The initials are innocuous enough--EEE, WEE, VEE--but the diseases they stand for can be deadly to both equines and humans. They are, in order, Eastern Equine Encephalomyelitis (EEE), Western Equine Encephalomyelitis (WEE), and Venezuelan Equine Encephalomyelitis (VEE). In each case, the disease normally attacks the brain and central nervous system, and, with some frequency, is fatal. The deadly agent that causes the disease is a virus. Each of the strains uses mosquitoes as a vector, with each strain often transmitted by a separate branch of the mosquito family. (The words enceph-alomyelitis and encephalitis are often used interchangeably. Technically, encephalitis is an inflammation of the brain, while encephalomyelitis is inflammation involving both the brain and the spinal cord.)
The following information on the three forms of encephalomyelitis is based on interviews with the individuals quoted as well as research material presented by a number of experts in the field.
The most deadly of the three strains is EEE. Statistics show that fatalities in horses that contract EEE range from 75-100%. With humans, the odds are a bit better. The fatality rate ranges between 50-75%.
The good news for both the equine and human population is that EEE does not strike a large number of victims. Cliff Windham of the United States Center for Disease Control in Atlanta, Ga., says that during the past 40 years, 152 EEE cases in humans have been reported. Of that number, approximately 50% were fatal.
Each year, however, there are a number of cases reported in the equine population, with the outcome for afflicted horses generally being either death or permanent brain and nervous system damage that can totally compromise their ability to perform and/or reproduce.
The most recent EEE scare occurred in Rhode Island this past September. An extraordinarily wet spring and summer resulted in the production of swarms of mosquitoes, a number of which were found to be carrying the EEE virus. At this writing, no humans or horses had been afflicted. Special precautions were taken to protect the human population, according to Richard Bolig, the communications coordinator for the Rhode Island Department of Health. Because mosquito activity is at its highest in the morning and evening hours, a number of schools delayed the start of classes and dismissed students earlier than normal in the day. Residents were also urged to wear long-sleeved shirts and to apply mosquito repellent before going outdoors.
In an effort to destroy as much of the mosquito population as possible, two crop-duster planes were employed to spray swampy areas with insecticide.
"We are just hoping for an early frost," said Bolig during the height of the mosquito invasion.
Two staff members of the Center for Disease Control in Atlanta were sent to Rhode Island to assist officials there. Their presence was formally requested by Rhode Island health officials, according to Windham.
Rhode Island proved to be a classic example concerning the ability of the disease to spread to other areas. Mosquitoes carrying the EEE virus were first discovered in a swampy area in the southern part of the state. Within a short time, virus-carrying mosquitoes were discovered in a total of five communities, all of which were widely separated geographically.
The reason the disease can spread quickly and to far-reaching areas is because birds are unwitting helpers. Birds, as well as some wild animals (generally small mammals) and reptiles, serve as reservoirs for the virus, although they are not adversely affected by it.
If a mosquito should bite an afflicted bird--a couple of types of mosquitoes feed heavily on birds--the mosquito can pick up the virus. If the virus is able to penetrate the mosquito's gut, it can then pass to oral glands, multiply, and subsequently be shed in saliva and other oral secretions. Normally, the mosquito will remain infected throughout its several weeks of life.
If the infected mosquito should bite a horse or human, the virus could be passed and that person or equine could become afflicted.
Except in rare instances, humans and horses are considered dead-end hosts for both EEE and WEE. In other words, if an uninfected mosquito should bite an afflicted horse or human, it would be unlikely that it would pick up enough of the virus to transmit the disease to another horse or human.
Because the mosquito plays such a vital role in transmission of the disease, it is no surprise to learn that encephalitis cases are most apt to be reported between June and November in temperate climates. In warmer climates where heavy freezes do not normally occur, the threat can be year-round. Florida, for instance, routinely reports several cases of EEE each year. Other states that have reported cases thus far this year include Alabama, South Carolina, North Carolina, Louisiana, Virginia, and Maryland.
The good news, of course, is that horsemen can vaccinate their animals and, thus, protect them from the viruses.
Cases of encephalitis in equines are monitored by the Center for Disease Control in Fort Collins, Colo. The theory is, says Robert Craven, MD, of the Center, that if there is an outbreak in the equine population, it might be followed in two to five weeks by humans being affected.
The equine population, in a sense, he said, serves as a sentinel for the human population.
Horses afflicted with EEE demonstrate classic symptoms. Typically, there will be loss of appetite, fever, and a change in behavior. Within 12 to 24 hours of the initial symptoms, the aberrant behavior will intensify, with head pressing, circling, and, often, blindness.
As the viral attack on the brain and nervous system continues, the horse might lose its ability to stand and might suffer seizures. In severely afflicted equines, there normally will be respiratory arrest two to three days after the onset of clinical signs and the horse will die.
Horses that do survive often are left with visual problems as well as behavioral and learning disabilities.
Unfortunately, there are no anti-viral drugs available, so treatment of an afflicted horse is generally supportive, such as administering phenylbutazone to help reduce fever, wrapping legs to prevent injury, and providing a diet that is both nutritious and laxative in nature to prevent impaction.
Western Equine Encephalomyelitis
While all is pretty much doom and gloom from a prognosis standpoint for horses and humans afflicted with EEE, the same is not true for Western Equine Encephalomyelitis (WEE). Also known as sleeping sickness, WEE is the most common and mildest of the three strains of encephalitis. Like EEE, it is transmitted by mosquitoes.
The mosquito strain responsible is known by the scientific name of Culex tarsalis. This species of mosquito feeds heavily on birds and birds serve as reservoirs for the WEE virus, though they, themselves, are not affected by it.
The mosquito that bites an affected bird can become a carrier of the WEE virus in the same manner as described above with EEE. When it bites a horse or human, the disease can be transmitted.
Typically, WEE outbreaks would be more common in the latter part of the mosquito season because at that time, as birds begin their migration patterns and leave the area, the mosquitoes must resort to feeding on animals, such as horses.
All ages of horses are susceptible, if not vaccinated, but the young are affected more often. And when young horses contract the disease, it is generally severe in nature. Mortality rates of 10-30% are not uncommon and might run as high as 50%. For humans who contract WEE, the mortality rate ranges between 5-15%.
Generally speaking, WEE occurs in the United States from the Mississippi River Valley westward and in Western Canada, although there are occasional outbreaks in the Eastern United States as well as in Mexico and Central and South America.
Once the mosquito has deposited the WEE virus in a horse, there is an incubation period of one to three weeks, followed by local multiplication in muscle, subcutaneous tissues, and regional lymph nodes. The virus then spreads through the body via the bloodstream to vascular endothelial cells (such as in the lining around the heart) and to the highly vascular organs such as the liver and spleen.
During this period, the horse might run a fever which can reach 105° Fahrenheit. Also during this stage, a blood test would reveal a strong viral presence in the bloodstream.
At this point, the horse's defense mechanism steps in and attempts to clear the virus from the body. If it is successful, there will be no more clinical signs, although the horse will likely have developed antibodies against the virus and these would show up in a blood test. The time period involved between onset of clinical signs and recovery--when recovery does occur--normally runs from 24 to 48 hours.
If, however, the horse's body is unable to eliminate the virus, the central nervous system comes under attack and the outcome is now much more in doubt. As this new phase of the disease begins, the horse can become restless and excitable. This is usually followed by compulsive walking and circling, with the animal sometimes crashing blindly into walls. Next comes extreme mental depression. The horse might be reluctant to move and standing postures can be abnormal, with head hanging low, eyes closed, and lips drooping. There might be tremors in the head and shoulders and, in severe cases, the legs might buckle. During these episodes, the horse might also have difficulty swallowing and when forced to move will travel with an uncoordinated gait, particularly in the rear legs.
The most severe signs of the disease normally last only a few days, but it can take two weeks or more before it has totally run its course.
If the horse is able to remain on its feet through the duration of the disease, it might recover completely, providing there are no other complications, such as secondary bacterial infections. However, if the horse is unable to remain on its feet and paralysis sets in, the outcome is usually grim. These horses often will die, and those that do survive will be severely impaired.
Treatment of horses with WEE is the same as that listed above for those afflicted with EEE--phenylbutazone to help control fever and a highly nutritious and somewhat laxative diet. Horses which are unable to stand can be aided with a sling. If this doesn't work, they should be bedded in deep straw and rolled frequently.
Venezuelan Equine Encephalomyelitis
If EEE is the most virulent of the encephalomyelitis strains, and WEE is the mildest, that leaves Venezuelan Equine Encephalomyelitis to occupy the middle ground.
VEE was first recognized as a separate disease entity following an outbreak of encephalitis in Venezuela in 1936. From 1936 to 1968, devastating outbreaks occurred in both horses and humans in Colombia, Ecuador, Peru, and Venezuela. In January of 1969, another epidemic of VEE erupted in Ecuador and spread into Peru. During that summer, the virus was transported by undetermined means from Ecuador to Guatemala. From there, it spread into El Salvador, Honduras, and Nicaragua. In 1970, it reached Costa Rica, then Mexico. By 1971, it had arrived in the United States.
The most recent outbreak of the disease occurred this past July in Oaxaca, a state on the southwestern coast of Mexico. According to Craven of the Fort Collins Center for Disease Control, some 100 horses were afflicted. In an effort to keep the disease from spreading, the U.S. Department of Agriculture imposed strict importation restrictions on horses entering the United States from Mexico. Horses from Mexico must complete a seven-day quarantine period at USDA-approved facilities in Los Angeles, Miami, New York, or in Mexico.
The Mexican government was also quick to act, setting up strict quarantine measures that prevented horses from leaving the outbreak area. In addition, emergency vaccination programs were implemented. At this writing, the outbreak had been contained.
While VEE is the "middle child" in this deadly encephalomyelitis family, it does have one feature that makes it more worrisome than the other two. Horses and humans, as mentioned above, are dead-end hosts for both EEE and WEE, but not so with VEE. There is enough of the VEE virus circulating in afflicted horses and humans that they become amplifiers of the disease.
While mosquitoes are the prime vectors, the disease can also be transmitted from animal to animal through eye and nasal discharges.
As with the Western strain, VEE can be either mild or virulent in nature when it attacks a horse. After the horse is infected, there is an incubation period that might be as short as half a day, or as long as five days. The first clinical sign of VEE is a rise in body temperature, often ranging from 103-105° Fahrenheit. This is usually accompanied by an increased pulse rate, excitability, and loss of appetite. When the attack is severe, this might be followed by depression, weakness, loss of coordination, muscle spasms, and convulsions. The horse might also develop diarrhea and colic. Some horses will stand quietly when afflicted, while others will wander aimlessly and/or press their heads against solid objects.
VEE is a less predictable disease than either EEE or WEE. At any point during its state of infection, the course of the disease (VEE) can be interrupted by recovery, or prostration and death. It might move rapidly, with death coming within hours after the first outward manifestation, or it might move slowly, with dehydration and extreme loss of weight occurring before either death or recovery.
The mortality rate for equines with VEE ranges from 40-80%, while for humans the death rate is listed at only 1%.
Protection and Vaccination
Fortunately, vaccines are effective against all three strains of encephalomyelitis, and they can be administered simultaneously. In fact, it is recommended that simultaneous vaccinations occur as the response to VEE vaccine is poorer in horses previously vaccinated for EEE and WEE.
Vaccination should occur each spring, several months before the heavy mosquito season. In warmer climates where the mosquito population is more of a constant, twice a year vaccinations are recommended.
A question remains as to just when to first vaccinate foals. The youngsters obtain passive immunity from their dams via the colostrum, and this protection could interfere with the foal's ability to mount an antibody response to routine vaccinations. The amount and duration of the passive immunity can vary considerably. One recommendation is to begin vaccination at six to eight weeks of age, with boosters given at six months and one year to ensure adequate protection. Still another recommendation is to give foals two to three monthly vaccinations beginning at two to four months of age. Vaccinating mares one month prior to foaling enhances the colostral antibody levels.
A further protection measure from an environmental standpoint can involve eliminating standing water where mosquitoes breed.
But, the best and most basic preventative is vaccination on at least an annual basis. Relatively economical and easily administered, the vaccine effectively protects horses from what otherwise can be a fatal malady.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
POLL: University Equine Hospitals