Equine coital exanthema

Equine coital exanthema

G P ALLEN AND N W UMPHENOUR

Introduction

Equine coital exanthema (ECE) is an infectious, venereally transmitted mucocutaneous disease of mares and stallions caused by a herpesvirus. The disease is characterized by the development of superficial pock-like eruptions and erosions or ulcers on the external genital organs.8, 15, 20, 51 The virus is highly contagious but is non-invasive and relatively benign. Reports of the disease have long been recorded in the veterinary literature under a variety of names.7, 11, 16, 19, 32, 34, 39, 41, 43, 44

The infection does not usually result in systemic illness, and neither infertility nor abortion occur as sequelae.12, 20, 24, 36, 38, 51 Its primary negative impact on equine breeding enterprises is the forced, temporary disruption of mating activities. In intensively managed stud operations employing heavily scheduled breeding dates for stallions, such disruptions may translate into significant end-of-season decreases in the mare-book size of affected stallions. Similarly, delayed foaling dates or reduced pregnancy rates may occur in mares that miss breeding opportunities because of the disease.

Aetiology

The causative agent of ECE, equid herpesvirus 3 (EHV-3), is a member of the Herpesviridae family and in size, virion architecture, and genome structure is a typical herpesvirus.4, 12, 29, 35, 46 Its biological features place EHV-3 in the Alphaherpesvirinae subfamily. EHV-3 is antigenically, genetically, and pathogenetically distinct from EHV-1, EHV-2, EHV-4, and EHV-5.2, 6, 12, 26, 45 It shares no protective or neutralization epitopes and only minor genetic homology with these four other herpesviruses of the domestic horse (Equus caballus).2, 45, 53 The restriction endonuclease cleavage patterns of the DNA of EHV-3 are unique when compared with those reported for the DNAs from EHV-1, EHV-2, EHV-4, and EHV-5.9, 29, 31, 46 Although causing disease of clinical similarity, the virus of ECE is unrelated, by serum neutral neutralization tests, to bovine herpesvirus 1 (BHV-1) that causes infectious pustular vulvovaginitis in cattle.12

The 96 Md double-stranded DNA of EHV-3 is high in G + C content (66 per cent) and has a buoyant density of 1,725 g/cm3 . 35 Purified virions of EHV-3 possess, in addition to the DNA-containing nucleocapsid, a proteinaceous tegument and glycoprotein-laden envelope.3 The virus is environmentally labile, and infectivity is quickly destroyed by lipid solvents, detergents, heat, and drying as well as by the common disinfectants available for veterinary use.12 Storage at temperatures below −60 °C is required for maintaining its long-term viability.

In cell culture, EHV-3 replicates only in cell lines derived from equids.12 The intracellular replication cycle and subsequent cytopathic effect (CPE) are extremely rapid. EHV-3 progeny DNA and virions are present by two and six hours post-infection (PI), respectively, and CPE is detectable as early as six hours PI after a high multiplicity of infection.1 The CPE of EHV-3 is typically herpetic in nature with rapidly enlarging foci of rounded, refractile cells. When infected cell cultures are stained with haematoxylin and eosin, eosinophilic, intranuclear inclusion bodies are visible.22, 40 The optimal temperature for in vitro replication of EHV-3 is 34 °C; at 39 °C the production of infectious virus is reduced to 10−6 of its maximum yield.9, 27, 30 No laboratory animal model of EHV-3 infection has been identified.

Although restriction endonuclease fingerprint analysis of viral DNAs has been used to demonstrate the genetic individuality of EHV-3 isolates,9 there is no reported evidence of antigenic diversity among clinical isolates recovered from different disease outbreaks.12 A related but antigenically distinguishable herpesvirus (equid herpesvirus 6) has been isolated from superficial cutaneous lesions of a donkey.12, 28 Small-plaque variants of EHV-3 arise during passage in cell culture and are characterized by alterations in their DNA restriction endonuclease patterns caused by the presence of a 5,7 kbp nucleic acid insert in the unique (U) sequence of the small (S) component of their DNA genomes.9, 12, 31

Epidemiology

The only known biological reservoir for the virus of ECE is the latently infected horse. Careful observations and frequent serological monitoring of a closed, pony-breeding herd has demonstrated the existence of latently infected carrier animals from which EHV-3 was periodically reactivated and transmitted to cohorts.14 By serological tests, it was shown that some pony stallions and mares acquired primary infection or reinfection by EHV-3 without signs of clinical disease. It is now believed that such episodes of virus reactivation from latency with subsequent recrudescence of clinical (or subclinical) infection serve as the source for spread of EHV-3 to other animals.7, 14, 16, 24 Epidemiological data suggest that the original viral source of an outbreak of ECE may be either a visiting mare brought onto the stud farm for breeding or virus reactivated from a member of the resident stallion or mare population.7, 14, 16, 24 Persistently infected horses that shed EHV-3 continuously have not been identified. The anatomical site that harbours the latent herpesvirus is unknown.

Surveys to estimate the seroprevalence of EHV-3 infection in several horse populations have demonstrated...

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