VIRAL DISEASES OF EQUINE
DISEASES DESCRIPTION |
EPIDEMIOLOGY
Genus: Orbivirus
Family: Reoviridae
caused by: African Horse
Sickness Virus (AHSV) bilehe • C. imicola- most important.
size: 55-70nm
• An arthropod-borne viral
disease of equids that is
endemic to sub-saharan Africa.
• It has nine immunologically
distinct Serotypes.
• can be inactivated:
at a pH <6
I •• by formalin
~
• B – propiolactone
- • Acetylethyleneimine
derivatives
~ • radiation.
• It can manifest as an Acute,
Subacute or subclinical disease
characterized mainly by both
respiratory and circulatory
lesions and clinical signs.
EPIDEMIOLOGY
- is first recorded south of the
Sahara Desert during
mid-1600s
- considered to be endemic to
African Horse Sickness equatorial, eastern and
southern regions of Africa
- is known to be endemic in sub-
sahara Africa and had spread
to Morocco, Middle East, India
and Pakistan.
- Recent outbreaks of the
disease have been reported in
Iberian peninsula and Thailand.
- There are no reported cases of
the disease in the Americas,
Easter Asia and Australasia.
- Epidemiology is dependent in
host- vector interaction, where
cyclic disease outbreaks
coincide with high numbers or
competent vectors.
TRANSMISSION
• Principal vectors of all 9
serotypes:
• Culicoides spp
• The virus also has been isolated
from:
• Rhipicephalus sanguineus
sanguineus (dog tick)
• Hyalomma dromedarii (camel
tick) during the winter in
southern Egypt, where the
disease is endemic.
• Dogs can be infected through
the bite of an infected
mosquitoes.
• Dogs and large African
carnivores such as lions and
leopards can also be infected by
ingestion of meat from AHSV-
infected equids.
CLINICAL SIGNS
Mortality Rate:
- Horses - close to 90%
- Mules - 50%
- Donkey - 10%
The disease do not usually
manifest in African donkeys and
Zebras despite the high virus
titers in blood, and are thought to
be the natural reservoir of the
virus.
AHS manifests itself in 4
different forms:
- Pulmonary Form (Dunkop)
- Cardiac Form (Dikkop)
- MixedForm
- Mild or Horse Sickness Fever
Form
DIAGNOSIS | DIFFERENTIAL
DIAGNOSIS
Viral Isolation
- 4°C/39°F to the laboratory
• Unclotted whole blood collected
in an appropriate anticoagulant
at the early febrile stage
• Collected specimen of Spleen,
lung and lymph node samples
from freshly dead animals are
placed in appropriate transport
media
Viral Identification
• Enzyme-linked immunosorbent
assay (ELISA) – rapid detection
of AHSV antigen in blood,
spleen and supernatant from
cell culture
• Virus neutralization (VN) –
until recently the ‘gold standard’
for typing as well as identifying
virus isolates, but takes 5 days
• RT-PCR is a highly sensitive
technique that allows the
detection of a very low number
of copies of RNA molecules
• Real-time PCR – can detect all
9 serotypes of the virus
AHS Typing
• VN test is considered to be the
gold standard test for identifying
AHSV’s isolated from the field
by using type specific antisera.
• Type-specific gel-based RT-
PCR and Real-time R-T PCR
were used for both identification
and differentiation of AHSV
genotypes which provides rapid
typing method.
Serological Diagnosis
Horses that survived from natural
infection will develop antibodies
against the infecting serotype
within a period of 8–12 days post-
infection.
• Blocking ELISA
• Indirect ELISA
• Complement Fixation
DIFFERENTIAL DIAGNOSIS
• Anthrax
• Equine infectious anemia
• Equine viral arteritis
• Trypanosomiasis
• Equine encephalosis
• Piroplasmosis
• Purpura haemorrhagica
• Hendra virus
TREATMENT PREVENTION AND CONTROL
There is no specific treatment
for animals with AHS apart from
rest and good husbandry.
Sanitary prophylaxis (free
areas, regions or countries)
• Live-attenuated virus vaccines
are available for immunization
of equids against AHS.
• Establish vector control
measures: destroy Culicoides
breeding areas; use insect
repellents, insecticides, and/or
larvicides.
