Equine Viral Arteritis is a disease that mainly affects horses whose causative agent is equine arteritis virus. This disease was first detected in 1953, however, it had affected equine animals globally for many years, and usually common to various breeds of horses in the United States. Its synonymous names are EVA, infectious cellulitis, pink eye and equine typhoid.
Etiology
Equine Viral Arteritis is a contagious disease of the equids that whose primary causative agent is equine arteritis virus (EAV), an only member of the genus Arterivrus within a nonarthropod-borne group of toga viruses ( Timoney & McCollum, 1993). EVA is a common disease globally, even though its prevalence of subclinical EAV infection and EVA differ significantly between states and horse breeds. The majority of EAV infections are noticeable, however, often occurrence of EVA are characterized by a mishmash of influenza-like sickness in adult horses, abortion among pregnant mares, and interstitial pneumonia among small foals ( Timoney, Cordes, McCollum, & United States. 2006, Del Piero, 2000 ). EAV develops a carrier state in adult male horses such as colts and stallions and not in mare or geldings or sexually young colts. The steadily infected carrier stallion plays a primary role in the continuation and upholding of EAV in the equine group ( Timoney & McCollum, 1993). The importation of EAV carrier stallions and infected semen has a played a significant role in the initiation of EAV into different nations across the world. The evident worldwide dissemination of EAV and the increasing incidence of EVA probable shows the progressive raise in state and global transfer of horses for both competition and breeding, and also an acknowledgment of the significance of EAV infection.
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Before 1984 epizootic of EVA in Kentucky, the primary mode of EAV transmission was considered to happen through the respiratory system including infective aerosolized nasal discharge. This was well portrayed in both natural and trial infections. In connection with the 1984 epizootic, it was ascertained that the transmission of EAV through venereal had played a huge role in the spread and dissemination of the virus ( Timoney & McCollum, 1993). The consequence of the indirect contact with diverse virus contaminated materials such as shank, twitches, people, clothes, and cars used for horse transportation played a little or no role in the spread of the EAV. Another important player in the transmission of this virus is the teaser stallion and nurse mare. The degree to which lateral spread of this virus can happen in infected premises varies significantly taking into consideration the existing epidemiological situations ( Del Piero, 2000). It has also been noticed that there are high spread and transmission of the EAV among horse in close contact in the racetrack, a barn or pasture field.
Clinical Signs
Taking into consideration the sprain of virus concerned and range of the virus problem, equine arteritis virus (EAV) infection may lead to the establishment of a clinical or noticeable infection ( Timoney, Cordes, McCollum, & United States. 2006). Even though the symptoms seen in natural cases of EVA highly differ in a variety and clinical strictness, general cases of the disease is characterized by high fever of up to 41degree centigrade that emerges after 3 to 14 days incubation period and continues for five to nine days; limb edema, particularly the hind limbs; nasal and optical discharges; rhinitis and conjunctivitis; periorbital/supraorbital edema; unpredictable anorexia and despair; skin rash usually on the neck; edema of scrotum and prepuce of the animal; abortion among pregnant mares; and less often respiratory pain, coughing; diarrhea, and ataxia ( Timoney & McCollum, 1993, American Association of Equine Practitioners, 2018). While all these are some of the major symptoms of this illness, the major question is whether it is naturally acquired or not since naturally-infected horses always make ordinary clinical healing.
Diagnosis
A successful diagnosis of the EVA cannot be achieved based only on the existence of the major clinical symptoms of the illness with no corroborative virus separation and/or seriological or histopathological data. The best specimens for virus separation from a live animal including but not limited to nasopharyngeal and conjunctival wash down; citrated blood tests, and semen for stallions. To maximize the likelihood of isolation of the virus, the appropriate specimens should be acquired immediately after the start of the clinical sickness. In a situation where the necropsy specimens are only available, detection of EAV can be tried from different tissues, particularly the nodes related to the alimentary tract and associated organs ( Timoney & McCollum, 1993). In case of abortion by a mare, placenta and fetal fluids and various placental, lymphoreticular and others tissues can be subjected to the tests to isolate the virus.
Blood/Serum Samples- venous blood should be taken from the equine animal to be tested for the presence of EAV by a separator tube and allowed to clot while 3 ml of serum put in a different tube and well labeled and date collected. This should be well packaged to prevent breakage of the tube while on transit.
