Equine viral arteritis is an economically important, contagious, viral disease of equids caused by equine arteritis virus (EAV). EAV infection is usually subclinical; however, EAV can cause abortion, respiratory illness, establishment of a carrier state in stallions, and interstitial pneumonia and death in young foals. Diagnosis of equine viral arteritis is based on detection of the virus in body secretions or fluids, whole blood, or tissues, or on serological testing. Equine viral arteritis is treated with general supportive care during the acute phase of infection. There is no treatment to eliminate persistent viral infection in stallions. Attenuated and inactivated vaccines are available in North America and Europe, respectively, for the prevention and control of equine viral arteritis.
Equine viral arteritis is a disease of equids (horses, donkeys, mules, and zebras) that is caused by equine arteritis virus (EAV). Although EAV infection is almost exclusively restricted to equids, limited data suggest that the host range might also extend to alpacas and llamas (1, 2, 3). Transmission of the virus between horses and donkeys has been reported (4).
EAV is present in equine populations worldwide; notable exceptions include Japan, Iceland, and New Zealand, which have successfully eradicated the disease.
The prevalence of EAV infection varies widely both between countries and within the same country among breeds. It is frequently highest in Standardbreds and warmblood breeds.
Etiology and Pathogenesis of Equine Viral Arteritis
Equine arteritis virus (EAV) is a small, enveloped, positive-sense, single-stranded RNA virus. It is classified as a member of the family Arteriviridae, subfamily Equarterivirinae, and genus Alphaarterivirus, in the order Nidovirales. The species is named Alphaarterivirus equid, commonly known as equine arteritis virus.
Although there is only one known EAV serotype (the prototype Bucyrus strain), genomic and antigenic variation exists among temporally and geographically distinct strains of the virus. Furthermore, EAV field strains differ in virulence, pathogenicity, and neutralization characteristics, resulting in a spectrum of disease outcomes ranging from subclinical infection to mild clinical signs to moderate or severe clinical disease (5).
Phylogenetically, EAV isolates are grouped into North American and European lineages, each further subdivided into two subclades: North American (NA-1 and NA-2) and European (EU-1 and EU-2).
EAV is readily inactivated by lipid solvents and by common disinfectants and detergents. The virus survives for 75 days at 4°C (39.2°F), for 2–3 days at 37°C (98.6°F), and for 20–30 minutes at 56°C (132.8°F). EAV can maintain infectivity in tissues and various body fluids, including semen, for years when stored at –70°C (–94°F) or below (6, 7).
After an equid has been exposed to EAV, the virus invades the upper and lower respiratory tract and multiplies in nasopharyngeal epithelium and tonsillar tissue and in bronchial and alveolar macrophages. Infected CD14+ monocytes and a small subpopulation of CD3+ T lymphocytes transport EAV to regional lymph nodes (eg, bronchial lymph nodes), where it undergoes an additional cycle of replication before being released into the bloodstream (viremia).
The cell-associated viremia that follows ensures the dissemination of EAV throughout the body. By days 6–8, the virus localizes to the vascular endothelium and medial myocytes of smaller blood vessels, especially the arterioles, and causes panvasculitis. It can also be found in the epithelium of certain tissues, particularly those of the adrenal glands and liver during acute infection.
Vascular lesions caused by EAV include endothelial swelling and degeneration, neutrophilic infiltration, and necrosis of the tunica media of affected vessels. These lesions give rise to edema and hemorrhage, which are believed to result from activation of the proinflammatory cytokines IL-1-beta (interleukin-1-beta), IL-6, IL-8, and possibly TNF-alpha (tumor necrosis factor alpha). Maximal vascular injury occurs by approximately day 10, after which lesions begin to resolve.
Except in certain infected stallions that become carriers of the virus, EAV is no longer detectable in tissues and body fluids beyond day 28 after primary infection (1, 8, 9).
EAV causes abortion in pregnant mares, and abortion rates during natural outbreaks of equine viral arteritis can vary from approximately 10 to 60% (10). However, the 1984 Kentucky outbreak resulted in an abortion rate of 71% (11). EAV-induced abortions can occur at any time between 2 and 10 months of gestation without premonitory signs. However, the pathogenesis of fetal infection and the mechanism responsible for abortion are poorly characterized.