• Establish a strict quarantine
zone and movement controls to
prevent possible spread of the
disease.
Sanitary prophylaxis (affected
areas, regions or countries)
• Annual Vaccination of
susceptible animals.
• Good vector control measures
Medical Prophylaxis
Live attenuated AHS vaccines
(polyvalent or monovalent) are the
only commercially available
vaccine for AHS.
Vaccination of non-infected
horses:
• Polyvalent live attenuated
vaccine – commercially
available in certain countries
Monovalent live attenuated
vaccine – after virus has been
typed
• Monovalent inactivated vaccine
– no longer commercially
available
• Serotype specific subunit
vaccine – currently in
development
cole.
 AFRICAN HORSE SICKNESS FORMS
Pulmonary Form “DUNKOP” Cardiac Form “DIKKOP” Mild or Horse Sickness Fever Form Mixed Form

- 3- 5 days
INCUBATION PERIOD

- Recovery is rare - Fever peaks at a later stage in the course of
the disease compared to the “dunkop” form,
and may remain high for 3 – 6 days before
OVERVIEW declining.
- The “dikkop” form of AHS is more protracted
and milder compared to the “dunkop” form,
with a mortality rate of about 50 per cent.
- It is a very mild form of the disease and not
usually diagnosed clinically.
- It usually occurs to horses that are immune to
one or more serotypes of the AHSV.
- It also occurs in species like zebras and
donkeys which are known to be resistant from
developing clinical disease.
- The most common form of AHS
- but is rarely diagnosed due to the other
preceding form that may predominate the
other form which becomes the basis for the
diagnosis.
- It manifest as both Pulmonary and Cardiac
form.

- Acute respiratory form - subcutaneous oedema of the head and neck, - sudden rise of rectal temperature (39-40°C)
CHARACTERIZED BY - interlobular edema and hydropericardium and particularly the supraorbital fossae. which lasts for 1 to 6 days followed by a drop in
temperature, and recovery.

- fever (40-40.5C) * Edema usually appears late in the course of - labored breathing
- dyspnea the disease, but if it appears early, the - loss of appetite
- spasmodic coughing condition is more severe, more acute and with - conjunctival congestion
- dilated nostril a higher mortality rate. - increase in heart rate
- standing legs part and head extended
- congested conjuctivae In severe cases:
- swollen or edematous supraorbital fossae - Edema (eyelids, lips, cheeks, tongue,
- large quantities of frothy, serofibrinous fluid intermandibular space) (sometimes also the
SIGNS seen in the nostril, trachea neck, chest and shoulders, but usually not the
lower parts of the legs.)
- Dyspnea
- cyanosis
Unfavorable prognostic signs evident after death:
- petechiae (conjunctiva mucosa, mouth—
ventral aspect of tongue)

• Interlobular edema of the lungs • Intramuscular edema - :

• Hydropericardium
• Pleural effusion
• Edema of the thoracic lymph nodes
• Petechial hemorrhages in pericardium
• Hyperemia and petechial hemorrhages of the
serosa and mucosa of small and large intestines
LESIONS
• Subcutaneous edema • As the edema worsens, dyspnoea and
• Epicardial and Myocardial ecchymosis cyanosis may supervene.
• Hemorrhagic gastritis
- Similar lesions described in dunkop form tends
to be more severe and are found in heart
- severe hydropericardium
- slightly congested and edematous lungs
- engorged liver
- nephrosis
- severe GI lesions
- severe esophageal paralysis
- moderate to severe edema
- congestion and petechiation of cecum, colon
ad rectum

Most characteristic lesion:

- yellowish gelatinous edema (IM and SC
connective tissue of head and neck
- severe cases: extends to the back,
shoulder and chest

- dies of anoxia, congestive heart failure or both - usually occurs within 4 to 8 days of the onset of - Mortality rate: approximately 70%
DEATH - occurs in 1 week the febrile reaction - Death usually occurs 3-6 days after the fever
manifests

cole.
 DISEASES OVERVIEW
Family: Paramyxoviridae
Genus: Henipavirus
Genus also includes: Nipah virus,
Cedar virus (apprently non-
pathogenic virus found in Aus
bats) and additional
uncharacterized henipaviruses in
various locations
- is an emerging viral disease of
horses and humans in
Australia.
