|Issue 6: Encephalitis in Horses
As defined, encephalitis is inflammation of the brain. Therefore, clinical signs of this disease state are that of dysfunction of the brain - depression, ataxia or incoordination, weakness, head tilt, circling, paralysis, muscle tremors, convulsions, and cranial nerve abnormalities.
Information concerning the West Nile Virus has dominated the news quite a bit lately. As of September 5, 2001, there were 66 confirmed cases of WNV infection in horses in the US this year. Most (54) have occurred in Florida. One horse each in Pennsylvania, Kentucky, and Connecticut were ill but are recovering. Five horses in south Georgia have been identified. At least 1 of these, a 30-year-old mare, and one in Louisiana have died . Twenty-five percent of the equine cases have died so far. Many dead birds from all over the East Coast have been diagnosed with WNV. And recently birds in Indiana, Michigan, Illinois, Wisconsin, and Alabama have been positive, indicating that it is moving inland.
Unfortunately, this virus is likely here to stay. However, we must keep in mind that at least five other viruses can cause encephalitis in the horse - Eastern Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), Venezuelan Equine Encephalitis (VEE), the necrologic form of Equine Herpes Virus I (EHVI) (also called Rhinopneumonitis), and Rabies. These must be differentiated from infection with the WNV. WEE, as the name implies, occurs in western states of the US. VEE is seen in Central and South America. Outbreaks occur occasionally in Mexico and can spread to areas of Texas along the Mexican border. EEE occurs every year in Florida and occasionally will be seen in Georgia, especially the southernmost counties. At least 10 cases of EEE have been diagnosed in Georgia so far this year, some have been fatal. EHV occurs sporadically worldwide as this virus is present in virtually all populations of equine. VEE most often causes respiratory disease; the necrologic form is less common and usually produces dysfunction in the hind limbs and urinary tract. Rabies causes a myriad of clinical signs and must always be considered in a horse with necrologic disease, especially when signs of encephalitis are present. If rabies is suspected and the patient dies or is euthanized, the animal must be autopsied and tested for rabies. All humans in contact with a rabies suspect must be identified so that prophylaxis treatment can be be initiated in a timely fashion if needed.
EEE, WEE, and VEE are closely related viruses. West Nile is similar but belongs to a family of viruses that cause encephalitis in humans, such as St. Louis Encephalitis, Japanese Encephalitis, and others. However, they are all arboviruses. They are arthropod-borne, which means that an arthropod organism (mosquito, tick, flea) is the intermediate host and important in transmission of the virus between species. For WNV, EEE, WEE, and VEE various mosquito species are the culprits. The natural host for these viruses is the bird. Many Asian species have been found to carry these viruses. Birds are the reservoir host, meaning that the virus survives for long periods in this species (ie, over winter, over time). The migration of birds may be important in the spread of the virus over a continent or perhaps even between continents. Mosquitoes must be present to transfer the virus to other species. Mosquito species have also been discovered recently in the US that were previously found only in other parts of the world. The pathogenesis of infection is as follows: during periods of mosquito activity (ie, late spring - early fall) a mosquito bites an infected bird during a viremic stage (virus is present in blood), picks up the virus during feeding, then bites another animal and gives the virus to this individual, again during feeding. The cycle proceeds: bird - mosquito - bird. However, some mosquito species feed on many different hosts, i.e., humans, horses, and other mammals. We and our equine companions are "accidental" hosts. Although susceptible to infection, we do not generally develop a level of viremia that is high enough to transfer the virus to a mosquito. Therefore, we are "dead-end" hosts as the virus stops here.
The WNV was first identified in a human with a febrile illness in Africa in 1937. Since then, it has been found in many parts of Africa, Asia, Europe, and the Middle East. Antibodies to WNV are now commonly found in birds in Africa where the disease is endemic in this species. It was first identified in the US in the summer of 1999 when large numbers of dead birds began appearing in New England. Cases of febrile illness sometimes with encephalitis in humans and horses soon followed. Investigation into the cause of the illness first identified a different virus. However, the work of a veterinarian in New York investigating the deaths of numerous exotic birds in her zoo helped to correctly identify WNV as the cause. The current situation with the WNV is an excellent example of the how the world is becoming one community via global commerce and transportation. It also demonstrates how a "new" disease can affect a naive population. In areas where the disease was previously unknown, more clinical cases are seen at first as the population responds to the new invader. In spite of this, subclinical infection is actually the most common scenario seen with exposure to WNV. No clinical signs are apparent, however, an antibody titer is measurable in the blood. Fever, malaise, headache, body ache, etc. similar to other viral infections, is the next most common clinical presentation. Signs of encephalitis actually occur in a low percentage of cases in both humans and horses, perhaps 15-20%. However, some of these cases will be fatal. It appears that about 1/3 of the horses who develop signs of encephalitis will die. The immunocompromised, the very old, and the very young, are the most susceptible and the most likely to die from infection, as their immune systems are unable to kill the virus.
A vaccine to the WNV has been produced for the horse. Initially, two injections are required 3 - 4 weeks apart to ensure adequate stimulation of the immune system. High demand has necessitated its delivery first to areas with the highest level of infection. We expect the vaccine to be in our hands sometime in September. It has been shown to stimulate antibody production, but efficacy is unknown . Side effects should be minimal as it is very similar to the vaccines already being produced for EEE, WEE. Immunity lasts about 6 months. We highly recommend that the timing of vaccination for the viral encephalitides such that high antibody levels coincide with mosquito season, ie booster in early spring and again 6 months later if mosquitoes are still present.
Points to remember:
- Exposure to and therefore illness due to the WNV is seasonal in occurrence as the presence of the mosquito is required for transmission to occur.
- Infected birds are seen first, seen in others species usually only w/in a 10 mile radius of areas with infected birds.
- Most cases are inapparent or mild. A few will develop encephalitis, 1/4 to 1/3 of these may die.
PREVENTION of West Nile infection:
Reduce exposure to mosquito bites via...
- removal of sources of standing water
- frequent use of mosquito repellents - humans should spray clothing as well
- house during periods of high mosquito activity (difficult since some species bite all times of the day)
- provide active immunity via vaccination.
For the most current info on West Nile Virus, consult the following Websites: