Overview: West Nile Virus

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:

Comerford, Pat. "West Nile Encephalitis in Horses." . N.p., 2008. Web. 14 Apr 2012. http://pubs.cas.psu.edu/freepubs/pdfs/un008.pdf.

Smith, Keith. "Extension Fact Sheet." What Horse Owners Should Know About West Nile Virus. N.p., 2008. Web. 14pr 2012. http://ohioline.osu.edu/wnv-fact/pdf/1007.pdf.

“CDC.” Vertebrate Ecology. N.p., 2009. Web. 14 Apr 2012. http://www.cdc.gov/ncidod/dvbid/westnile/birds&mammals.htm

 “Global Climate Change Impacts in the United States." Report 2009. N.p., 2009. Web. 27 Apr 2012. http://nca2009.globalchange.gov/west-nile-virus-transmission-cycle.