- Although this disease is
uncommon, cases in horses
have been reported with
increasing frequency since it
was first recognized in 1994.
- Hendra virus is maintained in
asymptomatic flying foxes
(pteropid fruit bats).
- Infected horses usually
experience a brief, severe
respiratory or neurological
illness with a high case fatality
rate, and are thought to be
incidental hosts.
SPECIES AFFECTED
Reservoir hosts: Bats of the
genus Pteropus (pteropid fruit
bats/ flying foxes)
Incidental hosts: other mammals
all clinical cases in animals, to
date, have occured in horses, but
other species may also be
susceptible
Hendra Virus Infection
GEOGRAPHIC DISTRIBUTION
- Hendra virus infections have
been seen only in Australia,
where this virus is endemic in
flying foxes.
- Cases in horses have only
been reported from eastern
Australia, in the states of
Queensland and New South
Wales.
- Antibodies detected in flying
foxes in Papua New Guinea
might be caused by Hendra
virus or a related virus.
- Currently there is no evidence
that Hendra virus exists in other
areas. However, henipaviruses
or antibodies to these viruses
have been detected in bats on
several continents.
- Most of these viruses are
poorly characterized.
TRANSMISSION CLINICAL SIGNS DIAGNOSIS | DIFFERENTIAL TREATMENT PREVENTION AND CONTROL
DIAGNOSIS
Humans: IP: 8-16 days Difficult to assess risk:
- direct contact with fluid from Death: Sudden,1-3 days after • Sick horses in endemic areas
infected horses (likely MOT) onset • Areas inhabited by fruit bats
- Unlikely MOT
- respiratory - Can be asymptomatic during In suspect cases:
- human-to-human incubation, but shed virus • Do NOT handle:
- bat-to-human - Depression • Infected tissues
- Infected individual without - pyrexia • Blood
protective gear has extensive - dyspnea • Urine
contact with horses - tachycardia
- not all exposed humans and - Initial nasal discharge (clear to To prevent bat to horse
horses became sick serosanguinous) transmission:
• Stable horses at night and
Research on-going during high risk months
• Do not use paddocks with
Animals: access to roosting trees used by
fruit bats
Bat-to-horses • Secure feed bins and water
- unclear troughs
- birth products (fetus, placenta) • Remove and destroy dead bats
- congestion of contaminated or birth products
feed • Call proper authorities for
- virus excreted in urine and removal
saliva
Prevent virus spread on
Horse-to-Horse fomites:
- not highly contagious • Rigorous hygiene
- close contact • Quarantine
- urine and oral cavity • Low rate of horse-to-horse
- mechanical transmission transmission
- Sensitive to heat and chemical
Cat-to-cat, cat-to-horse disinfection
(experimental) - Directly contaminated objects
- close contact - Autoclave or boil
- urine - 1% sodium hypochlorite
solution
- NaDCC granules
ZOONOTIC POTENTIAL
• Humans are susceptible to
Hendra virus.
• To date, all clinical cases have
been acquired during close
contact with infected horses
and/or their tissues.
• Necropsies are a particularly
high-risk procedure, but any
contact with blood, secretions or
tissues also carries a risk
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DISEASES OVERVIEW
Family: Beta Coronavirus
strand: ss RNA virus
Equine Coronavirus (ECoV) is an
important cause of enteric
disease in adult horses.
• Reported worldwide with
increasing incidence
Equine Coronavirus
Equine influenza virus is a RNA
virus which is endemic in horse
populations in many countries
worldwide and which occurs
sporadically in epidemic form from
time to time.
Countries free of equine influenza
include Iceland, Australia and
New Zealand. Outbreaks are
possible and occur in endemic
countries.
May be more severe in donkeys
and mules
Equine Influenza
TRANSMISSION
Transmission:
- Feco-oral
- Fomite transmission is possible
(e.g. ECoV- contaminated
stalls, muck forks , manure
spreaders, thermometers,
hands and clothing)
Risk factors: exposure to
infected horses
PREVALENCE
In a study of horses presenting for
gastrointestinal disease, ECoV
was isolated by PCR from only
1/258 fecal samples (Sanz et al
2019).
