|West Nile Encephalitis In Horses |
West Nile Virus (WNV) encephalitis is a viral disease that
is relatively new to the United
States. The disease gets
its name from the West Nile District of Uganda in Africa
where it was first recognized in humans in 1937. The first
cases of WNV infection in horses were recognized in France
in the early 1960’s. WNV infection was known to occur in
Africa, the Middle East
and parts of southern Europe, but the
virus was not isolated in the U.S.
until 1999, when an epidemic of WNV encephalitis and aseptic
meningitis was diagnosed in New York City.
Concurrent epizootics occurred in horses on Long
Island and in birds. The close genetic relationship
between WNV isolates from Israel
and New York
suggests that the virus was imported into North
America from the Middle East.
It is not known how the virus came to the U.S.
but, given the location of the first outbreak, it is likely
that it arrived via airline or boat in an infected bird or
WNV is a member of the Japanese encephalitis virus complex
of the genus Flavivirus, family Flaviviridae. This
genus includes nine viruses distributed around the world.
In the U.S.,
the complex has two other representatives, Powassan and
St. Louis Encephalitis viruses, both of which cause encephalitis
in humans. In 1999, 9 of 25 (36.0%) horses from Long
with clinical signs of the disease died or were euthanized.
In 2000, 60 cases of WNV were reported in horses from 7
states, and 23 (38.3%) horses either died or were subjected
to euthanasia. In 2001, 640 confirmed cases of WNV infection
in horses were reported from 20 states, and 156 (24.4%)
horses either died or were euthanized.
Wild birds of many different species are the reservoir
for WNV. The virus is transmitted by mosquitoes who acquire
it from infected birds. Horses and humans are considered
accidental or dead-end hosts. A mosquito that has fed on
an infected bird can bite people or horses (or other mammals)
and transmit WNV to them. Infected birds may die from the
disease though most avian species are resistant. Consequently,
birds may have the virus circulating in their bloodstream
for some time (viremic stage) allowing further infection
of other mosquitoes, but they do not develop symptoms of
illness. Horses and humans only develop a low-level and
transient viremia, thereby diminishing the importance of
their role in the transmission cycle of the virus.
Persistence of the virus in migrating birds is considered
to be one of the main factors in the spread of the disease.
At least 17 species were affected in 1999 and 76 in 2000,
particularly the American crow. The signs of illness in
these birds include convulsions, tremors, head tilt, wing
drop, paralysis, loss of balance, and circling. Less specific
signs, such as weakness and lying on the chest, may also
be observed. Although as many as 40 species of mosquitoes
are potential hosts and 14 different species were identified
as carriers of the virus in the U.S.,
the primary species involved are Culexpipiens
The incubation period of WNV infection is usually
5-22 days. Clinical signs in affected horses may include
both central and peripheral nervous system signs, consisting
most frequently of ataxia, lack of interest in surroundings,
weakness of limbs, muscle fasciculation, and loss of appetite.
Horses may become recumbent and may be unable to get up
without help. Some horses may develop fever. The target
organ of the virus is the brain and spinal cord where it
causes inflammatory reaction (encephalitis), manifested
by variable neurological signs. Affected horses, which
show no progression of gait abnormalities, usually recover
completely with no consequences within 5-15 days.
The clinical signs of the disease may be indistinguishable
from other equine encephalitides including rabies, equine
herpes virus-1, equine protozoalmyeloencephalitis, and Eastern,
Western, or Venezuelan equine encephalomyelitides. Therefore,
diagnostic tests are necessary for a definitive diagnosis.
Whole blood, serum, and cerebrospinal fluid (CSF) should
be submitted to the National Veterinary Services Laboratory,
through Purdue ADDL, with a complete history of the case.
If the animal presented rapidly progressive neurologic signs
including recumbency, it should be submitted to ADDL requesting
rabies and WNV testing. Field postmortem analysis should
follow USDA guidelines.
There is no specific treatment for WNV encephalitis.
General supportive care should be provided. Regardless
of the treatment, horses that survive usually recover quickly.
A new vaccine is available for prevention of WNV infection
in horses. It is a killed vaccine which must be given in
two doses initially, with an interval of three to six weeks.
Both doses should be completed at least three weeks prior
to mosquito season. Efficacy data of the vaccine are not
available at this time; however, the vaccine is considered
to be safe.
Since mosquitoes are associated with WNV transmission,
the key for preventing or controlling future outbreaks of
WNV among horses is to control mosquito populations and
prevent horses from being exposed to these insects. Recommendations
include reducing mosquito breeding sites, providing screened
housing, using insect repellants, and reducing outside exposure
of the animals. Horse owners also need to watch for dead
birds, particularly crows, on their property. Presence
of the virus in a given area may be first indicated by seeing
dead birds in the vicinity. Crows are particularly susceptible.
Diagnosis of WNV can be determined by submitting dead birds
to the ADDL or the Indiana Department of Health.
Testing at this time is limited to crows,blue jays or
raptors as these are the species most susceptible to the
-by Rajeev Nair, ECFVG Student
-edited by Dr. Ingeborg Langohr, ADDL Graduate student
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