The Ever-Present Threat
Editor's Note: This is the fourth in a 12-part series of articles on vaccinations for horses.
West Nile virus (WNV) might be the new kid on the block, the one gaining all the media attention, but unfortunately, it is not the only mosquito-borne disease to which your horse is vulnerable. Long before WNV ever reached North American shores, there were two other forms of viral encephalitis (literally, inflammation of the brain) for horse owners to worry about, as well as an occasional invader from South America. You probably know them as EEE, WEE, and VEE--Eastern, Western, and Venezuelan equine encephalitis (the encephalitides). Or you might be familiar with the older, more general term "sleeping sickness." Either way, these viruses are as dangerous today as they were decades ago.
Although they are three separate diseases with three separate vaccines, EEE, WEE, and VEE have several qualities in common:
- All three viruses are found in North, Central, and South America, with WEE being the most widely distributed. They have not been noted in Europe, Asia, or Africa.
- The main reservoirs for each disease are various migratory birds. Because multiple species are involved, from blue jays and chickadees to cardinals and catbirds, the distribution of encephalitides is widespread. Rodents can also harbor the viruses.
- Each is transmitted from birds to horses via mosquitoes that first bite an infected bird, then a healthy horse.
- Humans can also contract all of the equine forms of encephalitis, although the diseases are not generally considered transmissible from humans to horses or vice versa (dead-end hosts). The one possible exception to this is VEE, which in horses can develop high enough viremia (levels of virus in the bloodstream) for it to be picked up by mosquitoes and passed on to other species. VEE virus can be detected in the blood, saliva, and nasal discharge of an infected horse (potentially zoonotic). Horses also develop viremia with WEE and EEE infection, but not at high enough levels to pass it on to other horses or other species.
- The incidence of each disease is tied to the mosquito season. When mosquitoes aren't active, the risk is low; when mosquito populations are high, the risk is very real.
- All three diseases are extremely difficult to treat. There are no known anti-viral drugs that can tackle equine encephalitides, so veterinarians can only help an affected horse by treating the clinical signs (primarily with fluid therapy, anti-inflammatory drugs to help reduce fever and inflammation of the brain and spinal cord, and possibly anticonvulsants).
- Horses that survive a bout of WEE, EEE, or VEE often suffer from lasting neurological deficits. Essentially, they're brain-damaged, sometimes so much so that they're dangerous to ride or handle.
- The causative viruses for EEE, WEE, and VEE all belong to the family called alphaviruses. (By contrast, WNV, which behaves similarly in many ways, comes from a viral family called flaviviruses.)
- EEE, WEE, and VEE all attack the horse's central nervous system (brain and spinal cord). Although diagnosis can sometimes be made by isolating the virus in blood samples of acutely affected horses, the best confirmation is by post-mortem analysis of brain tissue.
- Cases of EEE, WEE, and VEE in the United States are all monitored by the Centers for Disease Control in Fort Collins, Colo., because horses are considered sentinels for possible outbreaks in the human population.
Differentiating WEE, EEE, and VEE
So what separates the three viruses? First and foremost, distribution.
EEE is usually found along the Eastern seaboard, from the Canadian maritime provinces down to Florida, and only rarely in the Midwest or points farther toward the Pacific. WEE, in contrast, is generally found west of the Mississippi. VEE, which was first diagnosed in Venezuela in 1936 after a major outbreak, generally stays south of the equator, but it is responsible for occasional outbreaks in horse populations in Central America (it was diagnosed in Mexico as recently as 2000, and Belize in December 2004). In 1971, VEE caused widespread alarm in the southern United States when it crossed the border and invaded parts of Texas. While it is a rare invader, it's not a disease to be dismissed lightly, as we'll see in a minute.
What else differentiates EEE, WEE, and VEE? Here's a rundown.
EEE: High Mortality, High Risk
With a fatality rate of 75-90%, EEE is the most deadly of the encephalitis trio. It's also one of the most opportunistic, as it's found in multiple species of birds with all kinds of migratory patterns. Several kinds of small mammals and reptiles are also possible reservoirs. EEE is considered endemic in the United States, eastern Canada, the Caribbean, and Central America; there was also a horse diagnosed with EEE in Venezuela in 2004.
Because it can also affect humans and other species, EEE is designated as a reportable disease in the United States (any positive diagnosis must be reported to federal authorities).
The progression of EEE is swift and ugly. The clinical signs usually appear abruptly and can kill a horse in as little as two to three days. It starts with a fever, which is sometimes accompanied by no other clinical signs and is easy to miss if the horse is turned out. The fever might break, only to rise again, this time accompanied by depression, loss of appetite, and a "sleepy" appearance. Soon, neurological symptoms begin to appear. Affected horses will struggle with muscle tremors, weakness, and staggering gaits, and might circle aimlessly or tilt their heads at odd angles. Within 24 hours, the clinical signs can progress to include a characteristic behavior called head pressing (the horse presses his face against walls or other solid objects, as if he's trying to hide), convulsions, and sometimes blindness. These clinical signs can be followed by recumbency; when a horse lies down, death from respiratory arrest often occurs within two to three days.
Horses that survive EEE have been described as "disabled" and often have lingering vision problems.
WEE: Widespread, But Less Virulent
Although its mortality rate (20-50%) is far lower than EEE, WEE is nothing to sneeze at. Sparrows and house finches seem to be the main reservoir hosts of the virus, and one species of mosquito, Culex tarsalis, is responsible for spreading WEE across the western U.S. and Canada, with occasional outbreaks in the eastern United States as well as in Central and South America.
Outbreaks of WEE tend to occur toward the latter part of the mosquito season. That's because Culex tarsalis normally prefers to feed on birds, but as birds start to migrate out of an area for the winter, the insects have to turn to other food sources. That's when they're most likely to bite mammals, including horses, and spread the virus.
It might take a horse one to three weeks of incubation time after he is bitten by an infected mosquito to show signs of WEE. Many of the clinical signs are similar to those seen in EEE, but with the Western form, some horses become agitated or excitable rather than sleepy. Every stimulus has the potential to send them into a frenzy. With a fever as high as 105ºF in the acute stage, it's not surprising that restlessness is also a clinical sign of WEE. With this disease, the first 24-48 hours will tell the tale; if the horse's immune system is able to beat the virus, it will usually do so in that initial window. If not, the central nervous system will come under attack as the virus replicates in lymph nodes and muscle and spreads to highly vascularized (supplied with lots of blood vessels) areas such as the liver, spleen, and the lining of the heart. By this time, the horse will exhibit severe depression, tremors in the head and shoulders, difficulty swallowing, loss of coordination, and circling or walking blindly into walls. These clinical signs might come on gradually over a couple of weeks. If the horse is able to remain on his feet, he still has good odds for recovery, but most veterinarians agree the prognosis is poor if he goes down or muscle paralysis sets in.
VEE: Somewhere in Between
VEE might be a rare disease in North America, but epizoologists keep a close eye on it nonetheless. With a mortality rate of 40-80%, VEE is an extremely dangerous and unpredictable disease. It's more variable than either EEE or WEE, with the ability to progress quickly or slowly, and be mild or extremely virulent. It's possible that's because VEE in horses can be caused by more than one variant of the virus.
Horses that contract VEE generally exhibit clinical signs similar to the Eastern and Western varieties of encephalitis, although the incubation period is shorter than WEE (usually only one to two days). Loss of appetite, excitability, an increased heart rate, and a fever of up to 105ºF are common. Severely affected animals might later suffer weakness, muscle spasms, depression, loss of coordination, diarrhea or colic signs, and might circle aimlessly or press their heads against solid objects. If the disease progresses to convulsions, the prognosis is usually grim.
Unlike WEE and EEE, which generally don't result in detectable viremia, the VEE virus can be detected in the blood, saliva, and nasal discharge of an infected horse. Although it's never been documented with absolute certainty, epizoologists believe that this gives VEE the potential to be spread directly from horses to humans who might come into contact with that saliva or discharge from the nostrils or eyes. This makes VEE a true zoonotic disease.
Shooting Down Encephalitis
As with rabies, tetanus, and WNV, by far the best strategy for avoiding encephalitis is to protect your horses with vaccines.
D. Craig Barnett, DVM, senior equine technical services veterinarian for Intervet pharmaceutical company, points out, "In 2003, there was a serious outbreak of Eastern equine encephalitis in the southeastern United States, thanks to some very wet weather and flooding, which resulted in high mosquito populations. There were a significant number of deaths spread over a number of states, and the horses that died were those that had not been properly vaccinated." Some of the horses were overdue for a booster vaccination or didn't receive the recommended number of doses for primary immunization.