• In a study investigating
seroprevalance, 9.6% of adult
healthy horses from the United
States tested seropositive to
ECoV (Kooijman et al 2017).
SHEDDING OF VIRUS
• Under natural conditions, fecal
shedding of ECoV has been
reported to range from 3 to 25
days.
• Horses with no clinical signs of
the disease can shed the virus.
- Respiratory transmission (most
common)
- Inhalation of infective droplets:
coughing and snorting horses
(may be able to spread as far
as 50 yards by this route)
- Respiratory shedding typically
lasts for 7–10 days post
infection in naïve animals;
much shorter shedding periods
occur in partially immune
horses (previously vaccinated
horses)
- Indirect transmission through
clothing, equipment, brushes,
shared water buckets, hands,
etc.
Risk Factors:
- Areas of high comingling of
horses such as race tracks,
show grounds, veterinary
hospitals
- Immunosuppression from
traveling, hospitalization,
training and showing
Age: horses 1–5 years of age
CLINICAL SIGNS
IP: 2-4 days
Clinical disease is generally mild,
but mortality from necrotizing
enteritis and hyperammonemic
encephalopathy has been
reported.
• Miniature horses appear to be at
higher risk of complications from
ECoV infection.
May occur as an individual case
or outbreak
- Fever up to 105° F (40.5° C)
- Leukopenia characterized by
neutropenia and lymphopenia
(can be severe)
- Inappetance
- Lethargy
- Diarrhea (consistent finding)
- Scant fecal production
- Colic
Complication that occur in rare
cases:
- Hypoproteinemia
- electrolyte and metabolic
derangements secondary to
intestinal inflammation
- Hyperammonemic
encephalopathy (lethargy,
obtundation, wandering, ataxia,
seizures)
- Death secondary to septicemia
IP: frequently as short as 24
hours and may be up to 3 days
- Fever up to 106°F (41.1°C)
- depression
- anorexia
- muscle pain/weakness
- Dry, harsh cough (sometimes
paroxysmal, can last up to
6wks.) usually precedes fever
- Nasal discharge is initially
serous, but rarely may become
mucopurulent with secondary
bacterial infections
- Secondary bacterial
infections are very common
in influenza affected horses
- Slightly enlarged
retropharyngeal lymph nodes
Rare clinical signs:
- distal limb edema
- cardiomyopathy
Clinical signs are usually present
3-5 days after exposure (i.e. 3–5
day incubation period)
Clinical signs are more common,
and more severe, in younger
horses; ages 1–5yo.
Older horses usually have milder
disease.
DIAGNOSIS | DIFFERENTIAL
DIAGNOSIS
• Presence of clinical signs
compatible with ECoV infection
• Detection of ECoV in feces
• Consistent hematological
abnormality observed is
leukopenia due to neutropenia
and/or lymphopenia
• Polymerase Chain Reaction
(PCR) – feces is used as
sample
• Post-mortem diagnosis
CARRIER STATUS
Carrier status is currently
unknown but subclinical horses
(horses with no clinical signs)
have been found to shed the virus
in feces, and likely serve as silent
reservoirs for infection.
• Virus isolation from
nasopharyngeal swabs.
• Real time PCR (RT-PCR) from
nasopharyngeal swabs (EDTA
blood is NOT an acceptable
sample)
• Immunoassay—stall-side kit
• Antigen capture ELISA
• Serology
TREATMENT
- supportive care based on the
clinical signs
- Severe cases may require
hospitalization for intravenous
fluid treatment, colloid support,
and/or correction of electrolyte
and metabolic derangements.
PROGNOSIS
Exposure to the virus can result in
up to 85% infection rate but most
animals do not show clinical
signs.
Mortality is generally low.
PREVENTION AND CONTROL
• There are currently no vaccines
for EcoV
• Minimizing contact between at-
risk horses
• Maintaining high standards of
sanitation
• Careful disposal of manure
Biosecurity
Horses positive for ECoV should
be isolated and strict biosecurity
measures and manure
management instituted to prevent
the spread of infection to other
horses in the vicinity.
Personnel working with infected
horses should use disposable
gloves and personal protective
equipment (gowns, boot covers)
and wash hands thoroughly with
liquid hand soap and water
followed by 70% ethanol hand
sanitizer after handing sick
animals.
