Equine coital exanthema - University of Kentucky College ...

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Equine coital exanthema

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

G.P. ALLEN AND N.W. UMPHENOUR

INTRODUCTION 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
Equine coital exanthema (ECE) is an infectious, venereally g/cm3.35 Purified virions of EHV-3 possess, in addition to the
transmitted mucocutaneous disease of mares and stallions DNA-containing nucleocapsid, a proteinaceous tegument and
caused by a herpesvirus. The disease is characterised by the glycoprotein-laden envelope.3 The virus is environmentally
development of superficial pock-like eruptions and erosions or labile, and infectivity is quickly destroyed by lipid solvents,
ulcers on the external genital organs.8, 15, 20, 51 The virus is detergents, heat, and drying as well as by the common
highly contagious but is noninvasive and relatively benign. disinfectants available for veterinary use.12 Storage at
Reports of the disease have long been recorded in the temperatures below -60 °C is required for maintaining its
veterinary literature under a variety of names.7, 11, 16, 19, 32, 34, 39, long-term viability.

41, 43, 44 In cell culture, EHV-3 replicates only in cell lines derived
from equids.12 The intracellular replication cycle and
The infection does not usually result in systemic illness, subsequent cytopathic effect (CPE) are extremely rapid. Equid
and neither infertility nor abortion occur as sequelae.12, 20, 24, 36, herpesvirus 3 progeny DNA and virions are present by two
38, 51 Its primary negative impact on equine breeding and six hours post-infection (PI), respectively, and CPE is
enterprises is the forced, temporary disruption of mating detectable as early as 6 hours PI after a high multiplicity of
activities. In intensively managed stud operations employing infection.1 The CPE of EHV-3 is typically herpetic in nature
heavily-scheduled breeding dates for stallions, such with rapidly enlarging foci of rounded, refractile cells. When
disruptions may translate into significant end-of-season infected cell cultures are stained with haematoxylin and eosin,
decreases in the mare-book size of affected stallions. eosinophilic, intranuclear inclusion bodies are visible.22, 40 The
Similarly, delayed foaling dates or reduced pregnancy rates optimal temperature for in vitro replication of EHV-3 is 34 °C;
may occur in mares that miss breeding opportunities because at 39 °C, the production of infectious virus is reduced to 10-6
of the disease. of its maximum yield.9, 27, 30 No laboratory animal model of
EHV-3 infection has been identified.
AETIOLOGY
Although restriction endonuclease fingerprint analysis of
The causative agent of ECE, Equid herpesvirus 3 (EHV-3), is viral DNAs has been used to demonstrate the genetic
a member of the Herpesviridae family and in size, virion individuality of EHV-3 isolates,9 there is no reported evidence
architecture, and genome structure is a typical herpesvirus.4, 12, of antigenic diversity among clinical isolates recovered from
29, 35, 46 Its biological features place EHV-3 in the different disease outbreaks.12 A related but antigenically
Alphaherpesvirinae subfamily. Equid herpesvirus 3 is distinguishable herpesvirus (Equid herpesvirus 6) has been
antigenically, genetically, and pathogenetically distinct from isolated from superficial cutaneous lesions of a donkey.12, 28
Equid herpesvirus 1 (EHV-1), EHV-2, EHV-4, and EHV-5.2, 6, Small-plaque variants of EHV-3 arise during passage in cell
12, 26, 45 It shares no protective or neutralisation epitopes and culture and are characterized by alterations in their DNA
only minor genetic homology with these four other restriction endonuclease patterns caused by the presence of a
herpesviruses of the domestic horse (Equus caballus). 2, 45, 53 5,7 kbp nucleic acid insert in the unique (U) sequence of the
The restriction endonuclease cleavage patterns of the DNA of small (S) component of their DNA genomes.9, 12, 31
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 EPIDEMIOLOGY
Although causing disease of clinical similarity, the virus of
ECE is unrelated, by serum neutralization tests, to bovine The only known biological reservoir for the virus of ECE is
herpesvirus 1 (BHV-1) that causes infectious pustular the latently infected horse. Careful observations and frequent
vulvovaginitis in cattle.12 serological monitoring of a closed, pony-breeding herd has

