A SPECIAL, NON-REVIEWED SECTION
REFERENCES
sylvatic VEE virus can be differentiated from those produced
in response to infection with epizootic VEE viruses only by
the viral PN test.
Control
During recent epizootics of equine encephalomyelitis,
control of the diseases has involved vaccination of equids
combined with vector control by ground or aerial application
ofultralow volumes of insecticides such as organophosphorus
compounds.
Safe and effective inactivated encephalomyelitis vac-
cines are commercially available for use in equids. These
monovalent, bivalent or trivalent vaccines should be used
annually for at-risk populations. The only safe and acceptable
inactivated VEE virus vaccines are produced from the attenu-
ated VEE vaccine, strain TC-83. Epizootics of VEE have
occurred from the use of formalin-treated preparations of
equine-virulent epizo0tic VEE virus; these products should
not be manufactured and should never be used in equids.
The attenuated VEE virus vaccine strain TC-83 was
derived from an equine-virulent epizootic VEE virus by serial
passage in fetal guinea pig heart cell cultures. It was produced
for use in "at-risk" laboratory workers and military personnel.
The vaccine is safe and effective for use in equids and
produces an immunity of long duration.
EQUINE VIRAL ARTERITIS -- EPIDEMIOLOGY AND CONTROL
P. J. Timoney and W.H. McCollum
SUMMARY
The epizootic of equine viral arteritis (EVA) in the
Thoroughbred population in central Kentucky in 1984
aroused concern for a disease whose previous sporadic occur-
rences had gone largely unnoticed.
The threat of spread of EVA through the internal move-
ment of horses led to the imposition of considerable restric-
tions by other major bloodstock-raising countries on the
importation of horses of all breeds from theUS. Though in no
way disputing the importance of spread of the EVA infection
at racetracks, sales and equestrian events, etc., it has become
evident that the long-term carrier stallion probably plays a
major epidemiologic role in perpetuating the virus from year
Authors' address: Depa~naent of Veterinary Science, University of Ken-
tucky, Lexington, KY 40546-0076. Published as paper #87-4-154 by per-
mission of the Dean and Director, College of Agriculture and Kentucky
Agricultural Experiment Station.
54
1. Calisher CH, Shope RE, Brandt W, Casals J, Karabatsos H,
Murphy FA, Tesh RB, and Wiebe ME: Proposed antigenic classification of
registered arbovimses. I Togaviridae, Alphavirus. Interviroiogy, 14:229-
232,1980.
2. Fenner F, Bachmann PA, Gibbs EPJ, Murphy FA, Studdert MJ and
White DO: Togaviridae and Flaviviridae. In: Veterinary Virology,eh 25, pp
451-472, Academic Press, New York, 1987.
3. Hanson RP: American arbovirnl encephalomyelitides of equidae.
Virology and epidemiology of eastern and western athoviral encephalomye-
lifts of horses. In: Proc. International Conference of Equine Infectious
Diseases, 3:100-114. Bryans JT and Gerber H, Eds. Karger, Basel, 1973.
4. Johnson KM AND Martin DH: Venezuelan equine encephalitis.
Adv Vet Sci Comp Med 18:79-116, 1974.
5. Karabatsos N (Ed): International catalogue of arboviruses includ-
ing certain other viruses of vertebrates, 3rd edition, American Society for
Tropical Medicine and Hygiene, San Antonio, TX 1985, 1147 pp.
6. Monath TP and Trent DW: Togaviral diseases of domestic ani-
mals. In: Comparative Diagnosis of Viral Diseases, 4:331-440. Academic
Press, New York, 1981.
7. Pan American Health Organization. Venezuelan encephalitis. In:
Proc. Workshop-Symposium on Venezuelan Encephalitis Virus, Sci. Publ.
243, Washington DC, 1972, 416 pp.
8. Walton TE: Venezuelan, eastern and western encephalomyelitis.
In: Virus Diseases of Food Animals. A World Geography of Epidemiology
and Control: Disease Monographs, 2:587-625, EPJ Gibbs, Ed., Academic
Press, New York, 1981.
9. Walton TE and Grayson MA: Venezuelan equine encephalomye-
lifts. In: Arboviruses: Epidemiology and control, Vol. 4. Monath TP, Ed.,
CRC Press, Boca Raton, FL, In Press.
10. Young NA and Johnson KM: Antigenic variants of Venezuelan
equine encephalitis virus: Their geographic distribution and epidemiologic
significance. Amer JEpidemiol, 89:286-307, 1969.
to year. In contrast to the stallion, the carrier state has not yet
been confmned in the mare, nor has there been any evidence
of a congenitally acquired carrier state in foals.