Release of animals from
isolation
Clinical and subclinical horses
should remain in isolation until
fecal PCR negative.
Zoonotic Potential
No known zoonotic potential.
However, standard hygiene
precautions and use of personal
protective equipment should be
utilized with any diarrheic patient
due to risk of coinfection with
zoonotic agents.
Vaccination
• Booster vaccination of healthy
animals in primary and
secondary contagion control
perimeters is likely to be of
value, and is not known to result
in complications. While annual
vaccination is currently
recommended, more frequent
vaccination is recommended for
young horses and specific
equestrian facilities and
organizations that require more
frequent (biannual) vaccination
• If animals are unvaccinated
prior to an outbreak, the use of
a modified live intranasal
vaccine is recommended as this
can achieve protection within 5
days of primary administration
Isolation and Biosecurity
• Any horse showing clinical signs
of any respiratory disease
should be immediately isolated
and standard respiratory
biosecurity guidelines should be
followed until a diagnosis is
confirmed
cole.

Formerly known as: Equine
rhinoviruses
Family: Picornaviridae
Genus: Aphthovirus (ERAV grp)
Erbovirus (ERBV1-3)
Genera: Equine Rhinitis A virus
(ERAV) and Equine Rhinitis B
virus (ERBV)
Strand: ss RNA viruses
Serotypes:
•ERAV
(formerly known as Equine
rhinovirus1)
Equine Rhinitis Viruses • ERBV1
• (formerly known as Equine
rhinovirus 2)
• ERBV2
• (formerly known as equine
rhinovirus 3)
• ERBV3 (formerly known as
acid-stable picornavirus).
- have been considered to be of
relatively low importance
among respiratory viruses and
were believed to cause only
mild upper respiratory disease
in the horse.
ENVIRONMENTAL
PERSISTENCE
• Virus can remain viable for up to
2 days on contaminated fomites
and solid environmental
surfaces like stall latches.
• In water, virus viability has been
reported up to 3 days. (Viability
in water is temperature
dependent; accordingly, viability
may be longer than 3 days in
cold water. Freezing water may
inactivate virus.
• Can survive in aerosols for
several hours and on hands for
a few minutes
ZOONOTIC POTENTIAL
• None known, but strains of
H3N8 virus can infect canines.
• Evidence implicating duck and
equine influenza viruses as
possible progenitors of the Hong
Kong strain of human influenza.
• The OIE document on EI also
states: There is little risk to
public health. In experimental
settings, the virus has shown
the ability to infect humans, and
a few people in contact with
infected horses developed
antibodies to equine influenza
viruses, but no humans exposed
to the virus have become ill.
• Another OIE reference states:
While equine influenza has not
been shown to cause disease in
humans, serological evidence of
infection has been described
primarily in individuals with an
occupational exposure to the
virus. During 2004–2006
influenza surveillance in central
China (People’s Rep. of) two
equine H3N8 influenza viruses
were also isolated from pigs.
Transmission of equine rhinitis
virus (ERAV and ERBV) has not
been well documented, largely
due to a lack of virus identification
in infected individuals and an
impression that it is of clinical
insignificance.
However, it is believed to be
similar to that of other equine
respiratory viruses.
• spread through groups of
horses in aerosolized secretions
dispersed by coughing
• Both direct contact and indirect
(fomite)
• contact with nasal secretions
are also likely routes of
infection.
POST-MORTEM
- It is very rare that equine
influenza infection would result in
a fatal outcome.
- Gross pathologic findings:
- bronchiolitis,
peribronchiolitis and
subacute interstitial
pneumonia.
SHEDDING
Shedding period: 7–10 days post
infection; not post resolution of
clinical signs.
(In most cases, virus shedding is
no longer occurring by the time
clinical signs resolve)
- An increase in body
temperature, 12 hours after
infection
- Swollen and painful
submandibular lymph nodes
- Seromucoid nasal discharge,
which progresses to
mucopurulent discharge (due to
bacterial involvement) on Day 5
to 7
- Serous ocular discharge
- Dry cough
- Occasionally lower leg swelling
- Some increase in respiratory
rate with increased bronchial
sounds on auscultation
- Reduced feed consumption
during the febrile phase.
ERVs are definitively diagnosed
by:
• Virus isolation
• RT-PCR testing
• Serology
Virus Isolation
• Nasal and nasopharyngeal
swabs are collected from horses
to attempt virus isolation when a
respiratory outbreak occurs.
• Samples collected through
bronchoalveolar lavage have
been used to attempt viral
recovery, in addition to lung
cytology and airway
immunologic assessment.
• Samples such as:
• whole blood
• tracheal biopsy specimens
• urine
• feces
• —are rarely collected for
virus isolation
• Treatment is mostly
symptomatic.
• For Acute form: is limited to
administration of a non-steroidal
anti-inflammatory agent to
control the fever and
concomitant administration of
antibiotics to minimize
secondary bacterial infections.
• Rest from daily exercise is also
as important since complete
repair of the mucosal epithelium
destroyed by the virus will take
at least 21 days.
• Any exercise prior to this will
cause prolonged
inflammation that can affect a
horse’s performance for the
rest of its life.
• Rest can include turnout,
which is preferred to get the
horse out of the dusty, moldy
environment of a stall.
Release of animals from
isolation:
• Maintain isolation procedures
(primary perimeter) for 21 days
after resolution of last suspect
case of new infection.
For horses having been housed
within a primary perimeter (i.e.
any horse housed in a
barn with a horse that showed
respiratory clinical signs):
• Isolate from the general equine
population for 14 days
For other horses:
• Vaccination requirements may
be considered when disease risk
is elevated
• Certificate of Veterinary
Inspection (CVI) specifications -
disclaimer regarding disease
exposure within a specified
interval of time
• Isolate all horses returning from
shows, exhibitions, or trail rides
for 10–14 days.
•Easily killed by many
disinfectants. Antec Virkon S with
potassium peroxymonosulfate
and sodium chloride killed EIV
regardless of time, temperature or
presence of organic matter
• Alcohol hand sanitizers are
effective against influenza
viruses.
• No commercial vaccines were
available to vaccinate for ERVs.
• More recently, a conditional
license has been issued for
Equine Rhinitis
A Vaccine, killed virus.
• Horse owners have historically
been and continue to be skeptical
about the efficacy of vaccines for
equine influenza virus and equine
herpesvirus. However, recent
findings have indicated that it is
often other viruses (such as
ERVs), which occur
concomitantly during respiratory
outbreaks, that give the
appearance of vaccine failure.
• Correct diagnosis of the cause
of individual respiratory events
should make horse owners more
confident that the vaccines are
effective.
cole.
 - Previous nomenclature has
caused confusion between the
terms “rhinopneumonitis” and
“rhinovirus infection.”
- Rhinopneumonitis, which is
caused by equine herpesvirus
infection, is not the same as
equine “rhinovirus” infection.
• Recent worldwide surveillance
and seroprevalence
investigations have
demonstrated that these viruses
are highly prevalent in the horse
population (with prevalence
ranging from 20% to 70%) and
are actively associated with
clinical respiratory disease.
• ERVs have not been well
characterized, and their role as
an active entity in clinical
respiratory disease is ill defined.
• ERAV, the most seroprevalent
serotype among horses, was
first documented in 1962 in the
United Kingdom and was
subsequently recognized
globally.
• There is sufficient evidence that
ERVs have circulated within the
horse population for decades,
and viral coinfection may play
an important role in viral
respiratory outbreaks.
• The presence of an ERAV
noncytopathic strain has been
reported in recent years. This
strain was implicated in clinical
respiratory disease when no
other viral agents could be
identified.
• Surveys of ERVs are clustered
in the United Kingdom, Canada,
• Australia, the United States,
Japan, New Zealand, and
Germany.
- it is a contagious viral disease
of equids
- Serological evidence of
exposure to the causal agent,
equine arteritis virus (EAV), is
present in equine populations in
many countries.
- The name equine viral arteritis
comes from the characteristic
vascular lesion that is produced
by the causal agent equine
arteritis virus.
- Infection with EAV is highly
species-specific
Equine Viral Arteritis - It is limited to members of the
family Equidae (includes
horses, donkeys, mules, and
zebras).
- The virus replicates primarily in
equine macrophages and
vascular endothelial cells
resulting in the characteristic
pathologies.