demonstrated the existence of latently infected carrier animals a horse. The virus is easily transmitted by simple contact with
from which EHV-3 was periodically reactivated and the skin; the epidermal surface need not be damaged for
transmitted to cohorts.14 By serological tests, it was shown that infection to be established.12, 33, 38, 53
some pony stallions and mares acquired primary infection or
reinfection by EHV-3 without signs of clinical disease. It is Viral replication is limited to the stratified epithelium of
now believed that such episodes of virus reactivation from epidermal tissue present within the skin or at mucocutaneous
latency with subsequent recrudescence of clinical (or margins. Destruction of epithelium by the lytic virus infection
subclinical) infection serve as the source for spread of EHV-3 elicits a vigorous, localised inflammatory response that gives
to other animals.7, 14, 16, 24 Epidemiological data suggest that the rise to the formation of the characteristic cutaneous lesions of
original viral source of an outbreak of ECE may be either a ECE. Viral invasion of tissue within blood vessels or the
visiting mare brought onto the stud farm for breeding or virus stroma of the dermis underlying the epithelial lesion does not
reactivated from a member of the resident stallion or mare occur, and systemic dissemination of EHV-3 has not been
population.7, 14, 16, 24 Persistently infected horses that shed reported. Secondary bacterial infection with Streptococcus
EHV-3 continuously have not been identified. The anatomical equi zooepidemicus is common and influences the character,
site that harbours the latent herpesvirus is unknown. severity, and duration of the epithelial lesions. Recovery from
ECE is complete in a matter of two to three weeks and occurs
Surveys to estimate the seroprevalence of EHV-3 infection without permanent sequelae.
in several horse populations have demonstrated the existence
of EHV-3 specific antibodies in 18 per cent to 53 per cent of The horse responds to infection by EHV-3 with the
horses of breeding age.5, 37, 47 Maternally derived antibody to production of serum complement-fixing (CF) and virus-
EHV-3 is present in new-born foals but decays to undetectable neutralising (VN) antibodies that reach maximal levels 14 to
levels by four months of age.37 The seroprevalence of 21 days after infection.12, 14, 37, 38, 53 In comparison to the equine
infection is low in young and in unmated horses, but increases humoral immune response mounted against the systemically
slowly with age in breeding animals.5, 37 infecting herpesviruses of the horse, peak antibody titres
against EHV-3 are relatively low.7, 12, 25, 38 Complement
Clinically apparent ECE occurs only sporadically in most fixation titres decline rapidly after infection (six to eight
breeding establishments. Its overall incidence is unknown. weeks), whereas VN activity declines more slowly with
Once recrudescence of EHV-3 infection has occurred, ECE is detectable levels persisting for a year or more.37 Post-exposure
highly contagious; postcoital infection rates as high as 100 per immunity to reinfection by EHV-3 is short-lived, and both
cent have been reported.7, 22 The primary method of virus stallions and mares have been observed to develop the disease
transmission is through direct skin-to-skin contact by coitus in consecutive breeding seasons.49, 50
with an actively infected, virus-shedding horse. The
incubation period is five to nine days. Experimental CLINICAL SIGNS
transmission of ECE from infected mares to stallions by coitus
has been demonstrated.25, 37 Evidence exists to indicate that The clinical presentation of equine coital exanthema is
subclinically infected horses without visibly noticeable lesions characterized by the presence of superficial lesions on the skin
can also transmit the virus to their breeding partners.14 The of the external genitalia of mares or stallions (Figures 78.1
potential for virus spread during artificial insemination has not and 78.2). The progress of each cutaneous lesion follows a
been explored. Iatrogenic transmission of infection can occur well-defined and predictable course.7, 8, 10, 11, 12, 15, 19, 20, 24, 25, 37,
by virus-contaminated objects, such as buckets, instruments, 39, 40, 41, 42, 43, 44, 51 Appearing initially as a small (1–3 mm)
tools and examination sleeves, used for the purposes of raised papule which often goes unnoticed, the lesion then
breeding, grooming, rectal palpation, or gynaecological progresses sequentially to a vesicle, a pustule, and, after
examination.8, 15 Reports of ECE lesions on the lips and epidermal sloughing of the necrotic dome of the pustule, to a
nostrils of some horses indicate that noncoital transmission of shallow, raw or encrusted erosion or ulcer. The progression to
infection by the genito-nasal contact associated with fully developed lesions is rapid, occurring over the period of
behavioural nuzzling/sniffing may be possible.13, 16, 17, 33 The only a few days. Initially, the individual erosions and ulcers
likelihood of mechanical transmission by stable flies has also are discrete and uniform in size (5 to 10 mm) and distinctly
been suggested.24 pock-like with raised borders and sunken centres. As they
develop in size, however, the lesions may coalesce to form
Because ECE is endemic in most horse breeding areas,5, 7, extensive epidermal erosions or ulcers. Localised
23, 24, 33, 41, 50 there are at present no international restrictions on inflammation is invariably present and gives rise to tissue
the export/import of horses from countries or from horse congestion and erythema as well as, in the mare, oedema of
populations in which ECE is known to occur. the vulvar labia, perineum and inner thighs. In the stallion,
oedema of the prepuce and sheath may occur and extend
PATHOGENESIS laterally onto the ventral abdominal wall and scrotum. Lesions
infected secondarily with bacteria may exude a whitish
Infection by EHV-3 occurs via direct cutaneous contact either discharge. The lesions may be few or many in number and
during the act of coitus or by the transfer of virus-containing may be at different clinical stages. Both the severity and
secretions from contaminated objects, such as hands, gloves, duration of the disease varies considerably among individual
instruments, palpation sleeves, sponges and the lips or nose of

