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Eastern Equine Encephalitis1
C.D. Morris2Eastern equine encephalomyelitis virus (EEEV) has been the cause of epizootics of eastern equine encephalitis (EEE) in North American horses as far back as 1831, but undoubtedly, the virus itself was present in its endemic cycle long before that (Hanson 1957, Simms 1950). The virus, however, did not receive its name until a major outbreak occurred in horses in coastal areas of Delaware, Maryland, New Jersey, and Virginia in 1933 (Giltner and Shahan 1933, Ten Broeck et al. 1935). There were additional outbreaks in 1934 in Virginia and 1935 in North Carolina. It was during the 1935 outbreak that birds were considered to be a possible reservoir host (Ten Broeck 1938), but it was not until 1950 that the first virus isolation was made from a wild bird (Kissling et al. 1951). Subsequent studies have shown that many birds, including virtually all passerine species, are susceptible to EEEV infection (Kissling et al. 1954a, 1955).
The first human cases of EEE were confirmed in 1938 by virus isolation from brain tissue in New England (Fothergill et al. 1938, Howitt 1938). The fact that the virus could cause encephalitis in wild birds and domestic pheasants was first documented in Connecticut in 1938 (Tyzzer et al. 1938). Other vertebrates besides human beings, horses and birds have been found naturally infected with EEEV. None of these are considered to play any role in the epidemiology of the virus nor is the virus considered a major disease of other animals.
Mosquitoes were first incriminated as potential vectors of EEEV in 1934, and a number of studies have shown species of Aedes, Culex and Coquillettidia perturbans could become infected with and transmit EEEV from one vertebrate to another (Mirrill et al. 1934, Davis 1940, Ten Broeck and Merrill 1935, Chamberlain et al. 1954).
Outbreaks of EEE are infrequent and, perhaps because of their infrequency, the disease has a significant economic and social impact once an endemic focus has been identified. The first time the disease occurs in an area, there is the loss of horses and/or poultry, perhaps human morbidity and mortality, and the human fear of the unknown.
The social and economic impact of mosquito control for EEE prevention is enormous once the potential for disease is recognized in an area. The economic impact entails costs for surveillance, prevention and control. In many cases these costs, especially for mosquito control, are not trivial.
The Virus
EEEV has been isolated from, or antibodies to EEEV have been found in, naturally infected ring-necked pheasants, pigeons, chukar partridge, Pekin ducks, turkeys, and a multitude of wild birds, particularly passerines, but also including owls, whooping cranes and shore birds (Moulthrop and Gordy 1960, Dougherty and Price 1960, Kissling 1958a, 1958b, Clarke 1961, Spalatin et al. 1961, Emord et al. 1984, Karstad et al. 1960).Virus and antibodies have been found less frequently in naturally infected mammals, even though most small mammals tested are highly susceptible (Trainer and Hanson 1969, Trainer 1970, Hayes et al. 1964, Wellings 1985, Syverton and Berry 1940, Main 1979, Hurst 1950, Sabin and Olitsky 1938a). Turtles and snakes have also been infected naturally and experimentally, as have swine, bovines, hamsters and fish (Hayes et al. 1964, Karstad and Hanson 1959, Karstad 1961, Purcell et al. 1972, Soret and Sanders 1954, Satriano et al. 1957).
The isolation of EEEV from mosquitoes is very common during epizootics but much less common during inter-epizootic periods. EEEV isolations have been reported in the literature from 23 species in six genera. More than 80 percent of these have been from Cs. melanura but there have been isolations made from (in roughly decreasing frequency) Culex nigripalpus, Cq. perturbans, Culiseta morsitans, Aedes sollicitans, Anopheles quadrimaculatus, Culex salinarius, Culex pipiens, Culex restuans, Culex species, Aedes canadensis, Aedes atlanticus-tormentor, Aedes cantator, Aedes infirmatus, Aedes species, Anopheles crucians, Culex (Melaniconium) species, Aedes vexans, Culiseta minnesotae, Culex territans, Uranotaenia sapphirrina, Culex quinquefasciatus, Aedes triseriatus, Aedes mitchellae and Anopheles punctipennis.
Disease in Humans
The course of infection of EEEV in the human is dependent on the age of the person and the route of virus entry (Hurst 1950, Wyckoff and Tesar 1939, Sabin 1938, Sabin and Olitsky 1938b). There are two types of illness, systemic and encephalitic. A systemic infection is abrupt and characterized by malaise, arthralgia, and myalgia. In a few hours the patient is chilly and experiences severe muscular shaking, which lasts for a few days. Maximum temperatures reach 100 to 104 F. The illness lasts one to two weeks, there is no central nervous system (CNS) involvement, and recovery is complete (Clarke 1961).The encephalitic form of the disease in infants is characterized by an abrupt onset, whereas, in older children and adults onset of active encephalitis typically occurs after a few days of indisposition (Ayres and Feemster 1949). Symptoms include fever of 102 to 106.4 F, irritability, restlessness, drowsiness, anorexia, vomiting, diarrhea, headache, cyanosis, convulsions, and coma (Hauser 1948, Clarke 1961, Ayres and Feemster 1949). Tremors and muscular twitching are usually accompanied by neck rigidity, which is continuous. Cerebrospinal fluid usually has increased pressure with 200 to 2000 cells, 60 percent to 90 percent neutrophils.
Death typically occurs in two to 10 days. During epidemics the initial mortality approximates 70 percent. Nearly all who recover have disabling mental and physical sequelae, which are progressive (Hauser 1948).
Disease in Domestic Animals
Four major patterns of infection in horses with EEEV have been observed, both by subcutaneous inoculation and mosquito bite (Kissling et al. 1954b). The first is characterized by a biphasic febrile reaction. The outcome can be fatal or the animals may recover with or without CNS sequelae. The maximum viremia of 19 inoculated equines in one study was 5.8 SMLDS50 (Byrne et al. 1964). The second type of infection is characterized by a single temperature rise where the horses show no signs of CNS involvement although virus can be circulating in the blood. The third pattern of infection is the presence of small amounts of virus without febrile illness and the fourth type is the absence of both a febrile response and demonstrable circulating virus even though there is development of specific antibodies.A survey of 67 equine deaths due to EEE in the US in 1971 showed that the most common signs of illness were: depression (49 percent of cases), fever above 103o (30 percent), ataxia (25 percent), paralysis (25 percent), anorexia (20 percent) and stupor (20 percent) (Maness and Calisher 1981). Other symptoms of note include irregular gait, grinding of teeth, incoordination, circling, staggering, recumbency and hyperexcitability.
Most species of domestic fowl and wild birds show signs referable to CNS involvement consisting primarily of leg paralysis, tremors, and somnolence followed by prostration and death (Tyzzer et al. 1938, Moulthrop and Gordy 1960, Spalatin et al. 1961, Coleman and Kissling 1972, Dein et al. 1986, Jungherr et al. 1958, Faddoul and Fellows 1965, Ranck et al., 1965). Younger animals, including people, birds, and rodents, are typically more susceptible to CNS disease (Tyzzer et al. 1938, Hurst 1950, Hanson et al. 1968, Sabin and Olitsky 1938b).
Disease in Wildlife
EEEV infection in wild birds may result in disease in introduced species such as the English sparrow (Stamm and Kissling 1956), ring-necked pheasant and domestic pigeon (Fothergill et al. 1938). Die-offs of native birds, especially small species, have been noted during EEEV epizootics, but the cause of death was not conclusively identified as EEEV (Emord and Morris 1984, McLean et al. 1985).Bats are susceptible to natural infection and by inoculation and mosquito bite in the laboratory, but not by ingestion of virus (Main 1979a, 1979b). Only one of 276 small mammals in Massachusetts had antibody-positive sera; none were viremic (Hayes et al. 1964). In contrast, 3 percent of 1,172 Florida raccoons and opossum sera had antibodies to EEEV (Wellings 1985). Voles, woodchucks, and cottontail rabbits are highly susceptible to and invariably die from experimental infections (Syverton and Berry 1940). The opossum survived inoculation without signs of disease.
