Equine coital exanthema

Synonyms: Genital horse pox, eruptive venereal disease, equine venereal vulvitis or balanitis, and coital vesicular exanthema

GENERAL INTRODUCTION: HERPESVIRIDAE

Introduction

Equine coital exanthema (ECE) is an infectious and highly contagious, venereally-transmitted mucocutaneous disease, characterized by the formation of papules, vesicles, pustules and ulcers on the skin of external genital organs of mares and stallions, caused by Equid alphaherpesvirus 3 (EHV-3). ^{4, 11, 55}

First reported in 1920 during an outbreak of the disease in one Thoroughbred stallion and six mares in Ireland,²¹ EHV-3 was then concurrently isolated during the 1960s in the United States, Canada and Australia.^{18, 30, 40} Since then, reports of ECE have been recorded almost worldwide under a variety of names such as genital horse pox, eruptive venereal disease, equine venereal vulvitis or balanitis, or coital vesicular exanthema.^{10, 12, 20, 27-29, 31, 41, 43, 51, 52, 58, 61, 62} The latest report was the confirmation, for the first time, of ECE in the native Icelandic horse population.⁵⁰

The infection is relatively benign and does not result in systemic illness, infertility or abortion.^{39, 52} However, the negative impact on the equine industry, mainly in the Thoroughbred breed, relies on the forced, temporary withdrawal of affected animals with the consequent disruption of mating activities in breeding facilities. For affected stallions, such disruptions may translate into significant end-of-season decreases in the mare-book size. Similarly, affected mares will miss breeding opportunities. In artificial insemination and embryo transfer centres, affected mares may be reluctant to be inspected, inseminated or transferred with the consequent loss of opportunity to become pregnant. In both scenarios (natural mating or artificial insemination), delayed foaling dates or reduced pregnancy rates may occur in those mares that miss breeding opportunities because of the disease.^{4, 10, 55, 58}

Aetiology

The aetiological agent of ECE, Equid alphaherpesvirus 3 (EHV-3), is a member of the Herpesviridae family (see Herpesviridae: General Introduction) with a typical alphaherpesviral architecture, size, and genome structure.^{4, 24, 32} Its biological features place EHV-3 in the Alphaherpesvirinae subfamily, within the genus Varicellovirus, which also includes Equid alphaherpesvirus 1 (EHV-1), Equid alphaherpesvirus 4 (EHV-4), Equid alphaherpesvirus 8 (EHV-8) and Equid alphaherpesvirus 9 (EHV-9). EHV-3 is antigenically, genetically, and pathogenically distinct from EHV-1 and EHV-4, and even more distantly related to equid gammaherpesviruses (EHV-2 and EHV-5).^{4, 24} It shares no protective or neutralization epitopes and only minor genetic homology with these other herpesviruses of the domestic horse (Equus caballus).^{4, 13, 15} The restriction endonuclease cleavage patterns of the DNA of EHV-3 are unique when compared with those reported for the genomic DNA from EHV-1, EHV-2, EHV-4, and EHV-5.⁴ Although causing disease of clinical similarity, the virus of ECE is unrelated, by serum neutralization tests, to Bovine alphaherpesvirus 1 (BHV-1) that causes infectious pustular vulvovaginitis and balanoposthitis in cattle.¹⁷ (see Chapter Infectious bovine rhinotracheitis/Infectious pustular vulvovaginitis and infectious pustular balanoposthitis)

As for physicochemical properties, the buoyant density of EHV-3 has been determined as 1.727 g/cm³, with a sedimentation coefficient of approximately 55.4 S, which corresponds to a molecular weight value of 90 to 100 megadaltons (Md).⁷ Regarding the structure of the EHV-3 genome, it has a double-stranded DNA class D genome consisting of a long and a short unique region (UL and US), both flanked by inverted repeats (TRL/IRL and IRS/TRS).^{7, 44} Its full-length genome sequence consists of 151,601 bp (G + C content of 68.1 per cent) encoding for 76 open reading frames (ORF), four of which are duplicated (ORFs 64, 65, 66, and 76), resulting...