| VETERINARY INFORMATION PAGE |
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| VIROLOGY: | Equine arteritis virus (EAV) is a small, enveloped RNA virus and the prototype virus of the genus Arterivirus , family Arteriviridae, order Nidovirales. Strains of the virus vary in their ability to produce disease, including abortion, with some causing only a mild to moderate fever (1). |
EPIDEMIOLOGY: |
Serologic isolation of EAV in North and South America, Europe, Africa, Asia, and Australia. Disease outbreaks in North America, Britain, Spain, Italy, France, Poland, The Netherlands, South Africa, and Germany. Outbreaks of EVA are uncommon and usually associated with the movement of horses or shipment of semen. The virus is known to infect many breeds of horses, however, the prevalence of infection varies widely, usually being highest in Standardbreds and Warmbloods. There is little evidence of infection in populations of wild equids. (1 and 5) Transmission of EAV infection can occur by respiratory, venereal, congenital, or indirect means. Aerosol transmission is the main mode of spread by horses in acute infections. It is primarily responsible for dissemination of infection among horses at racetracks, shows, sales, veterinary clinics, and on breeding farms. The virus can also be transmitted venereally by the acutely infected mare and by the acutely or chronically infected (carrier) stallion. The virus is shed constantly in the semen of stallions. Mares can be infected by the venereal route either following natural service or artificial insemination with infective semen. The virus can also be transmitted indirectly through the use of virus-contaminated fomites (eg, shanks, twitches, head collars, and breeding shed equipment) and on the hands or clothing of animal handlers. (1) |
CLINICAL PATHOLOGY: |
In one paper, experimentally infected mature horses were consistently leukopenic. The horses in this study presented with a biphasic leukopenia and neutropenia. Lymphopenia was consistently present postinfection (PI) in this group of experimentally infected horses. There is also clinical pathology finding for infected foals. (7) |
| GROSS PATHOLOGY: | There are various areas affected
by this virus: blood
vessels, lungs, lymphoid tissue, intestine, adrenal glands, kidneys,
skin, female reproductive tract, and the male reproductive tract. Gross lesions are mainly the expression of the vascular pathologic changes. Edema, congestion, and hemorrhage of the subcutaneous tissues, lymph nodes, and viscera are the most frequent gross lesions in horses that die after natural or experimental EAV infection. Moderate to abundant amounts of yellowish, clear exudate can be found in the body cavities. Congestion, lymphadenomegaly, edema, and hemorrhages can be observed along the course of the colonic and cecal vessels but also are evident systemically. Lungs, especially observed in the lungs of infected neonates, are wet and increased in weight, with a prominent lobular pattern. The trachea may contain froth. On occasion, lungs can be multifocally or diffusely reddish because of congestion and hemorrhage. The uterine endometrial surface of aborting mares may be swollen and diffusely congested, sometimes with hemorrhages. There is more information on each affected area on this webpage (7). |
PATHOGENESIS: |
Through experimental and naturally infected models, the possible pathogenesis of this virus is understood. The course of infection includes infection of the respiratory epithelium and alveolar macrophages first, and then onto the satellite lymph nodes. The next stage of infection occurs at the bronchopulmonary lymph nodes, endothelium, and circulating monocytes; replication occurs here. Systemic distribution of the virus follows and localization within the endothelium and medial myocytes of blood vessels and mesothelium occurs; severe damage occurs to blood vessels. Apparently, the last site of invation is the renal tubular epithelium, where the virus may persist for an additional two weeks. The virus is detectable in most tissues for about 28 days. (7)  |
| TREATMENT: | There is no specific EVA treatment. Symptomatic care (i.e. antipyretic, anti-inflammatory, and diuretic agents) may be required in severe cases, but most acute infections recover uneventfully. Supportive care and rest are ususally sufficient for a horse to recover. Treat according to the case that presents to you. Appropriate diagnostic samples may need to be taken prior to supportive therapy. |
CONTROL: |
The carrier stallion is the primary reservoir of the virus and serve as a long term source of infection. Therefore, an effective control measure would be to encourage all breeders in at-risk areas to do blood tests for EAV antibodies on all new breeding stallions before each breeding season. The semen of any anti-body positive, non-vaccinated stallions laboratory tested to identify any carrier stallions. Any EAV-carrier stallions should be physically isolated. Encourage strict hygienic procedures when breeding or collecting semen from carrier stallions. Restrict the breeding with EVA-carrier stallions to vaccinated mares or mares that have acquired a natural immunity to the virus. In breeds or geographic locations that are high-risk to EAV infection, encourage appropriate vaccination of immature male foals, 6-12 months of age against EVA. Over time, this will reduce the amount of carrier stallions and therefore, reduce the primary reservoir off which this virus will spread. For more information on control,, see the USDA's circulating bulletin(4). |
SAMPLING PROCEDURES: |
A diffinitive diagnosis is based on the isolation of EAV from affected cases or the demonstration of seroconversion or an increase in serum antibody titer.
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VACCINATION: |
Other then natural infection and recovery, the main way to induce a protective response against an infectious agent is through vaccination. With EAV the vaccine must be a modified live virus. It is suggested to vaccinate all at risk satllions with this vaccine 28 days before the beginning of the breeding season. Vaccination with the modified live vaccine protects mares exposed to stallions shedding the virus in semen and has been used to control outbreaks of the respiratory form on racetracks. Foals from non-immune mares can also be vaccinated. It is recomended to not vaccinate with a killed vaccine. The efficacy of a killed vaccine has not yet been reported and antibodies induced by the killed vaccine can not be differentiated from those resulting from natural infection; this creates problems with the import regulations. Import regulations require that the horse is sero negative, which is proof of lack of exposure to virulent EVA. (5) For more information on import regulations go to the "stallion owner page." The approved vaccine to our findings is Arvac, by Fort dodge laboratories, inc. (6). Vaccination protocol set by the AAEP (8) is:
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IN THE FACE OF AN OUTBREAK: |
According to the USDA, the state veterinarian must be reported when there is and EVA outbreak. In Canada, EVA is an annually reportable disease, therefore, should an outbreak occur it is recommended that an immediate quarantine be ordered on the affected premises. For this to be an effective quarantine, restrictions must be placed on all horses moving to and from that premesis. The following are suggestions (4):
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REFERENCES: |
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/52900.htm 2) OIE. Aug. 2005. “Equine Viral Arteritis.”http://129.186.78.52/Factsheets/pdfs/equine_viral_arteritis.pdf 3) McCue, P. November 2006. “Equine Viral Arteritis (EVA).”4) United States Department of Agriculture. April 2004. “Equine Viral Arteritis – Uniform Methods and Rules.” http://www.aphis.usda.gov/vs/nahps/equine/eva/eva-umr.pdf. 5) 6) 8) AAEP vaccination protocol, http://www.xcodesign.com/aaep/displayArticles.cfm?ID=36 |