Reptiles and amphibians have also been found to be naturally infected with EEEV (Hayes et al. 1964, Karstad 1961, Goldfield and Sussman 1967), to be susceptible to experimental infection (Hayes et al. 1964, Karstad 1961), to maintain high viremia over several months (Hayes et al. 1964, Smith and Anderson 1980), and to experimentally carry the virus through hibernation (Hayes et al. 1964).
Epidemiology
On a gross geographic scale, outbreaks of EEEV in North America have been documented in the Canadian province of Quebec and in essentially all of the United States east of the Mississippi River. West of the river, the virus has been isolated from Minnesota, Wisconsin, South Dakota and Texas. The incidence of EEE in humans since 1955 has ranged from zero to 36 (mean of seven) human cases per year (Monath 1979, Francy 1985). The number of inapparent cases per overt case was estimated at 23 for the 1959 outbreak in New Jersey, giving an attack rate of approximately one per 1,000 (Goldfield et al. 1968). Between 1956 and 1972 there were 684 reported equine cases with a range from 1 to 132 per year (Monath 1979). The equine attack rate in New Jersey varied from 0.4 to 80.5 cases per 10,000 animals between 1933 and 1959 (Goldfield and Sussman 1968).In the northern part of the virus range, both human and equine cases occur between July and October. Human cases occur year-round in Florida but are concentrated between May and August (Bigler et al. 1976). The virus or disease is often recognized first in either wild birds, penned pheasants or equines prior to human involvement (Goldfield and Sussman 1968, Beadle 1952, Morris et al. 1973, Howard 1985). Epizootic activity in a specific endemic area occurs about every five to 10 years. Peaks of equine cases occur approximately every five years, whereas peaks of human cases occur about every 10 years (Goldfield and Sussman 1968, Monath 1979, Morris 1985, Shope 1982).
People at greatest risk to EEE are children under 15 and adults over 55. Those age groups make up 70 percent to 90 percent of the cases in a given outbreak (Goldfield and Sussman 1968, McGowan 1973). Both sexes are equally affected, although typically there are more males than females (Bigler et al. 1976, McGowan 1973). Inapparent infections are the same for all age groups and for both sexes (Goldfield et al. 1959). The disease is rural in distribution, and most cases are associated with wooded areas adjacent to swamps and marshes. Horses of all breeds are susceptible (Gibbs 1985).
Transmission Cycles
The classical concept of EEEV epidemiology is based on the assumptions that: 1) EEEV activity in geographically isolated locations are interrelated epidemiologically, if not interdependent, and 2) there is one and only one EEE virus (with perhaps a latent phase) that is epidemiologically distinct from and independent of other arboviruses and microorganisms that share the same mosquito and avian hosts.Prior condensations of EEEV epidemiology typically conclude that: 1) Culiseta melanura is the principle endemic vector; 2) wild birds, primarily passerines, serve as the primary amplifying hosts; 3) epizootics begin in swamps and move locally outward through viremic birds; 4) in some cases, migrating birds introduce the virus into distant "clean" ecosystems; 5) humans and equines are dead-end hosts; 6) there is a single most important epidemic or epizootic vector; 7) nonavian vertebrates are potential but unproven maintenance hosts; and 8) the overwintering mechanism is unknown or an overwintering mechanism is not required.
Alternative interpretations of published data are possible given a different set of apriori conditions. New hypotheses stated within a scenario based on one such alternative framework will now be presented.
The first apriori concept is that there are many distinct, geographically isolated foci of EEEV subpopulations, each with its own isolated communities of invertebrate vectors and vertebrate hosts. These isolated foci are operative at the level of individual swamps or swamp complexes, not just between states or geographic areas of the continent.
The fact that each year EEEV epizootic activity in North America is typically in a different location or in several distant locations, rather than widespread, is presented as support. Even within a state or county, virus activity will be associated with one region or swamp complex one year, and another region or swamp complex the next (Bigler et al. 1976, Morris 1985, Gamble 1985).