In fact, there was a 690% increase in the total number of cases of EEE in Alabama, Florida, Georgia, Louisiana, Mississippi, North Carolina, South Carolina, Tennessee, and Virginia in 2003 compared to 2002. Says Barnett, "We have a concern that at the time everyone was so focused on West Nile that they might have neglected to vaccinate for EEE. West Nile gets a lot of press, but we have to remember that EEE has twice the mortality rate. It's by far the deadlier disease."
Barnett cites an earlier example of encephalitic virulence that should be enough to give all of us pause. "In 1931, there was an outbreak of WEE in California, which then spread eastward to the Midwest. Between 1931 and 1938, 180,000 horses died--which shows just how devastating these diseases can be.
"It's so important to remember that EEE and WEE are endemic in a lot of areas, and because it stays viable in bird populations, we're never going to eradicate it," he warns. "It's not going away, so vaccination, because it's so safe and so effective, should be a no-brainer."
The vaccines available for EEE, WEE, and VEE have been around since the diseases were first isolated in the 1930s. They're simple killed-virus vaccines, which are almost invariably packaged in a polyvalent form. In other words, a single vaccine will combine protection against EEE and WEE simultaneously, or EEE, WEE, and VEE, or even EEE, WEE, and WNV. Sometimes protection against rabies and tetanus is rolled in there, too, to simplify the routine for horse owners. There are even vaccines that can protect against all of these plus equine herpesvirus and influenza. The consistent part is that protection for EEE and WEE are almost always provided together.
"The main reason you get protection against both EEE and WEE in one formulation is that so many horses are transported across wide distances now that it just makes sense to protect them from the full spectrum," says Barnett. "It's also more economical for the company to combine them."
Whether you decide to protect your horse against VEE in addition to EEE and WEE will have mostly to do with geography; if your horses live in Central or South America, or in a state bordering Mexico (or you expect to be shipping to these regions), you'll want to add a VEE vaccine to your regimen. Interestingly, "(Horses) tend to respond better to the VEE antigen when the EEE and WEE antigens are also in (the same vaccine)," Barnett says.
Equine encephalitis vaccines are widely available from most pharmaceutical companies that make equine vaccines. The difference in the formulations is generally confined to the adjuvants (chemical carriers that enhance the formulation's immune-stimulating properties). Regardless of the brand name, equine encephalitis vaccines have all been demonstrated by decades of use to be extremely safe and nearly 100% effective. "The cases (of encephalitis) we do see are almost always in unvaccinated animals or improperly immunized ones, such as very young horses who might have received the first immunization but not the second," says Barnett.
It's important, he emphasizes, to stimulate a naïve horse's (one who has never been exposed to the vaccine or virus before) immune system properly by giving two doses of an encephalitis vaccine a month apart. In foals, a three-dose regimen is often done beginning at three or four months of age, but your veterinarian might recommend that you hold off until the foal is four to six months old (depending on the area's EEE risk) if his dam received an encephalitis booster four to six weeks before foaling. This is because foals can acquire maternal antibodies through nursing, the effect of which can protect them from the diseases for the first few months. Maternal antibodies can also have what Barnett calls "a blocking effect on immunization," so it's best to wait until their influence starts to wane before administering any vaccine or else any vaccinations you give the foal will have an unpredicatable response (the foal might not be adequately protected against the disease).
The choice of when to begin vaccinating foals will also have to do with mosquito activity at the time. "It doesn't make a lot of sense to begin providing protection when the vector (mosquito) is non-existent," Barnett says. "In the southern states, where mosquitoes are active year-round, it's a good idea to get that foal protected even if it's October or November, but in the north, you might want to wait till about a month before mosquitoes are due to appear in the spring."
No vaccine confers instant protection. In naïve horses, full immunity to encephalitides doesn't develop for about four weeks after the final injection, Barnett says, and even in horses who have previously been exposed to the vaccine, you should expect the process to take 14-28 days.
So think pre-emptive strike and ask your veterinarian to administer the vaccine(s) at least a month before bug season is due to start in previously vaccinated horses. In areas where mosquitoes are only active for part of the year, one yearly booster might be all that's needed, since the vaccines confer good protection for about six months. In the south, you'll be more likely to booster two, three, or four times a year, depending on the climate and mosquito populations. Consult with your veterinarian to design the best program for your conditions and your horses.
About the Author
Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.