DISCUSSION
The epizootic of equine viral arteritis (EVA) in central
Kentucky in the latter half of the 1984 breeding season marked
the In'st occasion this disease had been recorded in the Thor-
oughbred population of North America since the initial isola-
tion of the causal agent during an epizootic of abortion on a
Standardbred farm in Bucyrus, Ohio, in 1953.4 A clinically
similar disease of horses, "epizootic cellulitis-pinkeye," had
been described many years earlier in the veterinary literature
of the late nineteenth and twentieth centuries, 2s providing
evidence that EVA had probably been an affliction of horse
populations in various parts of the world for avery long period
of time.
EQUINE VETERINARY SCIENCE
 A SPECIAL, NON-REVIEWED SECTION
The results of various serologic surveys would indicate
that equine arteritis virus (EAV) is widely distributed
throughout the world ~s,19,'~3even though there are relatively
few occurrences of the disease reported in the scientific
literature.~Zo,t s ~ 3 3 Since 1984 there have been 3 additional
outbreaks/epizootics of EVA confh-med, 2 in North America
and 1 in Europe, 1 of which was an extensive epizootic
involving several hundred Thoroughbred and Standardbred
horses that originated at a racetrack in Alberta, Canada.
Abortion in pregnant mares, though of low incidence, did
occur in association with 2 of these outbreaks/epizootics.
Considerable variation in the prevalence of equine viral arteri-
tis (EAV) infection has been found not only between horse
populations in different countries but also between certain
breeds within a country. Serologic data from surveys under-
taken in the USA in 197119 and 1984-1985 (Timoney and
McCollum, unpublished data) revealed considerable disparity
in the distribution of EAV infection in Thoroughbred and
Standardbred breeds. Whereas 70 to 90 percent of Stan-
dardbred mares were seropositive for antibodies to the virus,
a comparable population of Thoroughbred mares was virtu-
ally seronegative, with only 3 percent of horses testing posi-
five.
Over the years since EVA was first recognized as a
separate viral entity of the horse4 and shown to be caused by
a virus belonging to the non-arthropod-borne group of toga-
viruses, 24few have regarded the disease of major significance
either economically or from a veterinary medical point of
view. Although the epizootic of EVAin Kentucky in 1984 was
not associated with any mortality or confirmed cases of
abortion, ~ the threat of outbreaks of abortion as was previ-
ously observed in Ohio, Pennsylvania, and Caiifomia in
1953,s and in Poland in 1976-1977,1° caused widespread
concern, fueled by the knowledge that spread of the disease
could follow the national/international movement of horses.
Additional fears expressed at the time were that the occur-
rence of EVA in the Thoroughbred might have resulted from
the emergence of a more velogenic variant of the virus. Both
factors led to the imposition of a temporary embargo on the
export of horses of all breeds from the USA to the important
bloodstock-raising countries comprising the Tripartite group,
namely France, Ireland, and the United Kingdom, a measure
unprecedented in the history of international commerce of
horses between these countries. The embargo, though short-
lived, was succeeded by restrictions on the export of any horse
either vaccinated against EVA or seropositive following natu-
ral exposure to the virus to these countries. The restrictions,
which have since remained if effect, have been financially
punitive especially for Standardbred owners and breeders,
since the sero-prevalence of naturally-acquired EAV infec-
tion in this breed in parts of the USA has been shown to
Volume 8, Number 1, 1988
average approximately 80 percent19 (Timoney and McCol-
lum, unpublished data).
Although research carded out over the years has provided
considerable information on various aspects of EVA includ-
ing the development of a safe and effective vaccine,6,16the
1984 epizootic in Kentucky underscored significant deficien-
cies in our current knowledge, more especially as it related to
the basic biology of the causal virus and the epidemiology of
this disease. Retrospective epidemiologic analysis of that and
subsequent epizootics has helped to provide additional insight
into modes of natural transmission of the virus and into the
carrier state in this infection. Natural exposure to EAV may
result in the development of clinical or inapparent infection
with the virus. The clinical signs characteristic of EVA closely
resemble those reported in horses infected with Getah virus,
an arthropod-borne member of the togavirus family. 14In view
of similarities in the clinical syndrome produced, differentia-
tion of these respective diseases can only be achieved on
virologic/serologic grounds. Although the signs observed in
natural cases of EVA can vary considerably in range and
clinical severity, typical cases present with the following:
fever of 5 to 9 days' duration; limb edema especially of the
hind limbs; nasal and ocular discharges; rhinitis and conjunc-
tivitis; periorbital/supraorbital edema; variable anorexia and
depression; skin rash most commonly on the neck but some-
times generalized; edema of the scrotum and prepuce of the
stallion; abortion in the pregnant mare; and less frequently,
respiratory distress, coughing, diarrhea, and ataxia. Regard-
less of the severity of illness, naturally infected horses invari-
ably make uneventful clinical recoveries. Mortality has only
been reported in horses experimentally exposed to the unat-
tenuated Bucyrus strain of the virus, 4,7 and very rarely in
sporadic cases of naturally acquired infection in foals a few
days to a few weeks of age" (McCollum, unpublished data).
Epidemiologic investigation of the 1984 epizoofic of
EVA in Kentucky revealed considerable variation in the
incidence of clinical disease in cases of naturally acquired
infection. Out of a total of 418 mares bred to a group of 17
EVA-affected stallions located on one farm, the ratio of cases
of clinical disease to inapparent infection was 38:28 or 1.4:1.27
In contrast, the corresponding ratio in a group of mares
bred to a stallion on a different farm that at no time had
exhibited signs of EVA and was a presumed chronic carder
of the virus was 3:18 or 1:6. Additional data have since shown
that mares bred to many of the stallions that have been
confirmed long-term carders of EAV, experience an inappar-
ent infection or else develop only very mild clinical signs of
the disease.
Analysis of the 1984 epizootic in Kentucky focused inter
alia on the extent to which inapparent infection occurred on
EVA-affected farms as a result of lateral contact with clinical
55
 A .SPECIAL, NON-REVIEWED SECTION
or inapparently infected cohorts. While the situation on some
farms was obscured in part by the fact that certain high-risk
horses had been prophylactically vaccinated against EVA, it
was found that the ratio of cases of clinical disease to inappar-
ent infection was 116:98 or 1:9.8. 27 A total of 57 percent of
affected farms had one or two cases of EVA and only 14
percent of premises had five or more cases of the disease.
Under the epidemiologic circumstances prevailing on these
farms at the time, lateral spread of infection between horses in
adjacent stalls or having across the fence contact at pasture did
not play a significant role in further dissemination of the virus.
These findings contrast sharply, however, with those from
more recent outbreaks/epizootics of the disease, in which
there has been ample evidence of widespread lateral transmis-
sion of EAV between horses having close association at a
racetrack, in a barn, or while at pasture (Timoney and McCol-
lum, unpublished data).
Although only one serotype of EAV has so far been
identified,9 evidence of limited antigenic variation among
certain isolates of the virus has been reported, s Using T1
oligonucleotide fingerprint analysis, genomic changes have
been demonstrated between isolates of EAV from both
acutely infected and long-term carrier horses covering a wide
geographic area (Murphy, Timoney and McCollum, unpub-
lished data). Based on currently available data, antigenic
modulation of EAV could not be considered a major epidemi-
ologic influence on the ability of the virus to persist in any
particular horse population. While the information available
on variation in pathogenicity between strains of EAV is, as
yet, incomplete, it is nonetheless apparent that the ability of
strains to produce disease can vary greatly, ranging from the
severe and often fulminating experimental infections caused
by the Bucyrus strain of the virus 4 to the clinically inapparent
infections transmitted by many of the long-term carrier stal-
lions (Timoney and McCollum, unpublished data).