Lab information
IDEXX Laboratories
7-10 working days
3 mL serum
List Price: $89.39
Methodology: SN
Interpretation
A serum dilution of <2 is equal to a Neg 1:4 (final dilution). The USDA recognizes this equivalency for regulatory purposes. In order to comply with international standards, the EAV (EVA) SN test starting dilution is 1:2 (final dilution of 1;4). The virus neutralization antibody titer is the reciprocal of the highest dilution of serum that neutralized the infectivity of the virus (endpoint dilution of 1:20 = antibody titer of 20). Titers are in units of antibody and as such all values reported without modifiers contain that specified amount of antibody in the sample. Values with a < (less than symbol) indicate no detectable antibody at the minimum readable dilution (<8 = no detectable antibody at a 1:8 dilution). An antibody titer can result from vaccination, infection, or passive maternal transfer.
Treatment
There is no explicit antiviral treatment available today for the EVA. Except for small foals, virtually all EAV acquired naturally by the horses make an absolute clinical recovery. Suggestive treatments such as antipyretic, anti-inflammatory and diuretic medicine are specified only in a severe situation, particularly in stallions ( Timoney & McCollum, 1993). Since congenitally affected foals are a prolific source of EAV, their possibility of survival is nil, and untimely euthanasia should be taken into consideration to reduce the risk of more spread to any close contacts, such as pregnant mares and small foals.
Control/Prevention
EVA is a controllable and avoidable disease that can be managed through observance of sound management practices and recommended vaccination programs. Currently, modified-live virus product is the only available vaccine in North America ( Timoney & McCollum, 1993, Timoney, Cordes, McCollum, & United States. 2006 ). The vaccine defends against the growth of EVA, abortion, and development of the carrier condition in stallions. Even though the vaccine is secure and immunogenic for stallions and mares, it is not recommended for use in pregnant mares or foal less than 6 weeks of age unless under unavoidable circumstances such as the high likelihood of infection. It is confirmed that there is no risk of vaccinating pregnant mares up to three months before foaling or during the postpartum period ( Timoney, Cordes, McCollum, & United States. 2006). Reducing or eradicating direct or indirect contact of unsecured horses with ill animals or virus-affected semen is key to the success of the prevention program.
The best control programs are associated with the observance of sound management practices like those suggested for other respiratory infections. These include separation of new arrivals on a building for about 3 to 4weeks before allowing them to mix with the resident equine group; safeguarding of pregnant mares in small secluded sets; ( Del Piero, 2000) recognition of carrier stallions; yearly immunization of non-carrier breeding stallion populations; and last but not least vaccination of six to 12 month aged colts to reduce risk of developing into carriers later in life. Carrier stallions should be controlled differently and bred to only naturally seropositive mares or mare immunized against EVA ( Timoney & McCollum, 1993). Since fresh-cooled or frozen semen can be a vital source of EAV, it should be evaluated in the laboratory with a suitable diagnostic profession to confirm its negative EAV status, particularly if its imported. Breeding a mare artificially using virus-infected semen is like breeding it with carrier stallion.
In case of an occurrence of EVA, appropriate animal health agencies should immediately be informed, with the infected and in-contact animals secluded, limitation promptly enforced on the movement of animals into and out of the infected premise ( American Association of Equine Practitioners, 2017). Necessary specimens should be gathered immediately after clinical symptoms are observed and delivered to the laboratory for test and diagnosis of the EVA. Breeding activity should be stopped to further dates to reduce the spread of this menace ( Timoney & McCollum, 1993). The affected premises should be properly sanitized. Also, vaccination of exposed equine group in the premise should be taken into consideration to avert further transmission of the disease. The free movement of the animals should not be allowed until at least three weeks have elapsed.
References
American Association of Equine Practitioners (2018). Equine Viral Arteritis (EVA). Retrieved from https://aaep.org/guidelines/infectious-disease-control/biosecurity-guidelines-control-venereally-transmitted-diseases/equine-viral-arteritis-eva
American Association of Equine Practitioners (2017).Infectious Disease Guidelines: Equine Viral Arteritis (EVA). .Retrieved from https://aaep.org/sites/default/files/Guidelines/EQUINE%20VIRAL%20ARTERITIS_Final.pdf
Del Piero, F. (2000). Equine viral arteritis. Veterinary Pathology , 37 (4), 287-296. Retrieved from http://journals.sagepub.com/doi/abs/10.1354/vp.37-4-287
Timoney, P. J., Cordes, T. R., McCollum, W. H., & United States. (2006). EVA, equine viral arteritis: A manageable problem . Washington, D.C: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service.
Timoney, P. J., & McCollum, W. H. (1993). Equine Viral Arteritis. Veterinary Clinics of North America: Equine Practice , 9 (2), 295-309. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1680490/pdf/canvetj00587-0017.pdf
