Equine viral arteritis

Equine viral arteritis



Equine viral arteritis (EVA) is an acute contagious disease of equids principally characterized by fever, dependent oedema, respiratory signs and, in the pregnant mare, the risk of abortion.87 It is caused by equine arteritis virus (EAV),22 which can frequently give rise to persistent infection of the reproductive tract in the stallion.92, 94

The older veterinary literature dating back to the late nineteenth century carries several reports of a disease clinically indistinguishable from EVA, which was referred to by various terms, such as infectious cellulitis-pinkeye, fièvre typhoide du cheval and Pferdestaupe.8, 12, 73, 75 It was not until 1953, however, following an outbreak of respiratory illness and abortion on a Standardbred breeding farm near Bucyrus, Ohio, USA, that EVA was defined as a separate equine viral disease and the aetiological agent was isolated for the first time.22

Little international significance was attached to EVA for many years until 1984, when it occurred on a widespread scale in Kentucky, involving an estimated 41 Thoroughbred breeding farms.80 Major concern over the potential risk of the virus spreading to susceptible Thoroughbred populations in the USA and abroad resulted in the imposition of stringent measures governing the international movement of horses between most countries.88 Many of these restrictions continue to impact on international trade in horses and equine semen.

There are very few equid populations throughout the world that have been confirmed to be free of infection with EAV.87 The virus has been introduced into South Africa on a number of occasions, either through the importation of a carrier stallion or infective frozen semen.24, 34 While such ingressions have not resulted in any reported occurrences of clinical disease, various studies have confirmed limited spread of infection among Lippizaner, Thoroughbred and certain Warmblood breeds of horses.24, 34 Evidence of EAV infection has also been found in the country’s donkey population, suggesting that the virus may have been present in South Africa for a considerable time.67, 68


Equine arteritis virus is an enveloped, positive-stranded RNA virus with quasispecies structure, which is the prototype virus of the genus Arterivirus, family Arteriviridae, order Nidovirales.10, 78 This classification is based on genomic structure, pattern of gene expression and replication strategies of the virus. Other taxonomically related arteriviruses include lactic dehydrogenase-elevating virus, porcine reproductive and respiratory syndrome virus and simian haemorrhagic fever virus.10, 72

Equine arteritis virus is a relatively small virus, with a genome of 12,7 kilobases and a 3’ polyadenylated tail.19, 79 It comprises nine open reading frames (ORFs 1a, 1b, 2a, 2b, 3, 4, 5, 6 and 7). Virus particles have a diameter of 60 ± 13 nm, and consist of an isometric core of 35 nm containing the viral RNA surrounded by an outer lipid envelope that is covered with spike-like subunits.37 Each virion is made up of five known structural proteins (E, GS, GL,Mand N), a viral replicase and at least two non-structural membrane glycoproteins (GP3 and GP4).19, 78, 79 The GL envelope glycoprotein encoded by ORF 5 expresses the major neutralization determinants of the virus.2, 4, 20, 29 An infectious cDNA clone of EAV has been developed97 and shown to replicate in horses.6

Equine arteritis virus may be grown in different cell cultures (see Diagnosis).

Only one serotype of EAV has been identified so far; the prototype Bucyrus strain.25, 87 Variation in antigenic and pathogenic properties have been observed among geographically and temporally different isolates of the virus.4, 60, 61, 87 A number of studies have shown that such isolates also differ significantly in their structural protein genes.1, 35, 66 Equine arteritis virus possesses a complement-fixing antigen but no haemagglutinin.87 The virus is readily inactivated by lipid solvents and disinfectants. It can survive for years at subfreezing temperatures.


A range of factors, which are virus-, host- and environment-related, are known to be involved in the epidemiology of EVA.85, 87 The most significant of these are: variation in pathogenicity and other phenotypic characteristics among naturally occurring strains of EAV, routes of virus transmission during acute and chronic phases of the infection, occurrence of the carrier state in the stallion, nature and duration of acquired immunity to infection, and changing trends in the horse industry.

The results of various serological surveys conducted over the years have confirmed that EAV is distributed in many equine populations throughout the world.86 It has been confirmed in countries in North and South America,51, 54, 65 Europe,16, 40, 59 Africa,59, 71 Asia44, 46 (with the notable exception of Japan44), Australia and New Zealand.38 In contrast to the currently known distribution of EAV, outbreaks of EVA are reported relatively infrequently. Indications in recent years would suggest that prevalence of the disease is on the increase,81 and is related in most cases to the movement of infected horses or use of virus-infective semen.34, 93

The prevalence of EAV infection differs considerably, both between countries and between particular breeds in the same country.87, 89

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