Equine practitioners devote a good deal of time in spring, and sometimes autumn, inoculating their patients against mosquito-borne viruses like Eastern and Western equine encephalitis (EEE and WEE) and West Nile virus (WNV). These viruses are members of the arbovirus family, which are transmitted to horses by insects such as mosquitoes.
Mosquitoes are considered the most dangerous “animal” in the world as they transmit some of the most ravaging diseases. Fortunately, the common mosquito-borne viruses relevant to horses are effectively prevented with annual vaccination. In portions of the country that enjoy mild weather, year-round mosquito populations can persist, thereby necessitating twice-annual boosters in those regions.
While EEE, WEE, and WNV also affect humans, they are not transmissible between horse and horse, horse and human, or human and horse. Transmission of virus to horse or human requires a mosquito vector that first feeds on birds (and sometimes rodents) that carry the virus.
A mosquito that takes a blood meal from an infected bird then bites a horse or person to transmit disease when it takes its next blood meal. Horses and humans are considered “dead-end hosts” for arboviruses because they don’t have enough infective virus in their bloodstreams for transfer of infection via mosquitoes or body fluids to another animal.
Within the general heading of arboviruses, there are three Alphaviruses of the Togavirus family in the United States—Eastern, Western, and Venezuelan encephalitis. A Flavivirus causes West Nile viral disease.
Mosquito-Borne Equine Diseases
Due to the seasonal nature of mosquito vectors in temperate climates, most cases of arboviral disease occur in late summer and fall, following a typical incubation period of two days to three weeks. Neurologic signs tend to be nonspecific, including lethargy, somnolence, excitability, incoordination/ataxia, circling, head-pressing, teeth-grinding, paresis, paralysis, dysphagia, bladder paralysis, and recumbency.
In some states, veterinarians are required to report any horse affected with neurologic disease to their State Department of Agriculture. Check your state regulations to see if you are required to report neurologic disease.
Eastern, Western, or Venezuelan Encephalitis (EEE, WEE, VEE)
There tend to be geographical dividing lines between two predominant encephalitic viruses in the United States. Eastern equine encephalitis typically occurs east of the Mississippi River. It’s transmitted from passerine birds to Culiseta melanura mosquitoes, which don’t feed on mammals.
However, Culex, Aedes, and a multitude of other “bridging” mosquito species can pick up the EEE virus and infect horses, resulting in serious neurologic disease with 70-90% fatality, even with aggressive treatment.
In Florida and South America, rodents can also play a vector role for EEE. Birds and rodents don’t develop clinical disease from EEE.
Viral encephalitis infection goes by the moniker “sleeping sickness” because horses with encephalitis appear sleepy. An infected horse develops a fever, involuntary muscle twitching, and an ataxic gait. Eventually, the horse goes to the ground, unable to get up. In temperate climate regions, most cases begin to appear in late summer into the fall months, but they can appear year-round in southern states.
Western equine encephalitis, a similar neurologic disease to EEE, is transmitted by the Culex tarsalis mosquito, which lives in the western part of the U.S. Besides birds, rodents and reptiles can also serve as intermediate vectors for virus transmission.
Fatality rate from WEE ranges from 20-50%. Equine cases have seen a dramatic drop in incidence in recent years, with no equine WEE infections reported in the western United States since 2004. However, in this geographic area, WEE continues to be identified in birds and mosquitoes. Therefore, annual equine vaccination practices should continue for the foreseeable future. Most infected birds are asymptomatic.
At this time, Venezuelan equine encephalitis is a reportable foreign disease. It causes death in 50-80% of infected horses. The bulk of VEE cases occur in Latin America, putting horses living near the southern borders of New Mexico, Texas, California, Louisiana, Mississippi, and Alabama and along the west coast of Florida at potential risk.
While no cases of VEE have occurred in the U.S. in 40 years (since 1971 in Texas), this could alter due to climate change if an influx of VEE-infected vectors moves north.
Rodents, opossums, bats, ticks, and black flies can be vectors for VEE.
VEE can develop a different epizootic cycle in which virus amplification in the horse or human host can lead to mosquito infection. In those situations, a horse or human is no longer a dead-end host. An E2 gene that amplifies various VEE strains might cause this mutation. There is also a possibility of aerosol transmission.
West Nile Virus
West Nile virus occurs worldwide wherever mosquitoes are found, especially Culex species. Mosquitoes are capable of vertical transmission that can sustain the virus without the presence of appropriate hosts. While birds are the primary amplifying hosts, reptiles can also play a vector role.
This Flavivirus was first identified in the United States in 1999 in New York. It is now found nationwide.
Equine infection with WNV is most prevalent in late summer and autumn in unvaccinated horses. Many avian species (Corvids such as crows, ravens, jays; house finches; waterfowl; owls and hawks) often succumb to WNV infection.
Not all unvaccinated horses exposed to WNV develop clinical signs. In fact, according to retrospective studies, only 8-10% of unvaccinated horses exposed to the virus develop progressive West Nile virus meningoencephalomyelitis. Study results have demonstrated that interferon receptors are protective against infection with WNV, and a specific gene (OAS1) also affords protection. Yet, when a horse becomes infected, the disease is quite serious.
WNV attacks the neurologic system of horses and humans and, to a lesser extent, a variety of other species (goats, sheep, llamas, dogs, bears, and reptiles). The blood-brain barrier normally limits access of bacteria, viruses, and fungi to the nervous system, but WNV can cross that barrier to cause inflammation and damage to the brain and spinal cord. Clinical signs are manifested according to which area(s) of the central nervous system is affected.
Fever and depression are common initial signs of WNV, along with limb weakness and inexplicable “lameness” or ataxia. Owners might see a horse stumble, drag its toes, or tilt to one side. The face, muzzle, and lips and/or the neck, shoulders, and chest often display muscle twitching or tremors. Difficulties occur with swallowing and vision; some are photophobic.
Horses that normally don’t mind being touched might become hypersensitive to touch and/or sound or might display other behavioral changes.
More severe cases exhibit a number of clinical signs, from aimless wandering and disorientation to colic, convulsions, paresis, rear quarter paralysis, and recumbency. Death occurs in 30-35% of horses infected with WNV. As many as 40% of survivors experience neurologic gait and behavior abnormalities for six months, and some deficits can persist indefinitely.
Hugh Townsend, DMV, MSc, and Tasha Epp, DVM, PhD, from the University of Saskatchewan’s College of Veterinary Medicine, have identified several specific risk factors for WNV infection and mortality:
- Lack of vaccination against the disease is a primary reason horses contract WNV.
- Older age is associated with a higher risk of exposure and more severe neurologic signs as well as higher mortality rates.
- Horses with clinical signs of WNV earlier in the season (Weeks 31-33) tend to have better survival rates than those developing signs later in the season (Weeks 36-38).
Other studies have identified a higher seroprevalence for WNV exposure in stallions relative to what is seen in mares or geldings.
In a study out of Egypt, mixed-breed horses had a higher seroprevalence than purebred Arabians and Thoroughbreds, possibly due to different management practices and a tendency for indoor stabling of purebred horses that limits mosquito exposure.
The Importance of Arbovirus Immunization for Horses
The American Association of Equine Practitioners (AAEP) lists arbovirus vaccines—EEE, WEE, and WNV—as part of the core vaccine schedule to be administered to every horse at least once a year regardless of location.
All available vaccine products against these mosquito-borne viruses are 100% protective, assuming the horse has a competent immune system. The most effective foundation for preventing arboviruses in horses is immunization, particularly in the spring prior to an active mosquito season.
For EEE, WEE, and VEE, a number of effective multivalent, killed vaccine products are available for horses. There are currently three effective USDA-licensed vaccine forms labeled for protection against WNV in horses—two killed (inactivated) vaccines and a chimera vaccine. Usually, these are available in multivalent forms combined with EEE, WEE, tetanus, and other respiratory risk-based vaccine products.
A killed virus product initiates antibody protection that covers the horse well for the five to six months of active mosquito season in temperate climates. Following a primary series of two to three immunizations, the WNV vaccine should be boosted annually. Depending on the vaccine form used, WNV vaccination might require two (or even three) yearly boosters if living in areas where mosquitos are active year-round.
Immunization of a pregnant mare with EEE, WEE, and WNV in the last four to six weeks of pregnancy confers maternally inherited antibodies in the colostrum. This gives passive transfer of antibodies to the foal for rapid activation of an immune response to protect against these viruses. Once a foal reaches four to six months of age, he can start on a three-dose primary vaccination series followed by regular boosters. A foal born to an unvaccinated mare should begin the WNV series at three to four months of age, as much ahead of the onset of mosquito season as possible.
Insect Mitigation
Part of a sound preventive management protocol for horses is to eliminate or at least minimize mosquito vectors that carry arboviruses. Client education about management practices on their properties can make a huge difference in alleviating the risk of EEE, WEE, or WNV infection.
Mosquitoes flourish in damp, warm, decomposing organic matter, such as in wet areas like ditches, stagnant ponds, and anything that holds standing water. A key element of insect control hinges on environmental cleanliness to reduce mosquito breeding sites.
Mosquito species vary in habitat preferences for laying eggs—some prefer to congregate in irrigation tail waters, while others propagate as “container breeders.”
Prior to mosquito season, eliminate open containers that collect even the smallest amount of water that could be a potential mosquito reservoir: Gutters, flowerpots, buckets and cans, swimming pool covers, hay tarps, wading pools, discarded tires, wheelbarrows, bird baths, pet bowls, and tractor buckets, to name a few. Even a hoof print in mud or near a water tank can hold a water depth conducive to the hatching of mosquito larvae. Turn water containers upside down, or drill holes in the bottoms for drainage.
Mosquitoes lay rafts of eggs atop standing water, especially water laced with organic debris. Cleaning water tanks regularly (once or twice weekly) removes organic debris such as hay and food particles as well as mosquito egg clusters and larvae.
Effective on-site drainage is important around gutters and water tanks to mitigate insect propagation. Fill in low spots on the property with sand or gravel. Keep vegetation cut short to diminish potential breeding sites for mosquitoes.
Aphids also live in standing vegetation and attract mosquitoes that feed on aphid excretions of digested sap and sugars.
Even if a concerted effort is made to eliminate containers as water sources for mosquitoes to lay eggs, it is likely that standing bodies of water still remain around a property. These might be managed by applying mosquito “dunks” as granules or floating briquettes that contains soil bacteria called Bacillus thuringiensis sub. israelensis (BTI) or Bacillus sphaericus (BS). In hot and humid climates, mosquito life cycles often shorten from seven to 10 days to just three to four days, so it is important to apply BTI weekly until the first killing frost. BTI is nontoxic to other aquatic life.
Biological controls such as mosquito-eating fish (fathead minnows or Gambusia species) consume mosquito larvae for management of ornamental ponds, irrigation waters, and watering ponds. Check with local bait and tackle shops as to which mosquito-eating fish species are native to your area. Aeration of small water areas is another good strategy to keep water moving and limit egg-laying by mosquitoes.
Another mosquito control strategy includes the use of permethrin insecticides to diminish mosquito populations. Mow and spray surrounding vegetation with insecticides as a barrier treatment. Follow application directions specified on insecticide labels. Permethrin applied around eaves and corners of stabling areas deters adult mosquitoes from overwintering in those locations. Eliminating attractive breeding sites for insects helps reduce their populations logarithmically over time.
In addition to environmental control methods, another strategy to protect against mosquito bites is to stable horses during high-risk periods. Fans help deter insect entry into stabling areas or at least shorten landing times on horses, thereby interrupting feeding periods. Screens with fine mesh, fly masks, fly sheets, leg mesh wraps, and mesh belly bands are helpful to reduce exposure to bites.
Pesticides (pyrethrins) are useful against adult insects when used directly on horse skin. Propane-fueled insect traps that emit carbon dioxide might collect insects within a breeding habitat, but they are relatively ineffective in windy areas. It is notable that fly zappers in and around barns can actually be insect attractants at night and might work against you, not to mention unintentionally kill good insects.
Take-Home Message
While arboviruses can wreak havoc on an equine community, we are fortunate to have commercial vaccines that are nearly 100% effective in horses in most cases. Coupling a diligent vaccination strategy against EEE, WEE, and West Nile virus with insect mitigation practices makes arbovirus risks a relative nonissue for veterinarians and horse owners. Good client education efforts help improve compliance with recommendations that follow core vaccine principles and keep horses up to date on immunizations.
Related Reading
- The Future of Equine Infectious Diseases in a Changing Climate
- Encephalitis in Horses
- Researchers Identify Potential New Transmission Method for West Nile Virus
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