EAV is vertically transmitted to the fetus, as evidenced by the high viral titers and abundance of viral antigen in fetal membranes and diverse fetal tissues. It is speculated that abortion occurs as a consequence of vasculitis of myometrial blood vessels and myometrial necrosis, which leads to placental dysfunction and chorionic detachment (12).
During the last trimester of pregnancy, foals can acquire EAV congenitally, resulting in weak neonatal foals. Infection in neonatal foals is frequently associated with interstitial pneumonia, which can be complicated by secondary bacterial infections.
After natural EAV infection, 10–70% of stallions become persistently infected and continuously shed virus in their semen, for either a short or a long period of time, without adverse effects on semen quality or reproductive capacity (1, 13, 14):
Short-term shedders/carriers shed virus for a period of several weeks up to approximately a year after infection.
Long-term shedders/carriers—ie, those with long-term persistent infection (LTPI)—shed virus for > 1 year after infection, possibly throughout life.
The EAV carrier state has been confirmed in sexually mature intact males, specifically postpubertal colts and stallions, but not in mares, geldings, sexually immature colts, or fillies. The establishment and LTPI of EAV in the reproductive tract of stallions is testosterone dependent; therefore, persistent infection does not occur in mares, foals, or sexually immature colts.
EAV persists exclusively in the male reproductive tract, despite the presence of high levels of neutralizing and mucosal antibodies (15), as well as a moderate to severe local inflammatory response (9).
Analysis of multiple tissues from the reproductive tract of EAV carrier stallions unequivocally confirmed the ampullae as the primary site of EAV persistence. During long-term persistence, EAV infects vimentin-positive fibroblasts and mononuclear cells (CD8+ T and B lymphocytes and macrophages) but not the glandular epithelium of the ampullae (9, 16).
It has been demonstrated that the establishment of EAV LTPI correlates with the in vitro susceptibility of a subpopulation of CD3+ T lymphocytes to EAV infection (17, 18). Consequently, stallions that have the CD3+ T lymphocyte susceptibility phenotype are at higher risk of becoming LTPI carriers than are those lacking this phenotype. Thus, variation in the frequency of the carrier state in certain horse breeds has been shown to be associated with the distribution of CD3+ T lymphocyte populations that are susceptible or resistant to in vitro EAV infection.
A genomewide association study demonstrated that these phenotypes are associated with the CXCL16 gene on equine chromosome 11. Subsequent studies identified two allelic variants of CXCL16 (CXCL16S and CXCL16r) that differ by four nonsynonymous nucleotide substitutions in exon 2 (14).
Of the two encoded proteins, the CXCL16S isoform has EAV receptor activity and is associated with the CD3+ T lymphocyte–susceptible phenotype and establishment of LTPI in stallions. The CXCL16R isoform, in contrast, lacks receptor activity, leading to a CD3+ T lymphocyte–resistant phenotype and early viral clearance in stallions (short-term carriers of the virus).
Carrier stallions are also the principal means by which genetic diversification of EAV can occur, with potential emergence of novel viral variants. Persistent infection is characterized by extensive genomewide purifying selection mediated by intrahost selective pressures. Nucleotide substitutions occurring in open reading frame 1a (ORF1a, the nonstructural protein-2 encoding region), ORF3 (which encodes the GP3 minor envelope glycoprotein), and ORF5 (which encodes the GP5 envelope glycoproteins that determine the major neutralization epitopes) have been found to be important in the evolution of EAV in carrier stallions over time (19).
Epidemiology and Transmission of Equine Viral Arteritis
The epidemiology of equine viral arteritis involves virus-, host-, and environment-related factors, including variability in pathogenicity among naturally occurring strains of the equine arteritis virus (EAV), modes of transmission, the occurrence of the carrier state in stallions, and the nature of acquired immunity to infection.
The carrier stallion is the natural reservoir of EAV and is responsible for maintaining and perpetuating the virus in equine populations in nature. Persistently infected stallions shed EAV constantly in the sperm-rich fraction of the semen, but not in any other secretions or excretions.
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Since the start of the 21st century, there have been no major global outbreaks of equine viral arteritis, and most reported cases have occurred as localized events on European breeding farms, resulting from the movement of carrier stallions or the shipment of virus-contaminated semen (chilled or frozen) and frozen embryos (20).
