West Nile Virus
West Nile Virus - Jul 20th, 05
A Bayer HealthCare Animal Health Brochure
Controlling the risk to your horse
How It Began
First isolated in Uganda in 1937, West Nile virus (WNV) is a virus that is transmitted principally by various species of mosquitoes and can cause inflammation of the brain and spinal cord (encephalomyelitis). Clinical disease caused by this virus is seen primarily in birds, equines and humans and very infrequently in goats, sheep, dogs, llamas, various reptiles and bears, among other species. Prior to its discovery in the northeastern U.S. in 1999, WNV was widely distributed in Africa, the Middle East, southwest Asia and parts of Europe.
West Nile virus was first recognized in the western hemisphere in September 1999, when it was isolated from the tissues of sick flamingoes and pheasants at the Bronx Zoo and from dead crows in the New York City area. By 2002 over 15,000 horses were diagnosed with West Nile Virus in 41 states.
Like Eastern and Western equine encephalomyelitis viruses, which historically have been identified with sleeping sickness in humans and equines in the U.S., WNV circulates in nature between birds and mosquitoes. Various species of birds serve as amplifying hosts of the virus, with at least 36 species of mosquitoes acting as vectors of WNV and transmitting it to a wide range of species. The strains of WNV present in North America are capable of causing disease in certain domestic and exotic species of birds, especially crows and blue jays, in which the infection is usually fatal. Humans, horses and a diversity of other mammalian species can also be infected with WNV. WNV infection in mammals does not result in large amounts of the virus in the bloodstream, as is seen in various bird species. This is important in terms of disease transmission. Because there is only a very small amount of the virus in the blood of infected horses, mosquitoes are unable to transmit the virus from horse to horse or from horse to human. The virus is transmitted when a mosquito takes a blood meal from an infected bird, then feeds on a horse. During the process of taking a blood meal from the horse, the virus is transmitted by the infected mosquito.
Horses and humans can become clinically affected by WNV. Typical of numerous other viral infections, many horses experience no clinical illness following exposure to the virus for the first time.
In horses infected with WNV, the virus may breach the blood-brain barrier and damage the brain and spinal cord. While the clinical signs of WNV encephalomyelitis can vary in range and severity, those most frequently observed include incoordination or ataxia (especially of the hind limbs); twitching of the muzzle and lower lip; and twitching of the muscles in the neck, shoulders or pectoral region. Signs may be bilateral or unilateral. Also reported are behavioral abnormalities (e.g., depression or heightened sensitivity to external stimuli, stumbling, toe dragging, leaning to one side and in severe cases, paralysis of the hindquarters, recumbency, coma and death. Other clinical signs that may be noted include fever, generalized weakness, impaired vision, inability to swallow, aimless wandering and convulsions. The nature and severity of clinical signs depend largely on the area(s) of the central nervous system affected by the virus and the extent of damage. The incidence of disease tends to be greater in older horses, where a favorable clinical outcome is less likely.
Diagnosis of WNV encephalomyelitis is usually based on the nature of the clinical signs displayed by an affected horse together with the detection of antibodies to the virus in the blood by laboratory examination. It is important to emphasize that many of the clinical signs of WNV encephalomyelitis closely resemble those observed in a number of other equine neurological diseases (e.g., Eastern equine encephalitis, rabies, equine protozoal myeloencephalitis, equine herpesvirus-1 and botulism) from which it must be distinguished.
At the present time, there is no specific anti-viral treatment for WNV encephalomyelitis. Management should focus on controlling pain and inflammation. Anti-inflammatory drugs should be provided as soon as possible to control inflammatory changes in the central nervous system. Other supportive measures such as intravenous fluids, sedatives and nutritional support can be important components of therapy. It is important to consult your veterinarian immediately if you suspect your horse is affected with WNV encephalomyelitis so that the appropriate treatment measures can be implemented without delay.
