April 2003

Eastern Equine Encephalitis - Rare But Devastating

Eastern Equine Encephalitis (EEE) is a disease of birds, humans and equines (horses, mules, ponies, donkeys, etc.) caused by a virus that is transmitted by mosquitoes. The mosquito that transmits the virus amongst the bird population in Florida is the Culiseta melanura mosquito, strictly a bird feeding specie.

            Maintenance and transmission of the EEE virus in nature remains a fascinating problem. Much of EEE’s disease and ecological pathway requires additional study and verification. Birds are the amplification host for the virus. When infected, native birds are minimally affected; they get infected, are lethargic for a few days, produce antibodies to EEE, and usually recover completely. From 3 to 7 days after the bird is infected and are in the process of producing antibodies, they are infective to mosquitoes. There are several possible means by which the virus is thought to be maintained in nature; the virus overwinters in the mosquito vector, the virus is maintained in reptile and amphibian reservoirs and/or by birds when recrudescence occurs. Recrudescence is the reoccurrence of the disease after antibodies have initially neutralized the virus. Over time, about a year, the antibody level declines and the virus or viremia reappears in the blood. When this occurs the bird becomes infective again without an outside source (a mosquito) re-initiating the disease.

            Conversions in our sentinel bird flocks, that is, the detection of antibodies to EEE in the blood samples we take, occur on a regular basis, averaging about one per month. This is normal and nothing to get alarmed about, but it does alert us to step up our control activities in a specific area. The problem with EEE is when it gets out of our native bird populations and into equines and humans. Most cases of EEE in humans and equines occur in late summer and fall along the eastern seaboard and eastern Gulf coast of the United States. Most people infected with the virus have no symptoms, others get a flu-like illness with fever, headache and a sore throat. In rare cases, infection of the central nervous system occurs causing sudden fever, severe headache, followed quickly by seizures and coma. In these cases, between 50% -70% of the patients die, those who survive usually suffer some degree of permanent brain damage, only 10% fully recover. There is no specific treatment for EEE. Antibiotics are not effective against viruses and no effective viral drugs or human vaccines have been developed. Patient care centers on supportive therapy, treating the symptoms and complications of the disease. Total case costs range from $21,000 for transiently infected individuals to over $3 million to care for a severely affected person over their lifetime. Horses and other equines are not as lucky. Once infected the disease is invariably fatal with mortality in the 95 - 98 percentile range. Animals that survive are brain damaged and labeled as “dumb” animals. When an animal is diagnosed by a veterinarian as infected with EEE, euthanasia is recommended to avoid the suffering before the animal eventually dies. The good news for equines is that there is a vaccine available. The vaccine is effective for only one year and booster shots are required on an annual basis.

            The only positive aspect of EEE is that it is very rare, only 163 human cases have occurred in the U.S. since 1964. Fewer than 5 cases are reported in most years. However, with equines, because of their sensitivity and exposure, epidemics can be common during the summer and fall.

            Why is EEE so rare? There are several reasons. First, EEE requires a bridge vector, a mosquito specie that will bite both birds and mammals and is capable of maintaining the virus. Such a mosquito will pickup the virus from a bird, become infective, and if its next bloodmeal is from a horse or human, pass on the disease. Equines and humans are dead-end hosts for EEE, that is, they get the disease but don’t develop a high enough viremia or virus level in their blood to become infective to other mosquitoes that feed on the person or equine that is sick with EEE, it’s a dead end for the viruses’ spread. The bridge vector in our area is the Coquillettidia perturbans mosquito. Second, because the amplifying host for the disease is birds, a large number of susceptible birds need to be available and exposed to infection. This situation occurs every spring with a new crop of hatchlings. When these “new” birds get infected with EEE they amplify the virus and become infective hosts for those few days before they develop the antibodies to the virus that eliminates the disease from the bird. The third reason EEE is rare is that the mosquito vector numbers must increase to higher than normal levels. For this to occur requires abnormal rain events and amounts which creates more habitat for mosquito production. The fourth, and probably the most important reason EEE is rare, is that all these components to the disease cycle must coincide. The weather events that provide “extra” mosquito habitat, high mosquito vector populations (both bird and bridge vectors) must occur, and a susceptible bird (hatchlings) population must be available - all at the same time. Then, of course, for the disease to be expressed in humans and equines, we need to be bitten by an infected mosquito.

            So what can be done to break the cycle that EEE needs to infect humans and equines? We can’t stop birds from breeding, we can’t control the weather but we can try to control mosquitoes. For equines the solution is easy - vaccinate your animals - judiciously. For people, on an individual basis, we can minimize getting bit by wearing long sleeved shirts, pants, applying repellents to exposed skin, avoid the times of day when mosquitoes are most active, and avoid areas with high mosquito populations, especially swampy areas. As a mosquito control agency we can larvicide, adulticide and a third weapon is to herbicide. The bridge vector for EEE, Coquillettidia perturbans, is an unusual specie in that it requires specific, emergent, aquatic vegetation to complete its larval stage. The larva of this mosquito penetrates the stem of cattails, below the water surface, with its siphon tube, to obtain the oxygen it needs to survive. By killing the cattails we remove the habitat this mosquito needs to support its life cycle, in essence, a form of source reduction. By minimizing the bridge vector’s population we can reduce, even further, the rarity of this disease.