Persistent EAV infection clears spontaneously in a variable percentage of stallions (ie, short-term carriers), with no evidence of subsequent reversion to a shedding state. Whereas acutely infected stallions can experience a period of subfertility lasting up to 4 months, the existence of the carrier state does not appear to impair the fertility of infected stallions or to otherwise adversely affect their health.
EAV can be transmitted via respiratory, venereal, and congenital routes or by indirect means:
The respiratory route is the principal mode of EAV dissemination during the acute phase of infection. It is primarily responsible for the transmission of EAV among susceptible equids kept in close contact (eg, at racetracks, shows, sales, or veterinary hospitals, and under conditions of intensive management on breeding farms). Respiratory transmission of EAV can also occur through contact with the placenta, placental fluids, and tissues from EAV abortions.
Venereal transmission of EAV occurs during natural or artificial insemination with infective semen from acutely and persistently infected carrier stallions. Mares can be readily infected via the venereal route after breeding to a carrier stallion either by live cover or by artificial insemination with fresh-cooled or cryopreserved semen.Limited evidence suggests that EAV can be transmitted through embryo transfer (21).
Importantly, EAV infection can be transmitted through indirect contact with virus-contaminated fomites (eg, breeding-shed equipment, buckets, shanks, or twitches) or through contact with the hands, apparel, or footwear of animal handlers.
Clinical Findings of Equine Viral Arteritis
Clinical signs of equine viral arteritis vary considerably among individual horses and among outbreaks. Exposure to equine arteritis virus (EAV) can result in clinical or subclinical infection, depending on the relative virulence of the strain involved, viral dose, age and physical condition of the animal, and various environmental factors.
Most cases of primary EAV infection are subclinical. The acute phase of infection, whether or not associated with clinical signs, is preceded by an incubation period of 2–14 days, which varies mainly with the route of exposure. The interval between exposure and the acute phase is 2–3 days after respiratory exposure and 6–8 days after venereal transmission of the virus.
Clinical signs of equine viral arteritis can vary in range and severity between outbreaks and between individuals within the same outbreak. Any combination of the following clinical signs is possible:
fever up to 41°C (105.8°F)
depression
anorexia
leukopenia
dependent edema (limbs, ventrum, scrotum, prepuce, mammary glands, peri- or supraorbital region; see and images)
conjunctivitis, with or without lacrimation
photophobia
serous to mucoid nasal discharge
stiff gait
petechial hemorrhages on oral mucous membranes
urticaria (localized on face, neck, or pectoral region, or generalized; see )
diarrhea
icterus
ataxia
abortion
fatal pneumonitis or pneumoenteritis in neonatal and young foals
temporary subfertility in stallions
Scrotal edema (swelling of the scrotum and sheath) in a horse with equine viral arteritis.
Courtesy of Dr. Peter J. Timoney.
Periorbital edema in a horse with equine viral arteritis.
Courtesy of Dr. Peter J. Timoney.
Urticaria-type skin reaction in a horse with equine viral arteritis.
Courtesy of Dr. Peter J. Timoney.
Strains of EAV can cause abortion throughout much of a mare's pregnancy (from 2 months to > 10 months). Abortion can occur late in the acute phase or early in the convalescent phase of infection, with or without prior clinical signs of equine viral arteritis. In natural outbreaks,abortion rates can vary from < 10% to as high as 60%.
No evidence suggests that mares bred with EAV-infective semen will abort. Mares that abort as a result of infection by the virus are already pregnant at the time of exposure, which occurs primarily by the respiratory route via direct proximity with an acutely infected animal, frequently sharing the same pasture or having across-the-fence contact. Abortion occurs 1–4 weeks after exposure.
Mares exposed to EAV very late in gestation might, instead of aborting, give birth to a foal congenitally infected with the virus. No evidence suggests that mares that abort because of EAV infection are subsequently less fertile.
Fetuses aborted as a result of EAV infection can be autolyzed or nonautolyzed. They might exhibit interlobular pulmonary edema, pleural and pericardial effusion, and petechial and ecchymotic hemorrhages on the serosal and mucosal surfaces of the small intestine.
Stallions with equine viral arteritis can experience short-term subfertility during acute infection. Such instances of subfertility have been observed in individuals that develop a high and/or prolonged fever and extensive scrotal edema.
