Overview:
West Nile Virus
By: Erika Beck
History:
West Nile virus is a mosquito-borne virus. The first case
of West Nile Virus was isolated from an adult woman in the West Nile District
of Uganda in 1937. There were outbreaks
recorded in Egypt in the 1950s, but it wasn’t until the outbreak in Israel in
1957 where the virus finally became recognized as a cause of severe human
meningitis or encephalitits (inflammation of the brain and spinal cord). The first equine case of the disease was
noted in the early 1960s in France and Egypt.
West Nile Virus did not appear in the United States until
August 1999. The first outbreak of the
virus in the United States occurred in New York City, where 62 people were
diagnosed with the disease, seven of which died. In October 1999, the first equine case of West
Nile Virus was diagnosed. Twenty-five
horses in Long Island, New York were diagnosed, nine of which died or were
euthanized from the disease. The virus, quickly
spread to Pennsylvania; having a confirmed case within a year of the first
reported in the United States. WNV quickly spread down the Eastern United States. Since then, horses have tested positive
throughout the US and in Canada. Of the
horses that are exposed to the virus, some may not show signs, but of those
that have clinical signs 35% are euthanized or die due to the virus.
Transmission:
The vector of transmission for West Nile Virus is the Northern
House Mosquito (Culex pipiens). Birds are the reserviors for the virus. Bird reservoirs will sustain an infectious
viremia for 1-4 days after the initial exposure, after which the host will
develop lifelong immunity. The virus is
maintained or cycles between vectors, amplification occurs within these
species. Vertical transmission must also
occur within these species for maintenance of the virus within the geographic
area.
Transmission of West
Nile Virus occurs when the uninfected mosquito takes a blood-meal from an
infected bird. The mosquito than becomes infected and proceeds to take a blood-meal
from another animal, such as a horse or a human, where it is injected upon the
meal and can multiply and cause disease.
The incubation period, the time between exposure to the
virus and the appearance of first signs, is thought to be between 3 and 15
days. Horses and humans are considered
“dead end” hosts. A “dead end” host
means that there are so few virus particles in their blood stream that a
mosquito cannot accumulate enough of the virus when taking a blood meal to
transmit the infection to anything else.
The mosquito must take a blood meal from a bird that is infected in
order to transmit the virus to another.
There are at least 326 species of birds that the virus
has been detected within. Although most
birds live, crows and jays seen to be more susceptible to complications from
the virus and they can become ill and die.
While there is no direct transmission between or amongst other species,
there has been direct contact transmission among caged crows.
While there is no evidence that suggests a
person-to-person transmission or even an animal-to person or horse-to-horse,
caution should still be used when handling species with the infection. Risk of transmission is no reason to
euthanize a horse just because it has been infected with West Nile Virus. In fact, evidence has been presented stating
that the virus is only present in the horse’s blood stream for a few days
during the entire course of the infection.
In the “dead end” hosts, the virus is not amplified and there is not
sufficient amount of virus to infect mosquitoes. It should also be noted that even in areas
that have high reports of West Nile Virus; it is unlikely that one bite from an
infected mosquito will be enough to cause the disease. Less than 1% of people who get bitten become
infected and will get seriously ill.
Other transmission of West Nile virus has been found in
North America. This consists of oral
ingestion and oral and cloacal shedding, and blood transfusion. The oral ingestion has been proven in both avian
and mammalian hosts and the oral and cloacal transmission has been proven in
birds. Blood transfusion can be a
possible source if donors are viremic.
Global Climate Change Impacts in the United States, 2009 Report
Clinical
Signs:
West Nile virus presents with many clinical signs, most
of which are correlated with central nervous system and cause encephalitis. West Nile Virus interferes with normal
central nervous system functioning causing inflammation of the brain. The most common clinical signs including lack
of coordination and stumbling, weakness, ataxia, muscle twitching or
tremors. Other clinical signs such as
altered mental state, hypersensitivity to touch or sound cataplexy or narcolepsy,
seizures, blindness, cranial nerve deficits, recumbency and fever may appear. When severe clinical signs affect horses,
many die as a result of the infection or are euthanized as a result of
secondary complications. The risk of
West Nile infection is not age dependent.
Foals as young as 3 weeks of age have been confirmed to have the viral
infection. However, the risk of the
infection seems to increase with age.
