports of naturally occurring viremia in any animal species. New lesions tend not to occur after initial lesions appear, and lesions are generally restricted to one anatomical area in each affected animal (Alderink, 1984). When secondary lesions do appear in anatomical sites distant from the primary lesions it may be due to either re-infection from the original source or contact spread from the primary lesion.

Epidemiology

Occurrence

Vesicular stomatitis is endemic and occurs seasonally every year in areas of southern Mexico, Central America, northern South America, and Ossabaw Island, Georgia (USA). Spreading north and south from these endemic regions into temperate regions of North and South America, the disease occurs sporadically but maintains a seasonal pattern, with outbreaks primarily occurring from early summer to late fall. Recent outbreaks in the USA have occurred in 1982-1983, 1985, 1995, 1997 and 1998.

Although most affected premises are spatially related to other affected premises during outbreaks, some cases may occur on single premises that appear removed spatially from other affected premises (Jenney et al., 1984). Acree (1964) described the pattern of spread both among neighbouring herds and among geographical districts as erratic.

Epidemiological cycle

The complete epidemiological cycle of VSV has not been elucidated. Virus can be transmitted to susceptible hosts by direct contact with lesions on infected animals, saliva of animals with oral lesions, or contaminated fomites such as watering tanks and milking machines (Strozzi and Ramos-Saco, 1953; Acree et al., 1964; Goodger et al., 1985). There are no reports of virus being shed in urine, faeces, or milk. Abrasions of skin or mucous membranes may facilitate transmission of the virus and subsequent lesion formation (Hansen et al., 1985). Virus has been isolated from non-haematophagous flies (e.g. Musca domestica), therefore arthropods may play a role in mechanical transmission of the virus (Webb et al., 1987b; Francy et al., 1988).

Available epidemiological data (e.g. seasonality of occurrence, specific ecology of zones of occurrence, increased attack rates in pastured animals) suggest a role for an insect vector in the transmission of VSV (Stallknecht et al., 1985; Brinson et al., 1992; Comer et al., 1993; Vanleeuwen et al., 1995; Hurd et al., 1999). In addition, VSV has been isolated from field-collected arthropods in VS-endemic and epidemic areas, and arthropod species (e.g. Culicoides spp.,Simulium spp., Lutzomyia spp., Aedes spp.) have been proposed as possible vectors (Jenney, 1967; Bergold et al., 1968; Walton et al., 1987; Brinson et al., 1992; Comer et al., 1994). Several proposed vectors have experimentally been shown to acquire the virus through a blood meal, support biological reproduction of the virus, transmit the virus transovarially, and/or transmit the virus to a host (Tesh et al., 1971, 1972; Cupp et al., 1992; Mead et al., 1999).

Despite the evidence for transmission via an arthropod vector, there are no reports identifying a naturally occurring viremia in any potential animal host studied to date. Many species of rodents throughout VS-endemic and epidemic regions have been shown to have been exposed to VSV, as indicated by circulating specific antibody in the serum (Jiménez et al., 1996). Donaldson (1970) experimentally induced viremias lasting 10 days in bats (Myotis lucifugus) using Cocal virus, although multiplication of the virus was not verified. More recently, Mead et al. (2000) observed transmission of VSV-NJ when infected and non-infected blackflies were simultaneously fed on non-viremic deer mice, suggesting that a viraemic host may be unnecessary for an insect to become infected with virus following feeding.

Persistence

Despite evidence that viral RNA has been detected in convalescent cattle that had been experimentally infected with VSV (Letchworth et al., 1996), and that persistence can be experimentally induced in rodents (Fultz et al., 1982; Hughes et al., 1985), there is no evidence that recovered animals infected with VSV under natural conditions or animals infected experimentally via natural routes of infection either maintain persistent VSV infections or shed infective VSV.

Impact: Economic

Background on economic significance

In the USA, the Department of Agriculture (USDA) requires all livestock with clinical signs of vesicular disease to be inspected by foreign animal disease-trained personnel from the USDA: Animal and Plant Health Inspection Service: Veterinary Services (USDA: APHIS: Veterinary Services), and laboratory confirmation of VSV infection is made only in approved laboratories. The costs of the mandated surveillance, investigation, testing, and control measures are borne by the USDA: APHIS: Veterinary Services, and therefore represent a significant economic impact of this disease.

Quarantines and other livestock movement restrictions are implemented at the local and regional levels during VS outbreaks in the USA (see Disease Prevention and Control section). The implementation of movement restrictions and increased regulatory surveillance has resulted in the cancellation of local and regional livestock shows, sales, and other events. As well, distant livestock events and the movement of animals for breeding and sale can be affected due to the inability of animals from affected areas to move freely across state borders, thus impacting livestock producers and the industry generally (Alderink, 1984; Hayek et al., 1998). Embargoes implemented by other countries during outbreaks of VS in the USA disrupt the livestock economy at every level. Costs are also incurred through increased serological testing and health examination requirements prior to shipment.

Impact of clinical disease

Clinical manifestations of the disease also result in economic losses during outbreaks of VS in all countries where it occurs. Decreased milk production, secondary mastitis, weight loss, and failure to gain have been reported in cattle (Acree et al., 1964; Leder et al., 1983; Alderink 1984; Goodger et al., 1985; Hayek et al., 1998). In addition, increased labour is required to care for ill animals, further increasing costs of clinical disease to the individual producer (Hayek et al., 1998).

Zoonoses and Food Safety

Vesicular stomatitis in humans can be an acute, severe, uniformly non-fatal illness that is generally characterized as flu-like, although the clinical manifestations of VSV infection vary and seroconversion without clinical disease occurs (Cline, 1976). It is believed that transmission to humans occurs through direct contact with active lesions or saliva containing infective VSV (Reif et al., 1987). There are no reports of humans transmitting the infection to other humans or to animals, although transmission via contaminated equipment, hands, gloves, and clothing probably occurs. Veterinarians, animal health technicians, livestock handlers, laboratory personnel and others working closely with infected animals or live virus are at increased risk (Patterson et al., 1958; Fields and Hawkins, 1967; Bridgewater, 1983). The VS virus does not appear to be transmissible through ingestion of milk from infected cows (Mohler, 1918), and no reports are available describing transmission through meat from infected animals. Due to the heat-lability of the virus, cooked meat and pasteurised milk would probably not contain infective VSV.

Disease Treatment

Unless secondary complications occur, VS is a self-limiting disease that resolves within 2-3 weeks after onset of clinical signs. No specific treatment is available or indicated. Symptomatic care may be indicated for secondary manifestations such as dehydration, anorexia, and secondary bacterial infections of lesions.

Prevention and Control

No VSV vaccines are currently commercially available in the USA or Mexico, although several vaccines are being developed or are being evaluated experimentally. A commercial VSV vaccine is in use in Colombia. In the USA, an autogenous killed virus vaccine was developed and made available during some outbreaks (most recently in 1985 and 1995), although vaccine efficacy was not determined (Bridges et al., 1997; Gearhart et al., 1987). Because of the potential international regulatory consequences of animals developing serum antibody titres against VSV, research is being conducted to develop a DNA vaccine which would elicit production of antibody that could be differentiated from that elicited through natural exposure (Cantlon et al., 2000).

Because the epidemiological cycle of VSV has yet to be completely elucidated, management factors to specifically reduce the risk of VSV exposure are ill-defined. Some research has suggested that minimising the exposure of livestock to arthropods (e.g. housing animals in barns, applying insecticides) may reduce the risk of VSV infection (Hurd et al, 1999). Disinfection of shared equipment such as watering tanks, feeders, and milking equipment may reduce the risk of transmission (Hansen et al., 1985). Isolation of animals with clinical lesions may be helpful to control spread, as contact transmission is known to occur. However, if one or more animals in a group housed together develop clinical signs it is likely that all animals in the group have been exposed, and therefore isolation of the entire group might be more effective.

Currently in the USA, premises with one or more animals confirmed positive for VSV infection are quarantined, and no movement of any susceptible livestock species off the premises is permitted during this time. Quarantine remains in place until 30 days after all animals on the premises are free from clinical signs. During VS outbreaks, many unaffected states impose embargoes or restrictions on animals from states where VS has been confirmed. Often, these restrictions include requirement of a health certificate specifically stating the status of the animals potential VS exposure. In some cases a negative serological test (usually SN test) is required. International embargoes and restrictions are also imposed on states, regions, and countries where cases of VS have been confirmed. Many of these restrictions also include a serological testing requirement.

See also Economic Importance and Impact section.

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