Stallions with acute EAV infection might exhibit decreased libido associated with decreases in total and progressively motile sperm, in curvilinear velocity, in the percentage of live spermatozoa, and in the percentage of morphologically normal spermatozoa. The changes in semen quality are believed to result from increased intratesticular temperature rather than from a direct effect of EAV on spermatogenesis and testicular function. Semen changes can persist for 14–16 weeks before a return to normal. No long-term adverse effects on fertility have been reported in fully recovered stallions.
The frequency and severity of clinical disease associated with EAV infection tend to be greater in very young, old, or debilitated individuals and under adverse climatic conditions. Regardless of the severity of clinical signs, affected horses almost always recover completely, even without supportive care.
Death in older horses occurs very rarely in natural outbreaks of equine viral arteritis. However, affected neonatal and young foals up to a few months of age can die from fulminating pneumonia or pneumoenteritis due to secondary bacterial infections.
Compared with other equine respiratory viruses, EAV induces a stronger, longer-lasting immunity that protects against clinical disease, including abortion. High levels of neutralizing antibodies, which frequently persist for 2–3 years, can be induced by natural exposure to the virus or vaccination.
During LTPI, EAV induces a local mucosal immune response in the stallion's reproductive tract, including the migration of antibody-producing plasma cells into the accessory sex glands.
Multiple antibody types are present in seminal plasma (IgA and several IgG subclasses); however, only some (IgG1 and IgG4/7) have virus-neutralizing activity. Importantly, even these neutralizing antibodies are not sufficient to eliminate EAV or prevent its shedding in semen. In contrast, the systemic (serum) antibody response is more limited, composed mainly of IgM and IgG1.
Overall, these findings indicate that EAV can persist in the reproductive tract despite the presence of a local antibody response.
Lesions of Equine Viral Arteritis
The gross and microscopic lesions observed in fatal cases of equine viral arteritis reflect the extensive vascular damage caused by the virus. These descriptions are based primarily on experimental infection with the horse-adapted highly pathogenic Bucyrus strain of EAV (EAV VBS strain).
The most important gross findings of equine viral arteritis include edema, congestion, and hemorrhages, especially in the subcutis of the limbs and abdomen; excess peritoneal, pleural, and pericardial fluid; and edema and hemorrhage of the intra-abdominal and thoracic lymph nodes and of the small and large intestines, especially the cecum and colon.
Unlike the EAV VBS strain, the low virulent and moderately virulent EAV strains do not produce severe lesions or death in infected horses.
Gross equine viral arteritis lesions are usually absent in aborted fetuses; if present, they are limited to an excess of fluid in body cavities and a variable degree of interlobular pulmonary edema. Pulmonary edema, emphysema, interstitial pneumonia, enteritis, and infarcts in the spleen have been reported in naturally acquired fatal cases of equine viral arteritis in foals.
The characteristic microscopic lesion in EAV infection is vasculitis involving primarily smaller arterioles and venules. Histologically, changes can range from mild cases with vascular and perivascular edema, occasional lymphocytic infiltration, and endothelial cell hypertrophy, to severe cases with fibrinoid necrosis of the tunica media, extensive lymphocytic infiltration, necrosis and loss of endothelium, and thrombus formation.
There are no characteristic histopathological features of EAV infection in fetuses; however, severe necrotizing panvasculitis of small vessels has been observed. Affected muscular arteries show foci of intimal, subintimal, and medial necrosis, with edema and infiltration of lymphocytes and neutrophils. Prominent vascular lesions also occur in the placenta, brain, liver, and spleen of aborted fetuses. Affected neonatal foals have severe interstitial pneumonia.
Fatal cases of EAV infection in young foals are characterized by interstitial pneumonia, emphysema, interlobular edema, congestion, and mononuclear cell infiltration in the lungs, as well as lymphoid depletion and hemorrhage in lymphoreticular tissues. Focal hemorrhages and necrosis of the intestinal mucosa have been described in cases with associated enteritis.
Substantial advances have been made in understanding the genetic basis of EAV carrier-state establishment, the pathology, and the pathogenesis of long-term persistent EAV infection in stallions.
The ampullae, rather than the testes, have been identified as the primary site of viral persistence. However, EAV was recovered from the prostate gland and from the bulbourethral glands in persistently infected stallions; mean viral titers for both of these accessory sex glands were very low (1.0 × 103 to 1.7 × 105 plaque-forming units [PFUs]/g of tissue) compared with the ampullae ([1.0–5.0] × 102 PFUs/g of tissue) (9).