Prior to the 1984 epizootic of EVA in Kentucky, the most
important mode of EAV transmission was considered to take
place via the respiratory route involving infective aerosolized
nasal secretions. This had been clearly demonstrated in both
natural and experimental infections,m,2°In association with
the 1984 epizootic, however, it became apparent that trans-
mission of EAV by the venereal route had also played a very
significant role in the widespread dissemination of the virus.27
This was based on the preponderance of cases of infection that
occurred in mares after breeding in conjunction with isolation
of the virus from the semen of certain stallions. It was felt that
mares when bred to certain EVA affected stallions, either in
the incubation or early convalescent phases of the disease,
may well have been exposed by both venereal and respiratory
routes. While difficult to assess, indirect contact through the
medium of virus-contaminated fomites, e.g., shanks,
56
twitches, personnel, apparel, and various other items used at
time of breeding, probably played a minor role in the spread
of EAV. 27Of further potential significance in the epidemiol-
ogy of EVA, is the role the teaser stallion and/or nurse mare
may play in the dissemination of the infection. Analysis of
data from the 1984 epizootic could not, however, confirm that
either had contributed significantly to the spread of the virus
on the majority of the farms investigated. Clinical and/or
serologic evidence of infection was observed in only 5 out of
a total of 29 teaser stallions located on 25 EVA affected
premises. 27
Of the various factors instrumental in persistence of EAV
in a horse population, perhaps the most significant in ensuring
perpetuation of the virus would be existence of the carder state
in the stallion, the mare, or both. In the aftermath of the 1984
epizootic of EVA in Kentucky, it became apparent that a
percentage of the stallions known to have transmitted the
disease remained persistently infected with, and constant
semen shedders of, the virus, z7 Both short-term as well as
long-term or chronic carders were shown to exist.29 Fre-
quency of the long-term carder state was found to vary widely
between different groups of stallions with as yet no acceptable
explanation to account for this variation. One of the factors
that has been proposed that may influence the carder rate in the
interval of sexual rest provided to stallions following expo-
sure to and infection with EAV. Failure to provide an adequate
period of sexual rest may predispose to the establishment of
persistent infection with this virus. Based on extensive epi-
demiologic field studies involving both Thoroughbred and
Standardbred breeds, it appears that the mean freq,uency of the
long-term carrier state in naturally acquired EAV infection in
the stallion is approximately 30 to 35 percent. 2s
Duration of the carder state can vary from a period of
several weeks after clinical recovery to years, perhaps even for
the remainder of the lifetime of a particular stallion,s° On the
basis of previous breeding data, 3 Thoroughbred stallions
identified in early 1985 have been carders and semen shedders
of EAV for a least 6 years.3x At this point, there is only one
instance of a long-term carrier stallion that, based upon an
extensive range of testing involving test breeding as well as
attempted virus isolation from semen, has ceased to shed virus
after being a carrier and semen shedder for a period of 18
months. 32
Investigation into the routes of virus transmission by
carrier stallions has confirmed that EAV is shed constantly in
the semen but is not present in detectable amounts either in
naso-pharyngeal secretions, urine, or in the buffy coat fraction
of the bloock3°The pattern of virus shedding in the semen tends
to be characteristic for individual carrier stallions and there is
not evidence to date either that some persistently infected
stallions are or can become intermittent shedders of the virus,
EQUINE VETERINARY SCIENCE

or of the phenomenon of latency with respect to persistence of
EAV in the stallion. ~ In a study of 18 naturally infected long-
term carder stallions, Timoney, McCollum and Roberts
(1986) have found that all of the mares test bred to these
stallions became infected with the virus and developed ho-
mologous serum neutralizing antibody titers 1:4 within 28
days after breeding. Based on these and other data (Timoney
and McCollum, unpublished data), there would appear to be
100 percent transmission of EAV to susceptible mares bred to
stallions that are chronic carders of this virus.
The constancy of virus shedding in the semen has greatly
facilitated and expedited the ease with which detection of the
carrier stallion can be achieved. The results of a study by
Timoney, McCollum and Roberts (1986) have indicated that
the carder state in the stallion can be detected with equivalent
accuracy either by means of a test breeding program or by
attempting invitroisolation of the virus from entire ejaculates.
In sharp contrast to the situation in the stallion, the carder
state has yet to be demonstrated in the mare. Many of the mares
involved in the 1984 epizootic of EVA in Kentucky were
screened virologically, the majority at time of foaling, for
evidence of the carrier state with completely negative re-
suits. 27In addition, the carder status of a significant number of
seropositive mares (74) bred to some of the shedding stallions
on a particular farm was investigated using susceptible in-
contact mares. Results of this study indicated that there was no
transmission of EAV within any of the experimental groups
even after close pasture contact for 7 to 8 months.3~
Offurtherconcern in view ofthetaxonomicclassification
of EAV, was the possibility of transplacentai transmission of
infection to the foal in utero with the development of a
congenitally acquired cartier state, this has been documented
for other members of the non-arthropod-borne group of toga-
viruses, e.g., the viruses of hog cholera, bovine viral diarrhea-
mucosal disease and Border disease. Follow-up investigation
of well over a third of the mares involved in the 1984 epizootic
in Kentucky and their 1985 foals didnot disclose any evidence
either of EAV-induced teratologic abnormalities or of a con-
genitally acquired carrier state in foals born of mares that were
pregnant at the time of infection or vaccination against EVA.3~
Based on currendy available data, it would appear that the
frequency of the naturally acquired carder state in the mare
and the foal, if it does occur, is low.