In all likelihood, the subpopulation of EEEV from different areas of the United States have different infection rates and transmission rates in different subpopulations of mosquitoes, similar to what has been observed for La Crosse virus and Aedes triseriatus. Behavioral differences have already been observed between subpopulations of Cs. melanura (Morris et al. 1980, Morris 1984, Howard et al. 1983, Hayes 1958, 1961, 1962, Burbutis and Lake 1956, Main et al. 1966, Nasci and Edman 1981a, 1981b).
The second apriori concept is that within a focus, the EEEV subpopulation is multi-phased or genotypically unstable, with the capability of changing from an avirulent phase which current techniques do not recognized to a virulent form of which we call EEEV.
Because EEEV has been isolated every month of the year in Florida, it has been proposed that there is active virus circulation year-round in the state, with no overwintering mechanism required (Bigler et al. 1976). This may be true in the southern tip of Florida, but in those parts of the state where EEEV is most prevalent there are long periods during the winter without adult mosquitoes. Thus, a winter reservoir seems prerequisite for virtually all North American endemic foci.
Each focus of EEEV is here considered allopatric, and while differences in the epidemiology of the virus should be expected among the foci, there remains the constant fact that Cs. melanura is present in all foci. Since over 80 percent of the EEEV have come from Cs. melanura, it is considered the prime candidate as the overwintering host for EEEV (Wellings 1985, Maxfield 1982).
Based on these concepts, the following is proposed as a typical transmission cycle of EEEV in North America: The virus, in an avirulent phase, resides in the overwintering invertebrate host, Cs. melanura. The spring brood, or perhaps only the summer brood, of Cs. melanura transmits the virus to its predominant hosts - passerine birds - and the virus is continuously circulated between these two host species. Sometime during this cycle the avirulent phase mutates to a virulent phase. This phase change occurs in the transfer from Cs. melanura to passerine bird and is thus essentially limited to the swamp and associated habitats where Cs. melanura is most abundant. At this point the passerines are viremic for the avirulent phase, but only a small percentage produce antibodies. The stage is now set for epornitic EEEV activity.
Following breeding, passerine birds undergo severe reproductive system regression and a complete feather molt (Meier and Russo 1985). This typically begins in mid-July for most passerines (Stokes 1979), and during this period birds are relatively quiet and inactive (Wallace and Mahan 1975). As any avid birder knows this is a bad time for bird watching. Molting is followed by metabolic and behavioral changes associated with post-breeding random wanderings and then fall migration (Meier and Russo 1985). These major avian physiologic changes provide the virus with a substantially different set of host parameters. If the virus is going to change to the virulent phase we call EEEV, this would seem to be the best time and location.
The consequences of the virulent virus in wild birds are the production of high viremias and antibodies, and perhaps some mortality. At this stage other bloodsucking arthropods in the swamp become involved as secondary vectors. There is no single epizootic vector species for all foci or for all hosts within a focus.
The post-nesting random wanderings of avians, particularly young birds, may serve as a mechanism of dissemination of the virulent phase within the limits of the premigratory range, which can be north or south from the breeding area (Wallace and Mahan 1975). Migratory birds that settle in an outbreak area should be as susceptible to infection as resident birds; the probability of becoming so being largely dependent upon the length of stay in the area. Any influx of susceptible migrants would tend to amplify the epornitic, and in that sense migratory birds could contribute to EEEV epidemics (Crans 1985). Viremic migratory birds may leave endemic foci but it is highly problematic that they serve as a source of new outbreaks. If they did it would be apparent by a spread of EEEV activity from north to south concurrent with fall bird migrations; this has not been demonstrated. What has been demonstrated is that EEEV outbreaks occur in the same foci repeatedly and only where there is Cs. melanura. If Cs. melanura were not essential in epidemic areas there should be outbreaks throughout the migratory range of infected passerines; this also does not happen.