Respiratory (most common)
-Droplet spread of respiratory
secretions from acutely infected
horses and congenitally infected
newborn foals
Contact with placental
membranes, fetal fluids and
tissues from cases of EAV
abortion
Venereal transmission
Acutely infected stallions or
mares.
- Virus present in infective fresh,
cooled, or frozen semen
- Carrier stallions act as a
reservoir of EAV and can become
chronic carriers and maintain the
virus in the horse population
-There is limited evidence of
transmission by embryo transfer
from a donor mare inseminated
with EAV-infective semen
VIRAL SHEDDING
- originally recovered from feces
- Commonly isolated from equine
respiratory samples and, on
rare occasions, recovered from
saliva, peritoneal fluid, urine,
and plasma.
- Only ERAV has been
recovered from samples other
than respiratory secretions,
whereas ERBV1 seems to be
recovered solely from
respiratory samples.
- It is debatable whether ERAV
replicates only in the upper
airways because there are
limited studies on this subject.
Studies in 1992 and 2010
suggested that ERAV may
replicate and persist in the
urinary tract; however, the
evidence is inconclusive.
- As previously reported, the viral
load in fecal samples may be
minimal, and current field and
experimental investigations
have not further characterized
and explored viral replication or
shedding in the urinary and
gastrointestinal tracts.
- Recovery and detection of
ERAV from urinary and fecal
samples does not confirm viral
replication at those sites.
Incubation Period
Respiratory spreads: 2-3 days
Post veneral spread: IP usually
6-8 days but may be up to 14
days in some cases
- The disease is frequently
confused with other illnesses
that produce similar clinical
signs.
- Widespread vasculitis may
result in non-immune
individuals leading to fever,
peripheral edema, pneumonia,
and abortion.
- fever (up to 106° F or 41.1° C)
- depression
- anorexia
- Edema: limbs, ventrum, peri or
supraorbital region, scrotum/
prepuce (male), mammary
glands (female)
- Conjunctivitis
- Epiphora
- Rhinitis
- Urticaria
- Leukopenia
RT-PCR testing
• required to detect viral antigen
and nucleic acid in samples.
• A positive RT-PCR does not
necessarily indicate a current
viral infection. This laboratory
technique is highly sensitive and
could detect viral particles
remaining after an infection.
Serodiagnosis
• has been widely used as either a
confirmatory tool or primary
diagnostic method in horses and
other species.
• The virus neutralization (VN) test
has been used to determine
ERAV and ERBV antibody levels.
• A four-fold increase in antibody
titers to any viral antigen in paired
(acute and convalescent) samples
is considered significant in most
cases.
• As a rule, serum samples should
be collected at least 10 to 14 days
apart and should be analyzed as
a pair.
• Serum VN titers as low as 1:32
may indicate recent exposure.
Clinical Signs:
• Diagnosis based on clinical
signs is problematic due to the
wide array of clinical signs, the
similarity of presentation to
those of certain other diseases,
and the frequency of inapparent
infection/horses mildly affected
with disease.
• Equine arteritis virus should be
suspected whenever high fever,
peripheral edema, and signs of
upper respiratory infection
(oculonasal discharge) are
present.
• Diagnosis cannot be based
purely on clinical signs alone as
they are non- specific.
• Subclinical EAV infection is
difficult to determine.
Laboratory Testing:
- Virus Isolation
- RT-PCR testing, and/or
- Serological Examination of
Paired Sera
EAV is stable at refrigeration or
lower temperatures.
• No specific antiviral treatment
for EVA is currently available
• Symptomatic treatment is
indicated in moderate to severe
clinical cases of the disease,
and is especially important in
affected stallions
• Use of GnRH antagonist may
facilitate clearance in some
stallions
• Immunization with GnRH has
been associated with elimination
of the carrier state in some
animals.
• Programs to control outbreaks
of ERBV should focus on the
other aspects of infectious
disease prevention.
• Along with strict hygiene
measures, good management
practices at equine facilities to
prevent the introduction or
spread of disease includes
providing separate housing for
transient or newly introduced
animals and for the isolation of
infected animals.
• Rapid tests to confirm the
diagnosis should be performed
whenever possible, and
quarantine of suspected cases
should be carried out.