Apart from the possible dissemination of EAV at race-
tracks, horse shows, sales, etc, it is now apparent that the
carrier stallion probably plays a major role in the epidemiol-
ogy of EVA and in the perpetuation of the virus from year to
year. It is proposed that the primary cycle of EAV transmis-
sion may, in many instances, take place at time of breeding
between a carder stallion and a susceptible mare, the latter
being exposed to the virus by the venereal route. Establish-
Volume 8, Number 1, 1988
A SPECIAL,NON-REVIEWEDSECTION ~ ~
ment of clinical or inapparent infection in the mare would be
succeeded by a period of profuse virus shedding into the
respiratory tract (McCollum, Timoney, Roberts, Willard and
Carswell, unpublished data). This, in tam, would provide the
opportunity for a secondary horizontal transmission cycle to
occur, involving exposure of susceptible in-contacts to infec-
tive aerosolized respiratory secretions and perhaps urine. 18,21
Evidence in support of this hypothesis has come from one of
the most recent occurrences of EVA in which EAV infection
had probably been introduced onto the particular affected
farm through a recently imported stallion that is thought to
have been a carder at time of importation (McCollum and
Timoney, unpublished data). The first cases of EVA were
observed in the initial group of mares artificially bred to this
stallion some 3 to 4 months after his arrival on the premise.
This was quickly followed by lateral spread of the disease
other other mares, foals, and stallions on the farm. The
imported stallion implicated in initiating this outbreak never
developed any clinical signs of EVA but was a semen shedder
of the virus when first tested shortly after the initial clinical
cases of the disease were detected.
In view of the sporadicity of reported occurrences of
EVA in the scientific literature in relation to the widespread
distribution of the casual virus, virtually no attempts were
made prior to the 1984 epizootic in Kentucky to formulate
measures for the prevention and control of this disease either
at a national or international level. Although a modified live
vaccine had been developed against EVA almost 20 years
earlier and had been shown to be both safe and effective on
an experimental basis, such was the lack of concern over the
medical and economic significance of this disease that few
felt the need to have the vaccine produced commercially. The
1984 epizootic, however, not only re-awakened awareness of
the abortifacient potential of EAV, but more importantly,
provided the f'trst indication that a relatively high percentage
of stallions become chronic carders and remain constant
semen shedders following infection with the virus. 27
The present EAV vaccine" has been produced in an
equine cell line culture system from an experimental vaccine
that was developed many years earlier by attenuation of the
prototype Bucyrus strain of the virus in cell culture. 6,16 In
vaccination studies involving immunization of horses with
European and American strains of EAV and subsequent
challenge with the Bucyrus strain of the virus, there was no
evidence, based on the immunity produced, of the existence
of more than one virus serotype. 16
Clinical immunity, lasting one to three years, was found
to develop rapidly following immunization with the original
experimental vaccine. 6,17Primary vaccination with the cur-
=Arvac)FortDodgeLabs,Inc.,FortDodge,Iowa.
57
 A SPECIAL, NON-REVIEWED SECTION
rent vaccine, while providing clinical protection, does not
prevent reinfection and limited replication of challenge virus
0VicCollum, Timoney, Roberts, Willard and Carswell, unpub-
lished data). The duration of virus shedding and the amount of
virus shed via the nasopharynx, is, however, very significantly
less than that observed in unvaccinated controls. Serologic re-
sponses are markedly enhanced in horses following revacci-
nation, with the development of high neu~alizing antibody
titers to the virus which persist for at least the duration of a
breeding season (Timoney, Umphenour, McCollum and
Roberts, unpublished data). While a high degree of safety has
been demonstrated with regard to the current EQUINE VI-
RAL ARTERITIS (EAV) vaccine, it is not recommended for
use in pregnant mares, especially during the last two months
of gestation or in foals less than six weeks of age, unless
possibly under circumstances of high risk exposure to natural
infection. Although the risk of fetal invasion by the vaccine
virus is slight, evidence has been presented that this can occur
in exceptional cases.~ Mild post-vaccinal febrile reactions
with transient lymphopenia have been reported in a small per-
centage of horses vaccinated for the first time. Studies in
stallions have demonstrated that vaccination did not result in
any adverse effects in semen quality nor any evidence of virus
transmission either to in-contact controls or to mares to which
they were bred 14 and 28 days after vaccination (Timoney,
Umphenour, McCollum and Roberts, unpublished data).