EAV shows a preference for stromal cells and certain immune cells (including T and B lymphocytes and macrophages) rather than glandular epithelial cells during long-term persistence.
Persistent EAV infection is associated with moderate, multifocal lymphoplasmacytic inflammation (ampullitis) characterized by infiltration of B and T lymphocytes, macrophages, and dendritic cells.
Findings also suggest that long-term persistence of EAV might be regulated at the molecular level, involving decreased expression of a specific miRNA (eca-miR-128) and increased expression of the chemokine CXCL16, indicating a role for the CXCL16/CXCR6 pathway in maintaining infection within the stallion reproductive tract (22, 23).
Diagnosis of Equine Viral Arteritis
Virus isolation
RT-qPCR assay
Viral antigen detection in tissues by immunohistochemistry
Viral nucleic acid detection in tissues by in situ hybridization
Serological testing
The clinical signs of equine viral arteritis can mimic those of a range of other equine diseases, both respiratory and nonrespiratory. Thus, differential diagnoses of equine viral arteritis include the following:
Primarily respiratory diseases:
equine herpesvirus 1 and 4 infections
equine rhinitis A and B virus infections
equine adenovirus infection
Primarily nonrespiratory diseases:
allergy-induced urticaria
toxicosis due to hoary alyssum (Berteroa incana; see the table )
Getah virus infection
Thus, confirmation of a provisional clinical diagnosis of equine viral arteritis should be pursued without delay in suspected outbreaks of the disease.
Abortion caused by equine arteritis virus (EAV) must be differentiated from abortion caused by equine herpesvirus 1 or 4.
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Furthermore, EAV-infected fetuses are often somewhat autolyzed at the time of expulsion, and very often they are devoid of any gross or even microscopic lesions. In contrast, herpesvirus-infected fetuses are invariably fresh and usually display characteristic gross and microscopic lesions.
Specimens for laboratory testing include nasopharyngeal, nasal, and ocular secretions; semen; whole blood (EDTA or citrate); serum (acute and convalescent); and tissues from aborted fetuses (placenta, fetal lymphoreticular, and other tissues, especially fetal lung and liver).
Laboratory confirmation of equine viral arteritis can be based on any of the following:
virus isolation
detection of viral nucleic acid by standard RT-PCR assay, real-time RT-qPCR assay, or RT–insulated isothermal PCR (RT-iiPCR) assay, along with in situ hybridization
visualization of viral antigen by immunohistochemical examination
demonstration of a humoral antibody response by testing paired (acute and convalescent) sera collected 3–4 weeks apart
Among the serological assays evaluated for detecting antibodies against EAV, the complement-enhanced virus neutralization test remains the most reliable for diagnosing acute EAV infection and for seroprevalence studies. Several ELISAs have been developed, but only one or two approximate the sensitivity and specificity of the virus neutralization test. None of the available serological tests can differentiate antibody titers resulting from natural infection from those due to vaccination.
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The most appropriate samples for EAV isolation and/or detection of viral nucleic acid by RT-qPCR assay are nasopharyngeal swabs, nasal swabs or washings, ocular secretions, and unclotted whole blood samples (citrated or EDTA). Samples should be collected as early as possible after the onset of clinical signs or upon suspicion of EAV infection, to optimize the chances of isolating or detecting the virus.
After sample collection, swabs should be transferred directly into viral transport medium and shipped refrigerated or frozen in an insulated container via an overnight delivery service to a laboratory with expertise and experience in testing for EAV infection. Unclotted whole blood samples should be transported refrigerated but not frozen.
In suspect cases of EAV-induced abortion, virus detection should be attempted from placental tissues and fluids, as well as from fetal lung, liver, lymphoreticular tissues (especially thymus), and peritoneal or pleural fluid. The chorioallantoic membrane and fetal lung are the tissues of choice for virus recovery.
When EAV is suspected in deaths of young foals or older horses, a wide range of tissue specimens, especially from the lymphatic glands in the thoracic and abdominal cavities and related organs, should be collected and submitted for laboratory examination, including viral nucleic acid detection by RT-qPCR assay or virus isolation, together with histological evaluation, immunohistochemical testing, and in situ hybridization.