Research shows this is likely due to elderly horses having a decreased
antibody titer. Horses over the age of 10 years have an age dependent decrease in neutralizing
antibody response after the vaccination is administered.
There are two proposed routes of neuroinvasion in the
horse. The first has West Nile virus
causing a low-level viremia followed by replication in the lymph nodes and
entry into the CNS across the blood-brain barrier. The second proposes transaxonal transmission.
Flaviviruses cause polioencephalomyelitis (inflammation
of the grey matter) with lesions that increase in number from the diencephalon
through the hindbrain and frequently increase in severity caudally through the
spinal cord.
Diagnosis
and Treatment:
Diagnosis of West Nile Virus infection in horses involves
testing the blood serum for antibodies against the virus. The laboratory diagnostic testing involves
the testing of serum or cerebrospinal fluid (CFS) to detect virus-specific IgM
and neutralizing antibodies. There are
four snap tests that have been FDA approved ELISAs. The ELISA kits are testing for IgM with
use of serum. The kits are to aid in
presumptive diagnosis based on laboratory signs and clinical symptoms of
meningitis or encephalitis. All positive
snap test results should be confirmed by additional testing at a state health
department. It is important to consider
vaccination status prior to interpreting the blood results since most horses are vaccinated for West
Nile Virus, especially for mares and foals. Vaccinated horses and foals
of positive-testing mares are likely to be positive for the virus. Veterinarians must confirm blood test
results, clinical symptoms, and the possibility of other neurologic diseases
when making a diagnosis. In cases that are fatal, the tissues upon autopsy can be
useful for nucleic acid amplification, hisopathology with immunohistochemistry
and virus culture of the tissue. The drawback is only a few state laboratories
are capable of the specialized tests.
Currently, there is no specific treatment for West Nile
encephalitis in horses. Supportive care
is recommended to help reduce clinical signs and help prevent secondary
infections such as joint and tendon infections, sheath infections, pneumonia,
and diarrhea. The main focus of the
treatment should consist of decreasing brain inflammation. Treatment should start with reducing the
fever and providing supportive therapy. Fluid therapy and oral or intravenous feeding should be started for horses
unwilling to drink and eat. For horses
unable to rise, a sling may be recommended to alleviate pressure points caused
from lack of circulation. Head and leg
protection is also needed frequently. Some
horses contract West Nile Virus but never show any clinical signs or have mild signs;
these horses will develop antibodies in response to the infection. The infected horses can acquire long lasting
immunity to the virus after recovery due to these antibodies. Encephalitis is the most severe sign, there
may not be full recovery and the horse may possibly have permanent CNS damage.
Recovery time is dependent upon health and age of the
horse affected. Many with improve within
5-7 days, however the horses that show severe neurologic deficits may take
several weeks to decrease the clinical signs.
Horses unable to rise are given poor to grave prognosis. Once the horse begins to show significant
improvement, full recovery is expected in 1 to 6 months and can be expected in
90% of the patients.
Prevention:
In order to protect horses from West Nile virus, there
are vaccines available. The initial
vaccination is a series of 2 shots; given 3 to 6 weeks apart prior to the start
of mosquito season (June to December).
It is not until 6 weeks after the second shot the horse is considered to
be fully protected. After the initial
vaccinations are complete, horses should at least receive a yearly booster
annually. Horses that are stressed such
as show and race horses should have two boosters annually, in April and
July.
Prevention of exposure to mosquitoes is the best method
to decrease risk of exposure. Practices such as housing horses indoors during
peak period or mosquito activity (dusk and dawn), avoid turning on lights
inside stable during evening and overnight, removing birds and chickens around
stables, use black lights because they don’t attract mosquitoes well, eliminate
areas of standing water, use of topical repellents, fans, etc. The most important of all prevention is to
reduce breeding sites. This primarily
includes removing standing water from the premises or anything not in use that
may collect water. Anything that can
hold water for more than 4 days needs to be drained and changed to help reduce
mosquito breeding. Preventing exposure will
help to reduce potential infection.
Public
Health Considerations:
West Nile Virus is considered a zoonotic disease. A bird reservoir maintains the virus life
cycle. Again, there is very little risk
to direct contact transmission, the greatest risk is with postmortem
transmissions from handling infected tissues.
Differentials:
Venezuelan (VEE), Eastern (EEE), and Western (WEE), and
Japanese (JE) and West Nile Virus.
Resources:
