Equine Viral Arteritis (EVA)
Are you currently breeding horses? Are you vaccinating your horses for Equine Viral Arteritis (EVA)? A 2005 study found that a mere 11.7% of breeding operations are vaccinating for this highly contagious, reportable, viral disease that causes sporadic outbreaks of respiratory infection and abortion in horses.
The virus was first identified in 1953, in the State of Ohio, but is now known to be worldwide in distribution. Equine Viral Arteritis is caused by an RNA-containing Arterivirus known as equine viral arteritis virus (EAV). The virus only infects the various members of the Equine family. Historically, the most commonly affected horses are warmbloods such as the standardbred and thoroughbred.
Infected horses may never show any physically apparent clinical signs of disease, a situation termed subclinical infection. These same horses may then spread the infection to other susceptible individuals.
Equine Viral Arteritis is transmitted in several ways including: contact with respiratory secretions, venereal transmission by natural breeding or artificial insemination, vertically from a mare to an unborn foal through the placenta, or fomites contaminated with infective body secretions such as tack equipment or an artificial vagina for the collection of semen from a stallion. Mares infected by a venereal route may, in turn, develop a viremia (the presence of virus in the blood) resulting in a respiratory infection that is capable of transmitting virus to other susceptible horses through respiratory secretions.
The most important source of viral transmission is through the use of a persistently infected stallion’s semen. Up to 70% of stallions will become persistent carriers of the virus without exhibiting any overt clinical signs of disease. The viral shedding may persist for years, sometimes resolving spontaneously for unknown reasons. It is theorized that the carrier state may be dependent on testosterone levels since mares, geldings, and foals do not become persistent carriers.
Artificial insemination does not prevent infection. Equine Viral Arteritis Virus may persist in frozen semen for years.
The incubation period is 2 to 13 days following infection with the average being 7 days before the onset of clinical signs of disease. Clinical signs of disease include: anorexia (lack of appetite), conjunctivitis (inflammation of the conjunctiva surrounding the eyes), petechial or small hemorrhages on the mucous membranes, and dependent ventral edema of the limbs, mammary glands, prepuce scrotum, and ventral body wall. Additional signs of disease include excessive tearing or lacrimation, edema surrounding the eyes (ocular edema), coughing, sneezing, nasal discharge, and a fever. Pregnant mares abort at any time between 3 and 10 months into gestation. Pregnant mares may not show any outward signs of illness. Aborted fetuses may be partially autolyzed (tissue disintegration through the action of the body’s own enzymes). There are no specific lesions that will indicate EVA. Foals that are born live are characteristically weak and may die from interstitial pneumonia or enteritis within the first few days following birth. Colostrum from immune mares may attenuate (lessen the disease) or prevent infection in foals not exposed to the virus in utero (during pregnancy).
The virus primarily infects macrophages (a type of white blood cell) and blood vessel endothelium throughout the infected animal’s body. The damaged blood vessels leak fluid thereby causing edema and petechia, most apparent on the mucous membranes of the host. Interference with macrophage function leaves the host’s immune system less able to fend off secondary bacterial infections.
Lab work is generally normal other than a leukopenia (lack of white blood cells) or possibly icterus (jaundice).
Horses that are acutely infected will typically shed the virus in nasal secretions for up to sixteen days following the onset of clinical signs. Treatment of young foals with pneumonia and/or enteritis has been largely unsuccessful although hyperimmune colostrum may help.
There is no viral specific treatment available for EVA. Treatment primarily consists of supportive care including rest, NSAID therapy, antibiotics to control secondary infection, and diuretics to control edema.
The prognosis following infection is generally good excluding young foals and in utero-infected animals. Most affected adult horses will recover completely.
The most commonly used test to confirm a diagnosis of EVA is viral neutralization by a USDA approved lab or the analysis of paired serum samples. Serum samples are taken 3 to 4 weeks apart from an individual horse to measure their antibody levels to the virus. A titer of 1:4 or greater on a single sample or a fourfold increase in the viral titer between individual samples indicates a recent infection. Unfortunately the viral titer does not distinguish between natural EAV infection and those antibodies produced from vaccination. Heparinized samples should not be taken since the presence of heparin in a sample interferes with PCR or virus isolation testing. Serum samples should be refrigerated and preferably shipped overnight on cold packs.
During an acute outbreak of the virus, nasal, conjunctival swabs, or various body samples from aborted fetuses including placental material may be submitted for viral isolation. These samples should be shipped on ice or preferably, frozen and shipped overnight.
Many countries will not allow the importation of horses that are seropositive for EVA. It is therefore important to document proof of a horse’s seronegative prevaccination status before beginning a vaccination program. Up to 50% of all stallions test seropositive for antibodies against EAV either by natural infection or vaccination. For this reason it is imperative that a prevaccination seronegative status be documented in a horse’s permanent record prior to vaccination and be included as part of the permanent medical record.
Currently there is only one approved vaccine for the prevention of EVA in the United States. The vaccine, called Arvac®, is produced by Fort Dodge Animal Health and is marketed for use in nonpregnant mares and foals greater than 6 weeks of age. A new vaccine, currently under investigation, shows promise in the differentiation between vaccinated animals and those that have been naturally infected with the virus.
In a comprehensive vaccination program, all colts that could possibly be used for breeding should be vaccinated at 6 to 12 months of age in order to prevent the establishment of a carrier state. The AAEP suggests the annual vaccination of seronegative mares 3 weeks prior to being bred to a carrier stallion. High-risk operations should vaccinate all horses 6 months of age and older with annual revaccination for Equine Viral Arteritis.
All semen should be tested by means of viral isolation before use. At least two semen samples should be evaluated prior to designating a stallion as free of the Equine Arteritis Virus. Carrier stallions and their semen cannot be imported into any country, other than the United States and Canada, even though the virus is worldwide in distribution.
The virus is easily inactivated by adverse environmental conditions and common disinfectants.
Barnett, Craig DVM. “Equine Viral Arteritis”, The Animal Health Solution. April 2007. pp 36-38
Ramirez, Julia. “Equine Viral Arteritis.” Compendium Continuing Education for Veterinarians Equine. Vol. 3(9), November/December 2008. Pp. 456-465.
Wetzel, Linda Marie, “Equine Viral Arteritis: Assessing the Threat, Causes and Prevention”. DVM . April 2007.Pp. 4E-5E.