Investigation of a stallion's putative EAV carrier status begins with determining whether the individual is seropositive or seronegative for antibodies against the virus. In the absence of a certified vaccination history, stallions with a virus-neutralizing antibody titer ≥ 1:4 are considered seropositive. They should be regarded as potential carriers of the virus until proven otherwise by the absence of detectable EAV in their semen (24).
Confirmation of the EAV carrier state is based on demonstrating the virus in a semen sample that contains the sperm-rich fraction of the ejaculate, either by isolating the virus in cell culture or by detecting it using an RT-qPCR assay. The carrier state can also be determined by test-breeding a stallion to two seronegative mares and then, 28 days after breeding, checking the mares for seroconversion to EAV.
Treatment of Equine Viral Arteritis
Supportive care
No specific antiviral treatment is currently available for equine viral arteritis. Aside from young foals, virtually all horses naturally infected with equine arteritis virus (EAV) make a complete clinical recovery, even without supportive care.
For moderately to severely affected horses, especially stallions, supportive treatment is indicated and should include the following:
antipyretics
anti-inflammatory drugs
diuretics
adequate rest
good nursing care
gradual return to breeding activity
Prompt supportive treatment of stallions with a high or prolonged fever and substantial scrotal and preputial edema can decrease the likelihood of short-term subfertility.
There is no effective treatment for equine viral arteritis–related cases of pneumonia or pneumoenteritis in foals. Because congenitally infected foals are very productive sources of EAV by the respiratory route, and because they have almost no chance of survival, early euthanasia is warranted to minimize the risk of further transmission of the virus to any susceptible contacts, especially pregnant mares and young foals.
The EAV carrier state can be permanently eliminated from a stallion by surgical castration.
Prevention and Control of Equine Viral Arteritis
Vaccination
Sound management of breeding populations
The primary focus of current equine viral arteritis control programs is to restrict the spread of the disease in breeding populations and to decrease the risk of outbreaks of virus-related abortion, death in young foals, and establishment of the carrier state in stallions and postpubertal colts.
Although equine arteritis virus (EAV) has occasionally caused extensive outbreaks of equine viral arteritis at racetracks, shows, sales, and veterinary hospitals, these outbreaks have been so sporadic that no specific control programs have been developed to prevent them.
Equine viral arteritis is a manageable and preventable disease that can be controlled through adherence to sound management practices and a targeted vaccination program. For prevention and control, live attenuated and inactivated vaccines are available in North America and Europe, respectively.
Vaccination against EAV induces antibody responses indistinguishable from those elicited by natural infection. Therefore, accurate vaccination records are essential for differentiating vaccinated from naturally infected horses and for preventing complications during international movement (ie, import certification and export certification).
The attenuated modified live vaccine available in North America protects against the development of equine viral arteritis (including abortion) and establishment of the carrier state in stallions. Annual revaccination of vaccinated horses is recommended to boost protective immunity.
Although the equine viral arteritis vaccine is safe and immunogenic for stallions and nonpregnant mares, the manufacturers do not recommend its use in pregnant mares, especially in the final 2 months of gestation, or in foals < 6 weeks old, unless there is a high risk of exposure to natural infection. Experimental and field studies have shown that there are no adverse consequences to vaccinating pregnant mares up to 3 months before foaling and during the immediate postpartum period. However, there is a low risk of abortion in mares vaccinated during the last 2–3 months of pregnancy (6, 25, 26, 27, 28).
All EAV-seronegative mares being bred to a persistently infected stallion should be vaccinated 21 days before natural breeding or artificial insemination. Previously vaccinated mares should be given a booster immunization.
Minimizing or eliminating direct or indirect contact of unprotected horses with EAV-infected animals or with virus-infective semen is critical to the success of any prevention program.
Equine viral arteritis control programs are predicated on the observance of sound management practices similar to those recommended for other respiratory infections, including the following:
isolation of new arrivals on a premises for 3–4 weeks before they are allowed to commingle with the resident equine population
maintenance of pregnant mares in small, isolated groups
identification of carrier stallions
annual immunization of noncarrier breeding stallion populations
vaccination of colts at the age of 6–12 months to minimize their risk of becoming carriers later in life
Carrier stallions should be managed separately and bred only to naturally seropositive mares or to mares vaccinated against equine viral arteritis. Personnel should take all appropriate precautions during the breeding of or collection of semen from such stallions, to ensure that EAV is not accidentally transmitted to other horses on the premises by indirect means via virus-contaminated fomites.