FIGURE 78.1 Equine coital exanthema in the mare, showing lesions present on the external cutaneous
surface or on the internal mucosal surface of the vulvar labia. A sequential progression of
the clinical stages of ECE lesions, from vesicular to pustular to ulcerative and then to
healed white scars, is illustrated in panels A to D. The photographs in panels A and B
were reproduced from reference #24 with permission of the publisher.

FIGURE 78.2 Lesions of equine coital exanthema on the shaft of the penis of stallions (panels A, B, and
C) and on the perineal skin of a mare (panel D)

horses. In uncomplicated cases, healing of the lesions of ECE mares, lesions commonly extend beyond the mucodermal
is complete by 10 to 14 days, but their locations may be junction of the vulva and may be present on its inner,
marked by depigmented cutaneous scars that persist for many nonpigmented mucosal surface as well as on the clitoris, fossa
weeks. The healing process is prolonged by centrifugal spread clitoridis, or the walls of the vaginal vestibule. On rare
of infection and the appearance of new lesions during the occasions, EHV-3 lesions have been noted also on the skin of
course of the disease. the ventral surface of the tail, buttocks, medial aspect of the
thighs, or abdomen adjacent to the genital areas 24, 40, 50 as well
The in vivo replication of EHV-3 in the horse is restricted as at extragenital epidermal sites on the muzzle, lips, or
to anatomical sites covered by true cutaneous (stratified nostrils.17,33
squamous) epithelium or by the transitional epithelium at the
mucocutaneous junctions of the nares, urethral orifice, and Experimental inoculation of EHV-3 into young horses by
female genital vestibule. Whether this represents a genuine the intranasal route resulted in ulcerations of the nasal mucosa
tissue tropism or merely reflects the demonstrated with accompanying pyrexia and nasal discharge.12, 13, 53 Unlike
temperature-sensitive nature of the virus is unsettled.9, 27, 30 coital exanthema of cattle, lesions within the cranial vaginal
Because of this anatomical restriction, the lesions of ECE are canal of the mare are not a prominent feature of EHV-3
most commonly located on the external (cutaneous) surface of infection.
the vulva and surrounding perineal skin in the mare, and, in
the stallion, on the glans and free body of the penis as well as Systemic signs of infection (e.g. fever, anorexia, or
on both the parietal and visceral folds of the prepuce. In dullness) in ECE is the exception, but vulvar discharge, tail
switching, frequent urination, or arching of the back have been

reported in severely affected mares.34 Occasionally, stallions Definitive identification of virus isolated in cell culture is
with extensive ECE lesions exhibit a stiff gait, pyrexia, best achieved by performing infectivity-neutralisation tests
inappetence and are so debilitated with discomfort from the with EHV-3 reference antiserum.22 Techniques to detect EHV-
disease that they lose libido and refuse to mount and copulate 3 in inoculated cell cultures or in clinical material by PCR
with mares.40 The disease is not known to cause any long-term have been described, 21 but immunohistochemistry assays
impairment of fertility in either mares or stallions.8, 36, 37 have not yet been routinely applied. Because the
Abortions caused by natural EHV-3 infection of the foetus immunofluorescence test for EHV-3 has been reported to
have not been reported. cross-react with EHV-1, it should be used with caution.26