A number of measures can be taken to help protect your horse against WNV. These are comprised of management strategies to reduce exposure to mosquitoes and immunizing against the disease. Horses vaccinated against Eastern, Western or Venezuelan equine encephalomyelitis are not protected against WNV. In February 2003, a vaccine was licensed by the USDA’s Center for Veterinary Biologics for use in healthy horses. The vaccine has been used extensively to prevent WNV infections in horses.
The vaccine should be administered as a series of two doses given three to six weeks apart. Foals should receive three immunizations starting at 6 months of age if the mare was immunized against WNV 30 days prior to foaling. The duration of immunity from vaccination is not known. It is recommended to vaccinate every four months in regions where the virus is active. Contact your veterinarian for the appropriate vaccination schedule for your location. In 2003, a recombinant canarypox vaccine was licensed for vaccination against WNV in horses. The vaccine has yet to be scrutinized in field conditions, but experimental studies reveal that it is protective against development of viremia involving WNV-infected mosquitoes.
Aside from vaccination against WNV, other measures should be taken to reduce the risk of your horse being bitten by a virus-infected mosquito. Concerted efforts should be made to eliminate or reduce potential mosquito breeding sites by disposing of old receptacles, tires and containers and eliminating areas of standing water on farms or at racetracks and wherever horses congregate.
Clean clogged roof gutters and turn over plastic wading pools or wheelbarrows when not in use. Thoroughly clean livestock watering troughs at least monthly. When it is not possible to eliminate particular breeding sites, measures should be taken to control mosquito populations through the selective use of larvicides and, under special circumstances, adulticides. Such action should only be taken, however, in consultation with your local mosquito control authority. If the application of such preparations is not advisable, use a species of fish that feed on mosquito larvae before they hatch. Keep horses indoors during peak mosquito activity periods (dusk to dawn). Screen stalls (if possible) or at least install fans over the horses to help deter mosquitoes. Avoid turning on lights inside the stable during the evening or overnight. Because mosquitoes are attracted to light, placing incandescent bulbs around the perimeter of the stable will attract mosquitoes away from the horses. Lights can also be used to draw mosquitoes to electric bug zappers.
The use of insect repellant that contain pyrethrin on horses can also reduce the chance of being bitten by mosquitoes. Remove any birds (including chickens) located in or close to a stable. Some veterinarians have success by hanging cattle ear tags on horse halters. These ear tags have been impregnated with insecticide and often reduce the effects of not only mosquito biting, but also midges and the effects of “fly-strike” dermatitis around the ears.
Because WNV can affect humans as well as horses, don’t forget to take actions to protect yourself as well. When outdoors in the evening, wear clothing that covers your skin and apply plenty of mosquito repellent.
You as a horse owner need to become well-informed of the potential consequences of infection with this virus, as with all diseases, and take appropriate measures to reduce the risk of transmission of WNV to your horse(s). Prevention is key to the control of this infection. You should consult your local veterinarian on how best to protect your horse(s) against this disease.
For more information, contact your veterinarian.
West Nile Virus Vaccination Guidelines
West Nile Virus - Jan 10th, 05
Information Updated March 2012
Developed by the American Association of Equine Practitioners
This information is intended as a supplement to the AAEP's Vaccination Guidelines (January 2008). Practitioners are directed to consult this publication as the following discussion is to be read in conjunction with those general guidelines for vaccination.
West Nile virus (WNV) infection was first diagnosed in horses in the United States in 1999 and is now an important consideration in the differential diagnosis of horses presenting with signs of neurologic disease in all areas of North America. West Nile virus, a flavivirus, was first identified as a cause of infection and fatal encephalomyelitis (inflammation of the spinal cord and brain) in horses and people in Egypt, Uganda and France in the early 1960s. Further epizootics of disease in horses have occurred in Morocco in 1996, Italy in 1998, France in 2000, and the United States from 1999 to the present. Since 1999, thousands of cases of equine West Nile Virus encephalomyelitis have been reported in the US, with an estimated 30 to 40 percent fatality rate. West Nile virus is now considered to be endemic in all areas of North America.
The flaviviruses, like the other encephalomyelitis viruses, are transmitted by mosquitoes, and infrequently by other bloodsucking insects, to horses, human beings, and a number of other mammals from avian hosts, which serve as natural reservoirs for these viruses in nature. Horses and humans are considered to be dead-end hosts of the West Nile virus and, therefore, do not contribute to the transmission cycle. The virus is not directly contagious from horse to horse or horse to human. Similarly, indirect transmission via mosquitoes from infected horses is highly unlikely because horses do not experience a significant viremia (i.e. they have negligible amounts of virus circulating in their blood).
The incubation period for West Nile virus in horses appears to be 3 to15 days. Clinical signs of WNV infection in horses may include fever, ataxia (stumbling or incoordination), depression or apprehension, stupor, behavioral changes, weakness of limbs, partial paralysis, droopy lip, teeth grinding, muscle twitching, muscle fasciculation, muzzle tremors, difficulty rising, recumbency (inability to rise), convulsions, blindness, or death. Data has supported that 40% of horses that survive the acute illness caused by WNV exhibit residual effects, such as gait and behavioral abnormalities that were attributed to the illness by owners, 6 months following diagnosis.
The variable clinical signs associated with WNV infection necessitate inclusion of many neurological disorders in the differential diagnoses. These include: rabies; equine protozoal myeloencephalitis (EPM); neurological equine herpesvirus-1; botulism; eastern, western and Venezuelan encephalomyelitis (EEE,WEE,VEE); heat stress; trauma; bacterial meningitis; cervical vertebral myelopathy (wobbler syndrome); myeloencephalopathy; and equine degenerative myelopathy.
Serologic tests (blood tests) used to diagnose WNV include plaque reduction neutralization (PRNT), virus neutralization, hemagglutination inhibition, complement fixation, ELISA and antigen (IgM and IgG) capture ELISA. The virus can also be identified in central nervous system tissue using techniques such as virus isolation, PCR and immunohistochemistry. The IgM-capture ELISA is currently the most reliable test for confirmation of recent exposure to West Nile Virus in a horse exhibiting clinical signs. Horses exposed to WNV typically develop a sharp rise in West Nile virus-specific IgM antibody that persists for 4-6 weeks after infection. Little IgM is demonstrated in horses that are recently vaccinated. The antibody measured by the PRNT is stimulated both by vaccination and recent exposure, making this test difficult to interpret in the suspect horse.
Risk of exposure and geographic distribution of West Nile virus vary from year to year with changes in distribution of insect vectors and reservoirs of the virus. Because of the unpredictable nature of those factors and the effects of the disease, it is recommended that all horses in North America be immunized against West Nile virus.
Preventive management practices may minimize the risk of the spread and transmission of West Nile virus from infected mosquitoes. Reduction of mosquito numbers and exposure can be achieved by reducing or eliminating stagnant or standing water in your area, removing old tires, keeping horses in the barns from dusk to dawn (prime mosquito feeding times), setting out mosquito traps, keeping air moving with fans, use of mosquito fish in water troughs and removing organic debris promptly. Chemical controls include the use of topical anti-mosquito repellent agents approved for the horse and use of mosquito dunks in areas of standing water.
Vaccination is the primary method of reducing the risk of infection from West Nile Virus to the horse, although clinical disease is not completely prevented. There are several licensed vaccines currently available. One is an inactivated (killed) vaccine, one is a recombinant canarypox vector vaccine, and the third is an inactivated flavivirus chimera vaccine. Vaccination with a two-dose series of any of these vaccines has been proven in an intrathecal challenge model to be effective in the prevention of viremia in experimentally infected horses 28 days after vaccination. In contrast, non-vaccinated control horses in that study developed both viremia and neurological signs. Earlier studies using mosquito and needle challenges also demonstrated protection against viremia in vaccinated horses. The results of the studies to date indicate high efficacy of vaccination. Given the widespread nature of the disease and efficacy of vaccination, WNV vaccination is recommended as a core vaccine for all horses in North America. Consult your veterinarian to discuss selection of the most appropriate vaccine and vaccination schedule for your horses.