An experimental, modified live EAV vaccine12was used
successfully for the first time in the field in helping to curtain
lateral spread of infection on affected farms during the 1984
epizootic of EVA in Kentucky. Restriction of movement of
breeding stock and closure of the breeding sheds were addi-
tional control measure implemented at the time that were
considered of equal ffnot greater significance in restricting the
further spread of EVA in the Thoroughbred population. ~ In
the 2 subsequent outbreaks/epizootics that have taken place in
North America, the commercial vaccine has been used
extensively as part of the respective control programs, with no
reports of any adverse sequelae even in pregnant mares. An
additional measure aimed at minimizing frequency of the
carrier state in the stallion, has been the recommendation that
all breeding stallions be provided a period of several weeks
sexual rest after infection with EAV.
Currently, very few programs have been formulated
specifically for the prevention and control of EVA. Those that
have been developed, e.g., in the states of Kentucky and New
York in the USA, have been primarily directed toward con-
trolling the spread of EAV in the respective Thoroughbred
breeding populations. Though in no way excluding the pos-
sible dissemination of the virus at racetracks, horse shows,
sales, etc., it has become evident since the 1984 epizootic of
EVA in Kentucky that the carrier stallion plays a major
58
epidemiologic role in perpetuation of the virus from year to
year?~ This finding provided the essential basis for formula-
tion of the first Guidelines for the Control of EVA in Ken-
tucky, in which state the disease was made notifiable in 1984.
A mandatory statewide serologic survey of the Thoroughbred
stallion population to determine the prevalence of EAV infec-
tion and subsequent identification of long-term carriers of the
virus, were prerequisite steps in development of the control
program. It was felt that by embarking upon a program of
strategic vaccination of the seronegative stallion majority,
effective control over establishment of the carrier state in the
stallion and further increases in the number of carrier stallions
could be achieved. This would also provide a means of short-
circuiting dissemination of EAV in the breeding sheds while
at the same time minimizing restrictions on the breeding of
any high-risk mares. As no effective means of detection of the
carrier mare is currently available, there is an unwarranted risk
of exposing an unvaccinated stallion to EAV infection
through contact with such a mare or with a mare in the
incubation stage of the disease or inapparently infected with
the virus) 2 Since the inception of the EVA Control Program
in Kentucky early in 1985, the EAV status of all new additions
to the state's population of Thoroughbred breeding stallions
has been monitored to detect additional carrier animals. The
current policy of mandatory annual vaccination of the state's
Thoroughbred stallion population is considered the most
effective means of preventing EAV infection and possible
establishment of the carrier state and of safeguarding the
Thoroughbred population against future epizootics of the
disease similar to that experienced in 1984.
Perhaps one of the more contentious issues to be consid-
ered in the formulation of any EVA control program is
whether to allow the continued commercial use of stallions
that are confirmed carriers and semen shedders ofEAV. Based
on experience derived from the 1985 and 1986 breeding
seasons in Kentucky, it is evident that carrier stallions can be
used successfully for breeding purposes subject to certain
stringent requirements being met. 3zCarrier stallions should be
kept physically isolated and bred only to mares vaccinated not
less than three weeks previously or seropositive from previous
natural exposure to EAV. After being bred, mares should be
kept isolated from other non-vaccinated or seronegative
equines for a period of three weeks. Although these measure
have been regarded by some as excessively restrictive and
f'mancially punitive, they have nevertheless provided the
necessary safeguards enabling the continued commercial use
of the carrier stallions without any attendant recurrences of
EVA.31~z
While much remains to be learned about aspects of the
epidemiology of EVA and the basic biology of the causal
virus, especially as it relates to the carrier state in the stallion
EQUINE VETERINARY SCIENCE
 A SPECIAL, NON-REVIEWED SECTION
and possibly in the mare, there are however, sufficient data
currently available to formulate effective programs for the
prevention and control of this disease. Characterization stud-
ies o f strains o f E A V isolated in recent years have not revealed
any evidence of the emergence o f a m o r e velogenic variant o f
the virus. In view o f this and the apparent world-wide distri-
bution o f EAV, there would seem to be little valid scientific
justification for continuing restrictions on the intemadonai
m o v e m e n t of horses between certain countries purely on
serologic grounds. Since it is evident that the carrier stallion
provides the greatest risk o f inadvertently introducing E A V
into a susceptible horse population, specific measures arrived
at identifying carrier stallions, including the screening o f
frozen semen shipments for the presence o f the virus, cur-
rently represent the most rational and feasible approach to-
ward achieving control over the spread o f E V A at both a
national and international level.
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