EEE in man and equines is closely associated with the swamp breeding grounds of Cs. melanura. Disease in either vertebrate host seldom occurs beyond five miles from these foci (McLean et al. 1985, Morris 1985, Shope 1982), and prevalence of antibodies in birds decreases with distance from the swamp (Emord and Morris 1984, McLean et al. 1985). This distance is within the flight range of Cs. melanura and the mosquito species which probably serve as epidemic vectors, such as Cq. perturbans, Ae. vexans, Ae. canadensis, Ae. sollicitans, Cx. nigripalpus and others (Horsfall 1973, Crans et al. 1976, Crans 1977, Nayar 1982, MacCreary and Stearns 1937). Thus, both mosquitoes and birds are capable of disseminating the virus from the swamp foci.
It is generally believed that equines are dead-end hosts, yet experimental studies have shown viremias high enough to infect mosquitoes (Chamberlain et al. 1954, Howard and Wallis 1974, Byrne et al. 1964). Thus, horses may enter into the epidemic maintenance of EEEV (Kissling 1958b).
While a number of laboratory studies have evaluated the vector potential of many mosquito species, results of these studies should be viewed with caution, since both the virus and mosquitoes have been laboratory adapted (Howard and Wallis 1974, Chamberlain and Sudia 1955). A case in point is that laboratory infection and transmission studies classified Cs. melanura as only a fair to poor vector (Chamberlain et al. 1954).
EEEV is frequently isolated from different Aedes species and different Culex species in different parts of the continent. However, EEEV has been isolated from a single species, Coquillettidia perturbans, in many parts of the virus range, including Georgia, Florida, New York, Michigan, Massachusetts and New Jersey (Howitt et al. 1949, Maxfield 1977, Wellings et al. 1972, Morris and Srihongse 1978, Francy 1982, Veazey et al. 1980).
Cq. perturbans is an opportunistic feeder and feeds equally on birds and mammals, avidly on man and equines, thus making it an ideal potential vector (Means 1968, Edman 1971, Tempelis 1975).
Adult mosquito population densities are closely linked to environmental conditions, and densities are highest during years with high rainfall. Associations between EEEV outbreaks and excessive rainfall have been observed (Howard 1985, Maxfield 1982, Hayes and Hess 1964). It is important to reemphasize that mosquito population density is not, in itself, a presage of either detectable endemic or epidemic EEEV activity.
In any given endemic focus, the hypothesized avirulent-phase virus is probably active annually in the mosquito-bird cycle, but goes unrecognized due to the insensitivity of our current techniques. Virus mutation rate is a function of, among other things, the physiologic conditions of the avian and mosquito populations and the frequency of transmission among different host species and the prior exposure of the avian host (Smith 1960). Consequently, the more mosquitoes and susceptible hosts there are in the focus, the greater the likelihood for mutations. This is not to say that simply having large numbers of mosquitoes and/or birds will be sufficient to trigger an outbreak. In fact, we know there can be high mosquito populations without epidemic EEEV activity (Howard 1985). The relationship between bird densities and the potentials for epidemics remains unstudied.
EEEV was isolated from overwintering larval Cs. melanura (Philbrook et al. 1958), and there is laboratory evidence of transovarial transmission of EEEV by Cq. perturbans (Chamberlain et al. 1956, Schaeffer and Arnold 1954). One isolate of EEEV has also been made from male Cs. melanura but concurrent isolations of EEEV from females in the same collection suggests the possibility of contamination (Chamberlain and Sudia 1961). More recent laboratory studies indicate, however, that EEEV in Cs. melanura does not infect ovarian tissue and that the virus is not transovarially transmitted (Sprance 1981, Scott et al. 1984). Although species other than Cs. melanura have been suggested as possible overwintering hosts, recent field studies on populations of Cs. melanura, Cq. perturbans, Cs. morsitans and Ae. cantator all failed to demonstrate virus in males, first-brood females, or overwintering larvae (Morris and Srihongse 1978, Sprance 1981, Watts et al. 1986, Muul et al. 1975, Hayes et al. 1962, Howard and Francy 1985, Clark et al. 1985).