Vaccination Schedules: (from AAEP’s Core Vaccine Guidelines)
Adult horses previously vaccinated Vaccinate annually in the spring, prior to the onset of the insect vector season.
For animals at high risk or with limited immunity, more frequent vaccination or appropriately timed revaccination is recommended in order to induce protective immunity during periods of likely exposure. For instance, juvenile horses (<5 years of age) appear to be more susceptible than adult horses that have likely been vaccinated and/or had subclinical exposure. Geriatric horses (>15 years of age) have been demonstrated to have enhanced susceptibility to WNV disease as well as those horses that are immunocompromised. Therefore, more frequent vaccination is recommended to meet the vaccination needs of these horses.
Booster vaccinations are warranted according to local disease or exposure risk. Protection against disease for 12 months is likely with all WNV vaccines. However, more frequent vaccination may be indicated with any of these products depending on risk assessment.
Adult horses previously unvaccinated or having unknown vaccinal history
Inactivated whole virus vaccine: A primary series of 2 doses is administered to naïve horses. A 4- to 6-week interval between doses is recommended. The label recommended revaccination interval is 12 months.
Recombinant canary pox vector vaccine: A primary series of 2 doses is administered to naïve horses with a 4- to 6-week interval between doses. The label recommended revaccination interval is 12 months.
Inactivated flavivirus chimera vaccine: A primary series of 2 doses is administered to adult horses with a 2nd dose given 3-4 weeks after 1st dose. The label recommended revaccination interval is 12 months or prior to the onset of the next vector season.
Pregnant mares
Limited studies have been performed that examine vaccinal protection against WNV disease in pregnant mares. While none of the licensed vaccines are specifically labeled for administration to pregnant mares at this time, practitioners have vaccinated pregnant mares due to the risk of natural infection. It is an accepted practice by many veterinarians to administer WNV vaccines to pregnant mares as the risk of adverse consequences of WNV infection outweighs any reported adverse effects of use of vaccine.
Pregnant mare previously vaccinated
Vaccinate at 4 to 6 weeks before foaling.
Pregnant mares previously unvaccinated
Initiate a primary vaccination series (see Adult horses previously unvaccinated) immediately. Limited antibody response was demonstrated in pregnant mares vaccinated for the first time with the killed vaccine. It is unknown if this is true for the other products. Vaccination of naïve mares while open is a preferred strategy.
Foals of unvaccinated mares
First dose: given at 3 to 4 months of age. Second dose: 4 weeks after 1st dose. Third dose: 60 day interval after 2nd dose.
Foals of vaccinated mares
Administer a primary 3-dose series beginning at 4 to 6 months of age. A 4- to 6-week interval between the first and second doses is recommended. The third dose should be administered at 10 to 12 months of age prior to the onset of the next mosquito season.
Data indicates that maternal antibodies do not interfere with this product; however protection from clinical disease has not been provocatively tested in foals.
Animals may be vaccinated more frequently with this product if risk assessment warrants.
Recombinant canary pox vector vaccine: Administer a primary 3-dose series beginning at 4 to 6 months of age. A 4- to 6-week interval between the first and second doses is recommended. The third dose should be administered at 10 to 12 months of age prior to the onset of the next mosquito season.
There is no data for this product regarding maternal antibody interference. Protection from clinical disease has not been provocatively tested in foals. Animals may be vaccinated more frequently with this product if risk assessment warrants.
Inactivated flavivirus chimera vaccine: Administer a primary 3-dose series beginning at 4 to 6 months of age. A 4- to 6-week interval between the first and second doses is recommended. The third dose should be administered at 10 to 12 months of age prior to the onset of the next mosquito season.
Animals may be vaccinated more frequently with the product if risk assessment warrants.
Foals of unvaccinated mares
The primary series of vaccinations should be initiated at 3 to 4 months of age and, where possible, be completed prior to the onset of the high-risk insect vector season.
Inactivated whole virus vaccine: Administer a primary series of 3 doses with a 30-day interval between the first and second doses and a 60-day interval between the second and third doses. If the primary series is initiated during the mosquito vector season, an interval of 3 to 4 weeks between the second and third doses is preferable.