• Biosecurity Guidelines
• Control measures are primarily
directed at restricting
viral spread in breeding
populations to:
a) minimize risk of virus-related
abortions, deaths in young foals
and
b) prevent establishment of the
carrier state in stallions and
sexually mature colts.
• Identify of any carrier stallions
• Separately manage any
carrier stallions
• Vaccinate non-carrier
stallions annually
• Restrict breeding carrier
stallions to EVA vaccinated mares
or mares naturally seropositive for
antibodies to EAV
• Isolate mares bred with infective
semen for the first time from EAV
seronegative horses for 3 weeks.
Indirect transmission
- Fomites such as breeding shed
equipment, phantoms,
contaminated twitches, head-
collars, clothing, and the hands of
animal care personnel
- Artificial insemination
- Semen
- Vaginal secretions
- Urine
- Feces
Congenital
- Infection in foals born to mares
infected in late gestation
Risk Factors:
• Inapparent carrier stallions shed
virus constantly in their semen.
• Fresh cooled or frozen semen is
highly infectious.
• Acutely infected shedding
mares and stallions (first-time
vaccinated mares bred to
infected stallions can experience
a limited reinfection cycle and
shed EAV).
- Abortion- can be associated
with ‘abortion storms’
- Temporary subfertility in
stallions
- Fatal pneumonitis or pneumo-
enteric syndrome in neonatal/
young foals
SHEDDING
• Carrier stallions shed EAV
constantly in semen, but not via
the respiratory tract, in urine, nor
is it present in blood.
• Only stallions and sexually
mature colts can develop the
carrier state.
Differential Diagnosis
• EHV-1&4
• Equine influenza
• Equine rhinitis virus A & B
infections
• Purpura hemorrhagica
• Equine infectious anemia
• Allergic reactions
• Toxicosis from ingesting hoary
alyssum (Berteroa incana)
POST- MORTEM
• EAV infection rarely results in a
fatal outcome in horses;
however, it can be associated
with isolated cases or outbreaks
of multiple cases of abortion.
• Evidence suggests lethal EAV
infection of the fetus is the
cause of abortion.
• Because the aborted fetus
contains high levels of virus, all
appropriate biosecurity
precautions should be taken to
limit spread of the virus.
• Screen semen intended for AI
use for virus, particularly if
imported
• Observe sound management
practices, especially of
pregnant mares
• Vaccinate colt (male) foals
between 6 and 12 months of
age to prevent possible
development of carrier state
later in life Under circumstances
of intensive management and
limited facilities, it is advisable
to consider vaccination of all at-
risk animals
OTHER CONTROL MEASURES
• For horses having been housed
within the primary perimeter:
• Certificate of Veterinary
Inspection w/ affidavit
indicating that within the
previous 21 days the horse
has not exhibited signs of
EVA, has not been exposed
to nor housed with horses
that exhibited signs of the
disease, or were suspected
or confirmed as being
infected with EAV.
• For other horses:
• Require health certificate w/
disease specific disclaimer and
proof of vaccination.
• Mares or fillies shipping from a
premise of exposure should
follow the requirements as
listed for exposed and
unexposed individuals as
above.
• Breeding farms:
• Colts and stallions should also
follow these restrictions (in
addition to any State veterinary
restrictions) if these animals are
to enter the breeding
population.
ENVIRONMENTAL
PERSISTENCE
The virus is heat sensitive but can
persist at freezing temperatures
for extended periods of time.
 CONSIDERATION
• Primary vaccination provides
protection from clinical disease
for at least 1–3 years.
• First time vaccination may not
prevent re-infection or potential
replication of challenge virus
• Revaccination results in an
enhanced serologic response
• It is recommended that at-risk
stallions be re-vaccinated
annually
• Stallions must be screened
serologically before primary
vaccination implications
regarding export must be
considered when vaccinating at
risk horses
• Currently it is not possible to
differentiate a vaccinated horse
from one naturally infected via
serology
• ‘Pony’ horses/outriders’ horses/
catch horses (or those with
close contact to multiple
horses) should be vaccinated or
withdrawn from use until
vaccinated
• Approximately 50% of
vaccinated horses may
experience a brief period of
viremia during the week
following vaccination and some
may shed low levels of virus
into the respiratory tract for a
few days.
• Risk of respiratory transmission
of vaccine virus is very minimal.

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