Horses with chronically recurrent ECE in which lesions A serological diagnosis of recent infection with EHV-3
recrudesce annually during the terminal period of pregnancy can sometimes be made, retrospectively, by the demonstration
or after foaling have been observed, most commonly in aged of a significant rise in the level of neutralising antibody
broodmares.11 between acute and convalescent serum samples. Because the
equine antibody response to infection with EHV-3 may be
PATHOLOGY minimal, a failure to demonstrate the conventionally required
four-fold rise in antibody titre may occur and should not
Detailed histopathological examination of exanthemous ECE necessarily be interpreted as evidence for the absence of
lesions through the course of their development remains to be infection.24 Detection of serum CF antibody to EHV-3 has
conducted. been reported to be indicative of viral infection within the
previous 60 days.38
Necrotic epithelium covering the erosions or ulcers is
sloughed and replaced by a fibrin exudate in which are trapped DIFFERENTIAL DIAGNOSIS
polymorphonuclear and mononuclear leukocytes. The Clinically typical cases of ECE can usually be diagnosed in
underlying dermis is oedematous and heavily infiltrated with the field without difficulty. In ECE-like outbreaks
inflammatory cells. The transition from necrotic tissue to accompanied by exanthemous lesions on the lips or nostrils of
normal epithelium at the edges of the erosions/ulcers is horses, vesicular stomatitis must be considered. In
sharply defined. Typical herpesvirus intranuclear inclusion geographical areas where true horse pox still occurs, this
bodies are usually present in some epithelial cells at the border orthopox virus disease should be included in the differential
of the erosions. diagnosis. Contagious equine metritis (caused by Taylorella
equigenitalis) should be excluded by careful laboratory
DIAGNOSIS examination in mares in which a mucopurulent vulvar
discharge is a prominent feature of the clinical picture. It
The genital lesions of ECE in both mares and stallions are should be borne in mind that exanthemous lesions on the
usually characteristic enough in their appearance for a clinical external genitalia of mares as a result of infection with equid
diagnosis to be made with reasonable certainty. If necessary, a herpesvirus 1 have, on occasion, been reported.12, 41, 48, 52
presumptive diagnosis can be confirmed in the laboratory by
polymerase chain reaction (PCR), by isolation of the virus or CONTROL AND TREATMENT
by demonstration of either seroconversion or a four-fold or
greater rise in antibody titre in paired serum samples. A commercial vaccine against ECE has not been developed.
Because of the existence of latently infected carrier animals in
Important specimens to be submitted for laboratory most horse populations, occasional reactivations of latent virus
confirmation of ECE are (1) clinical material collected from with recrudescence of clinical or subclinical infections with
the edges of fresh, active lesions by firm swabbing or EHV-3 are unavoidable. As reactivation of latent virus is not
scraping, and (2) two clotted blood samples without preventable, the basis for controlling the impact of outbreaks
anticoagulant, one taken during the acute illness and the other of ECE in breeding establishments is containment of the
three to four weeks later. Specimens for virus isolation should spread of infection.
be submitted in 2–3 ml of tissue culture medium (containing
antibiotics and antimycotics) on ice to a competent laboratory. A stringent code of practice should be implemented within
breeding sheds following observation of a case of ECE. The
Isolation of EHV-3 requires inoculation of equine-derived three priorities necessary for successful ECE control are:
cell cultures; e.g. equine dermal (E-Derm), foetal equine
kidney (FEK), or equine embryonic lung (EEL) cells. • cessation of breeding of clinically affected animals;
Increased success of virus isolation is achieved if material • heightened vigilance on the part of personnel for early
collected from cutaneous erosions is inoculated directly (i.e.
without prior homogenization, centrifugation, or filtration) recognition of new clinical cases; and,
onto monolayers of susceptible cells. Greater than the usual • strict adherence to breeding shed hygiene procedures
concentrations of antibiotics and antimycotics may be
necessary to control bacterial and/or fungal contamination in designed to eliminate mechanical transmission of the
such inoculated cell cultures. Cytopathic effect by EHV-3 is virus.
generally evident by one to two days after inoculation of cell
monolayers. The most effective method for restricting the transmission of