Recombinant canary pox vaccine: Administer a primary series of 3 doses with a 30-day interval between the first and second doses and a 60-day interval between the second and third doses.
Inactivated flavivirus chimera vaccine: Administer a primary series of 3 doses with a 30-day interval between the first and second doses and a 60-day interval between the second and third doses.
Horses having been naturally infected and recovered
Recovered horses likely develop life-long immunity. Consider revaccination only if the immune status of the animal changes the risk for susceptibility to infection. Examples of these conditions would include the long-term use of corticosteroids and pituitary adenoma.
|
Foals/Weanlings |
Yearlings |
Performance Horses |
Pleasure Horses |
Broodmares |
Comments |
|
Born to unvaccinated mare:First dose: 3 to 4 months. Second dose: 30 days after 1st dose. Third dose: 60 days after 2nd dose. Born to vaccinated mare: First dose: at 4-6 months of age. 2nd dose: 4-6 weeks after 1st dose. Third dose: 10-12 months of age. |
Annual booster, prior to expected risk. Vaccinate semi-annually or more frequently (every 4 months), depending on risk. |
Annual booster, prior to expected risk. Vaccinate semi-annually or more frequently (every 4 months), depending on risk. |
Annual booster, prior to expected risk. Vaccinate semi-annually or more frequently (every 4 months), depending on risk. |
Annual, 4 to 6 weeks prepartum (see full text inguidelines). |
Annual booster is after primary series. In endemic areas, booster as required or warranted due to local conditions condusive to disease risk. Vaccinate semi-annually or more frequently (every 4 months), depending on risk. |
Note: As with the administration of all medications, the label and product insert should be read before the administration of all vaccines.
10 Tips for Reducing Your Horse's West Nile Risk
West Nile Virus - Sep 2nd, 03
Updated February 2012
Since first being recognized in the United States in 1999, West Nile virus (WNV) has posed a serious threat to horses and humans alike. In the equine population, the virus is transmitted when a mosquito takes a blood meal from a bird infected with WNV, then feeds on a horse.
While many horses exposed to WNV experience no signs of illness, the virus can cause inflammation of the brain and spinal cord. In some cases, especially in older horses, WNV can be fatal.
As a horse owner, prevention is the key to reducing your horse’s risk of contracting WNV. Follow these guidelines from the American Association of Equine Practitioners (AAEP) to protect your horse against WNV:
1. Vaccinate your horse against the disease with one of the available vaccines. Talk with your veterinarian about the most appropriate vaccination schedule for your horse.
2. Eliminate potential mosquito breeding sites. Dispose of old receptacles, tires and containers and eliminate areas of standing water.
3. Thoroughly clean livestock watering troughs at least monthly.
4. Use larvicides to control mosquito populations when it is not possible to eliminate particular breeding sites. Such action should only be taken, however, in consultation with your local mosquito control authority.
5. Keep your horse indoors during the peak mosquito activity periods of dusk to dawn.
6. Screen stalls if possible or at least install fans over your horse to help deter mosquitoes.
7. Avoid turning on lights inside the stable during the evening or overnight.
8. Using insect repellants on your horse that are designed to repel mosquitoes can help reduce the chance of being bitten.
9. Remove any birds, including chickens, located in or close to a stable.
10. Don’t forget to protect yourself as well. When outdoors in the evening, wear clothing that covers your skin and apply plenty of mosquito repellent.
For more information about the virus, ask your equine veterinarian for the “West Nile Virus” brochure, produced by the AAEP in conjunction with Bayer Animal Health, an AAEP Educational Partner. Additional information about WNV can be found on the AAEP’s horse-health Web site, www.aaep.org/horseowner.
The American Association of Equine Practitioners, headquartered in Lexington, Ky., was founded in 1954 as a non-profit organization dedicated to the health and welfare of the horse. Currently, AAEP reaches more than 6 million horse owners through its nearly 10,000 members worldwide and is actively involved in ethics issues, practice management, research and continuing education in the equine veterinary profession and horse industry.