Because fresh-cooled or frozen semen can be an important source of EAV, it should be tested by a laboratory with appropriate diagnostic expertise to confirm its negative EAV status, especially if imported. When breeding a mare artificially with virus-infective semen, the same precautions apply as if breeding by live cover to a carrier stallion.
Specific measures to prevent or control equine viral arteritis on breeding farms include the following:
identifying carrier stallions
separately managing carrier stallions
vaccinating noncarrier stallions annually
restricting the breeding of carrier stallions to mares vaccinated against equine viral arteritis or to mares naturally EAV-seropositive
isolating mares bred for the first time with infective semen from EAV-seronegative horses for 3 weeks
screening semen intended for artificial insemination use for EAV, particularly if the semen is imported
observing sound management practices, especially of pregnant mares
vaccinating colt (male) foals between 6 and 12 months of age to prevent possible development of a carrier state later in life
under circumstances of intensive management and limited facilities, considering vaccination of all at-risk animals
In the event of a suspected outbreak of equine viral arteritis, the following actions should be taken:
Relevant animal health authorities and federal, state, or other officials should be promptly notified.
Affected and in-contact horses should be isolated.
Restrictions should immediately be imposed on the movement of horses onto and off of the affected premises.
Appropriate specimens should be collected as soon as possible after the onset of clinical signs and submitted for laboratory confirmation.
Breeding activity should be suspended on breeding farms to minimize risk of further spread of the infection.
Stalls and equipment that might have come in contact with infected animals should be thoroughly sanitized.
In consultation with a veterinarian, vaccination of the at-risk equine population on a premises should be seriously considered as a means of restricting further transmission of EAV and of expediting control and resolution of an outbreak. Movement restrictions should not be lifted until at least 3 weeks after the last clinical or suspected case of equine viral arteritis or laboratory-confirmed case of EAV infection.
Because CXCL16 genotypes have been shown to predict the likelihood that stallions will develop LTPI after exposure to EAV, a CXCL16 genotyping assay has been developed. Prepubertal colts can be genotyped for CXCL16 (CXCL16S/S, CXCL16S/r, or CXCL16r/r) using this duplex allelic discrimination real-time PCR assay (29). This tool is recommended for targeted vaccination and selective breeding, whenever possible.
Colts that carry the susceptible genotype (CXCL16S) should be vaccinated after the age of 6 months to prevent the establishment of EAV LTPI (14). In addition, the CXCL16 genotyping assay opens avenues for selective breeding, which is critical for equine breeding enterprises worldwide and for disease control. If no genetic testing will be performed, all colts should be vaccinated between 6 and 12 months of age.
In summary, the equine industry can control and eliminate EAV infection or disease, and ultimately achieve eradication, by combining genetic screening of colts/stallions, serological screening of stallions and mares before breeding and movement, and improved biosecurity and management practices.
There is no evidence that EAV is a zoonotic agent.
Key Points
Equine viral arteritis is an economically important, contagious respiratory, systemic, and reproductive disease of equids.
Carrier stallions are the primary reservoir of equine arteritis virus. There is no analogous carrier state in mares, geldings, sexually immature colts, or fillies.
Diagnosis is based on detection of the virus or of viral nucleic acids in body fluids or tissues, the visualization of viral antigens in infected tissues, and serological testing.
Supportive care (eg, antipyretic, anti-inflammatory, and diuretic drugs) is indicated, especially in severely affected stallions.
Available vaccines can protect against clinical disease, including abortion and establishment of the carrier state in stallions.
For More Information
Balasuriya UBR. Equine viral arteritis. Vet Clin North Am Equine Pract. 2014;30(3):543-560.
Balasuriya UBR, Carossino M, Timoney PJ. Equine viral arteritis: a respiratory and reproductive disease of significant economic importance to the equine industry. Equine Vet Educ. 2018;30(9):497-512.
Equine Viral Arteritis (EVA) Vaccination Guidelines American Association of Equine Practitioners.
Animal and Plant Health Inspection Service, USDA. Equine Viral Arteritis, Uniform Methods and Rules, Effective April 19, 2004. APHIS 91-55-075. USDA; 2004.
Also see pet owner content regarding equine viral arteritis.
References
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