EHV-3 infection remains the immediate cessation of mating Finally, all instruments, buckets, and assist devices used
activities of clinically affected stallions and mares. The during the breeding procedure should be washed and sterilized
decision to return an EHV-3 infected stallion or mare to between use or fitted with clean disposable covers or liners.
breeding service should be based on a clinical evaluation of
whether the genital lesions are still infective rather than on a The therapeutic objective of the treatment of breeding
prescribed length of time. Lesions should be fully granulated stallions and mares exhibiting ECE is shortening of the
and regressed to a point that the likelihood of virus still being required period of suspended mating by promoting the rapid
shed is low. The quarantine time interval, which may vary and uncomplicated healing of genital lesions. Treatment
from horse to horse, will be influenced by the extent and usually consists of daily cleansing of the genitalia, reducing
severity of the lesions and by the rapidity of the healing any inflammation, and preventing secondary bacterial
process. The recovery period may be prolonged by secondary infection. Therapy is thus palliative and prophylactic rather
bacterial infection. For stallions, this period of breeding than curative. Three functional categories of medicinals form
inactivity may, with appropriate management, be reduced to as the basis for most reported treatment regimens: antimicrobials
little as seven days.49 for control of secondary bacterial infection of the lesions;
antiseptics/stringents for cleansing and drying of the lesions;
Personnel assisting with the preparation of mares or and, glucocorticosteroid anti-inflammatory agents. All are
stallions for breeding should be informed of the importance of applied topically, once or twice daily, as creme- or ointment-
early detection of new cases of ECE and trained in recognition based emollients. During cleansing or topical application of
of the lesions characteristic of the disease. Assistants in the medicinals, care should be taken to avoid accidental, traumatic
mare chute area responsible for preparing mares for cover (e.g. removal of the crusts of healing sores. Although effective in
washing the genitalia and wrapping the tail) can be reducing inflammation, corticosteroids may slow the healing
instrumental in identifying animals with suspect lesions. process. Representative treatment regimens have included
Similarly, stallion crew members working close to the animals topically applied mixtures of (1) nitrofurazone, neomycin,
during mating often have the best vantage point for prednisolone creme;36 (2) oxytetracycline, polymixin B
recognition of a new case of ECE. opthalmic ointment;36 (3) chlorohexidine creme and
dimethylsulfoxide mixture;22 (4) nitrofurazone, silver
Strict adherence to hygienic measures designed for sulfadiazine creme,49 and (5) sodium propionate, gentian
preventing the mechanical spread of EHV-3 during an ECE violet, acriflavine mixture.49 Acceleration of the healing
outbreak is a critical component of the disease control plan. process by laser treatment of the lesions, in conjunction with
Care must be taken to avoid iatrogenic transmission of the vitamin E ointment, has also been explored.49 In severely
virus through contaminated equipment such as rectal sleeves, affected animals exhibiting pyrexia and/or anorexia,
vaginal specula, insemination utensils, etc. Breeding shed systemically administered antibiotics have been included in
personnel who have direct contact with horses should wear the treatment regimens. 22, 40
long, disposable examination sleeves and short latex gloves
which are changed between each horse handled. Mare Though theoretically promising as a treatment modality,
preparation chutes should be washed down with water and the topical use of the antiviral compound, acyclovir, for
then disinfected between the preparation of each mare to facilitating the healing of ECE lesions has not been fully
prevent cross-infection. A thorough rinsing of each stallion's explored. A 5% topical, creme formulation of acyclovir
penis and prepuce with plain warm water after each mating marketed for use in the treatment of herpetic skin lesions in
has been used with the aim of reducing the virus load of any people has recently been used in the treatment of coital
potential inoculum of EHV-3 acquired from the covered mare. exanthema in both stallions and mares. 18

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