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EQUINE VETERINARY EDUCATION / AE / SEPTEMBER 2018


a)


c)


e)


f) d) b)


g)


Fig 2: Clinical signs of equine viral arteritis (EVA). a) Urticaria; b) lacrimation, photophobia, and supraorbital oedema; c) congestion and petechiae in oral mucous membranes; d) limb oedema; e) conjunctivitis; f) scrotal and preputial oedema; g) abortion.


observed clinical signs include: icterus; photophobia; corneal opacity; coughing; dyspnoea; colic; diarrhoea; ataxia; petechiation of the nasal mucosa, conjunctiva, and oral mucous membranes; submaxillary and submandibular lymphadenopathy; and adventitious oedema in the intermandibular space, beneath the sternum or in the shoulder region (Bryans et al. 1957b; Doll et al. 1957a; Jones 1969; Gerber et al. 1978a; Cole et al. 1986; Clayton 1987; Collins et al. 1987). The most consistent clinical features include pyrexia and leukopenia (Doll et al. 1957a,b; MacLachlan et al. 1996; Balasuriya et al. 2007).


Reproductive consequences Equine arteritis virus is a well-recognised abortigenic agent that can cause reproductive loss in pregnant mares. Abortions may occur either late in the acute phase or early in the convalescent phase of infection, and frequently take place anytime between 2 and >10 months of gestation with an attack rate ranging anywhere from <10 to 71% and no premonitory signs (Bryans et al. 1957a,b; Coignoul and Cheville 1984; McCollum and Timoney 1984; Cole et al. 1986; Clayton 1987; Timoney and McCollum 1993). Even though the abortigenic potential of different strains of EAV has not been adequately compared, it may be that EAV strains differ in their abortigenic potential as they do in the severity of the clinical response to infection. Additionally, venereal or respiratory infection of susceptible mares does not appear to result in short- or long-term infertility. Equine arteritis virus infected stallions can undergo a


period of subfertility during the acute phase of the disease ranging from 6 to 11 weeks after infection and associated


© 2016 EVJ Ltd


with decreased libido, sperm motility, concentration and percentage of morphologically normal sperm cells (Neu et al. 1992; Campos et al. 2014). Most importantly, EAV causes persistent infection in a high proportion of infected stallions and sexually mature colts (10–70%) (Timoney et al. 1987a; Timoney and McCollum 2000). Carrier stallions continuously shed virus in their semen for a variable and frequently extended period of time that can range from several weeks post-infection (convalescent or short-term carrier) to months, years or life-long (long-term carrier), with apparently no alterations in the semen quality despite viral shedding (Timoney and McCollum 2000). Viral shedding in semen begins 5 days post-infection (Neu et al. 1992; Campos et al. 2014) and is associated with the sperm-rich fraction of the ejaculate (Timoney et al. 1987a). Viral titres in seminal plasma are frequently high, ranging from 101 to >107 PFU/mL (Little et al. 1991; Campos et al. 2014). It has been demonstrated that the carrier state is androgen-dependent, and that is why persistent infection has not been demonstrated in mares, geldings or prepubertal colts (Little et al. 1991; Timoney and McCollum 1993; McCollum et al. 1994).


Pathogenesis


The pathogenesis of EVA has been studied in both natural outbreaks and experimentally infected horses with different viral strains (Jones 1969; McCollum et al. 1971, 1998; McCollum 1981, 1986; Cole et al. 1986; MacLachlan et al. 1996; McCollum and Timoney 1998; Balasuriya et al. 2002a, 2007). It is to be stressed that, with the notable exception of fetal and neonatal infections, EAV infection of horses is


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