Equine Viral Arteritis: Historical Versus Contemporary Significance
ACVIM 2008
P. Timoney
Lexington, KY, USA

Equine viral arteritis (EVA) is a contagious disease of equids caused by equine arteritis virus (EAV), a single, positive stranded RNA virus and prototype member of the genus Arterivirus, family Arteriviridae, order Nidovirales.3,4 Principally characterized by fever, depression, leukopenia, dependant edema and respiratory signs, the disease is typically not life-threatening to otherwise healthy adult horses.20 Equine viral arteritis owes its name to the widespread vasculitis involving the smaller blood vessels, especially the arterioles that is characteristic of the disease.7 It should be emphasized that like many other infectious diseases, the majority of primary infections with EAV are asymptomatic. Equine viral arteritis is of primary industry concern because of the potential of the etiologic agent to cause abortion in the pregnant mare, illness and death in young foals, and persistent infection in the stallion. From a historical perspective, EVA or a clinically indistinguishable disease known by a variety of descriptive terms, e.g., infectious cellulitis-pinkeye, rotlaufseuche, typhoid fever, has probably afflicted horse populations in Europe and perhaps elsewhere, for a great many years. There are some very insightful reports on the modes of transmission and epidemiology of what was very probably EVA in the veterinary literature of the latter part of the nineteenth century.14,15

The global distribution of EAV has become more extensive over the past 30 to 40 years as a direct result of the continued growth in numbers of horses being transported both within and between countries worldwide.18 Of special significance in this respect has been the shipment of stallions that are asymptomatic carriers of EAV or in more recent years, virus infective semen. There have been numerous recorded instances where EAV was introduced into naïve, resident equine populations by either means and been responsible for economically damaging outbreaks of EVA.1,10,13,19 It is ironic that for over 30 years following its initial identification as a separate viral disease of the horse in 1953, scant attention was paid to EVA in terms of its veterinary medical and economic significance, notwithstanding the known abortifacient properties of the causal agent. That changed dramatically in 1984, however, following the widespread occurrence of the disease on an estimated 41 Thoroughbred breeding farms in Kentucky.17 A sea-change in attitude ensued in how equine industries worldwide viewed EVA and the threat of large-scale outbreaks resulting from the international movement of infected horses. With the exception of the United States, other horse breeding countries imposed major import restrictions because of the disease, many of which remain in force today.20

While many regard EAV as one of the three major equine respiratory-borne viral pathogens, the others being equine influenza and equine herpesviruses 1 and 4, some question this arbitrary grouping, based on the fact that clinical evidence of respiratory system involvement is absent from some outbreaks of EVA.16 Another feature that is unique to EVA and not shared by either of the other aforementioned viral infections is that EAV can be spread very efficiently by the venereal route by the acutely or chronically infected stallion.17,20 The ease with which the virus can be disseminated by this means was highlighted by the 2006 multi-state occurrence of the disease in the US19 and more recently, by widespread outbreaks of EVA in five departments in France.13 In each case, the source of infection was shipped semen from a carrier stallion. Continued growth in the practice of artificial insemination and embryo transfer will undoubtedly enhance the risk of spread of EAV and influence the frequency of outbreaks of EVA in naïve or unprotected breeding populations. There is every indication that aside from greater awareness of the disease and improved diagnostic capability, the actual incidence of EVA is on the increase, due, in major part, to changing economic trends in the equine industry worldwide.

Occurrence of the carrier state in the sexually mature, intact male (colt or stallion) and not in the sexually immature colt, mare or gelding is unique to EAV infection. There is no other known example of a testosterone dependant carrier state among viral pathogens of equids or other livestock species.8 The carrier stallion is widely considered the primary natural reservoir of the virus.22 Spontaneous clearance of the carrier state has been documented in an increasing number of stallions. Efforts continue to try and emulate nature by developing a safe and reliable therapeutic means of eliminating EAV from the reproductive tract of the persistently infected stallion. In this regard, primary emphasis has been placed on the use of GnRH antagonists6 or GnRH immunization2 as a means temporarily down-regulating testosterone production. While successes have been claimed for both treatment modalities, neither has, as yet, proven uniformly reliable. Efforts are currently being directed at removal of EAV from infective semen using a density gradient centrifugation based procedure.12 So far, this has not been fully successful. Increasingly, it is being accepted that the key to achieving greater prevention and control of EVA is through immunization of naïve stallions and immature colts against the disease and over time, reducing frequency of the carrier state and the natural reservoir of the virus.20

An often over-looked feature of EVA, and one that distinguishes it from other respiratory viral infections of the horse, is the uniqueness of the immune response of the horse to EAV. Natural infection with the virus stimulates a strongly protective, long-lasting immunity against the disease that can last for several years or longer5,9 and which is of much greater magnitude and duration than that engendered by equine influenza virus or equine herpesviruses 1 and 4. Vaccination can achieve a level of immunity that is protective against development of clinical disease and establishment of the carrier state in the stallion.21 However, first-time vaccinates may undergo a limited reinfection cycle upon natural exposure to the virus.11 Efforts are underway to develop either a marker (DIVA) vaccine and companion diagnostic test or a disabled infectious single cycle (DISC) vaccine against EVA which hopefully, would increase the marketability of vaccinated horses abroad and also, eliminate the risk of abortion from vaccination in mares immunized even in the latter stages of pregnancy. What is frequently not realized by many horse owners, breeders and even some veterinarians is that EVA is a disease that can be readily controlled through observance of sound management practices and a targeted vaccination program.

Reference

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2.  Burger D, et al. Anim Reprod Sci 2006; 94:107-111.

3.  Cavanagh D. Arch Virol 1997; 142(3):629-633.

4.  Doll ER, et al. Cornell Vet 1957; 47:3-40.

5.  Doll ER, et al. Cornell Vet 1968; 58(4):497-524.

6.  Fortier G, et al. Theriogenology 2002; 58:425-427.

7.  Jones TC, et al. Cornell Vet 1957; 47:52-68.

8.  Little TV, et al. Proc 6th Intl Conf Equine Infect Dis 1992; pp 225-229.

9.  McCollum WH. Proc 2nd Intl Conf Equine Infect Dis 1970; pp 143-151.

10. McCollum WH, et al. Proc 8th Intl Conf Equine Infect Dis 1999; pp. 559-560.

11. McCollum WH, et al. Proc 5th Intl Conf Equine Infect Dis 1988; pp. 13-18.

12. Morrell JM, et al. Equine Vet J 2006; 38(3):224-229.

13. Pitel PH, et al. Prat Vet Equine 2007; 39(156):19-27.

14. Pottie A. J Comp Pathol Therap 1888; 1:37-38.

15. Reeks HC. J Comp Path Therap 1902; 18(2):97-102.

16. Scollay MC, et al. Proc 39th Ann Conv AAEP 1993; pp. 255-256.

17. Timoney PJ Proc Grayson Foundation Intl Conf TB Breeders Org EVA 1984; pp. 24-33.

18. Timoney PJ. Vet Clinics North America: Equine Practice 2000; 16(3):537-551.

19. Timoney PJ, et al. Proc 110th Ann Mtg USAHA 2007; pp. 354-362.

20. Timoney PJ, et al. Vet Clinics North America: Equine Practice 1993; 9(2):295-309.

21. Timoney PJ, et al. In: Coetzer JAW, Tustin RC, eds. Infectious Diseases of Livestock. Volume 2. 2nd Ed. South Africa: Oxford University Press Southern Africa, 2004; pp. 924-932.

22. Timoney PJ, et al. J Reprod Fertil 1987; 35:95-102.

Speaker Information
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Peter Timoney
Lexington, KY


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