Virus latency in birds, as a possible reservoir mechanism of EEEV cannot be disproven by current knowledge. From a virus evolutionary standpoint, however, one must question the need for latency in an avian host which the virus can kill when the virus is so common and widespread in a commensalistic host, the mosquito. It is also difficult to justify latency in birds as a reservoir when the interval between epornitics in a given focus usually exceeds the one-to-two-year average life span of most passerines (Wallace and Mahan 1975). If latency in nonculicine hosts does serve as a reservoir, new research initiatives should emphasize long-lived reptilians (especially snakes and turtles) from which avians evolved, and which seem to be less susceptible to disease when infected with EEEV.
Ecology
The primary habitats for EEEV are lowland areas in the eastern half of North America. The microenvironments in these foci are quite similar and specific and the sizes of the foci quite small. Swamps and environs in Maryland, New York, New Jersey, Massachusetts, Florida and Michigan have been described as being associated with muck-peat soil associations dominated with hardwoods (McLean et al. 1985, Crans 1985, Gamble 1985, Muul et al. 1975, Moussa et al. 1966, Joseph and Bickley 1969, Morris et al. 1980). In the northern part of the virus range, the indicator tree species are red maple and hornbeam. In New Jersey, Maryland and Florida the key species are red maple, cedar and loblolly bay (Gamble 1985, Moussa et al. 1966, Morris et al. 1980).The bionomics of Cs. melanura larvae require wet, dark, highly organic water (Joseph and Bickley 1969, Pierson and Morris 1982, Williams et al. 1971, Siverly and Schoof 1962). Breeding is usually concentrated on the edge of the swamps but also occurs in the swamp interior (Pierson and Morris 1982, Williams et al. 1971). Overwintering larvae pupate in early spring and the first adults emerge in late May in the north, earlier in the south. In late June to early July in the north (earlier in the south) there is typically a second emergence in summer. Since EEEV is not normally found in mosquitoes until after the summer brood emerges, there may be some significant difference in the physiology of the two broods, which influences vector potential.
The blood-feeding habits of Cs. melanura are universally similar and ideally suited for EEEV transmission. All subpopulations of Cs. melanura examined so far are almost exclusively ornithophilic, and typically over 90 percent feed on passeriformes (Morris et al. 1980, Nasci and Edman 1981a, Tempelis 1975, Edman et al. 1972). They do occasionally feed on reptiles and less frequently on mammals and man (Morris et al. 1980, Hayes 1961, Hayes and Doane 1958, Schober 1964). The low incidence of EEE in humans may be the result of these infrequent feedings by Cs. melanura rather than a secondary vector.
Surveillance
Most states where EEEV is endemic have a statewide diagnostic service for veterinarians and physicians to submit blood and organ samples from suspected EEE cases. Reporting is required in some states, voluntary in others. These systems are inappropriate as an early warning system since the turnaround time of most is too long. They do, however, monitor nonendemic activity for the historical record.Where veterinarians and epidemiologists are familiar with the parochial signs and symptoms of equine EEE, field diagnosis becomes an accurate and more-rapid system upon which to base increased mosquito control efforts. By the time EEEV has become epizootic, however, prevention of additional cases often requires the widespread spraying of mosquito adulticides. With or without spraying, human and equine cases typically persist in the north until the advent of cold weather, which interrupts the man- or horse-mosquito interactions. In the south, epizootics seem to abate as a result of drier weather or high immunity levels in wild birds.
Tracking horse cases is an excellent monitoring system, although the method is biased by the levels of vaccination in the population at risk. The higher the level of vaccination in the equine population, the less reliable the EEE monitoring system (Maxfield 1982).
Sentinel chickens are used for monitoring EEEV activity, but substantial evidence indicates they are inappropriate as an early warning system for epidemic activity (Kissling 1958b, Bigler et al. 1976, Crans 1985, Sudia et al. 1969).
In some foci, endemic passerine birds and mosquitoes are monitored for endemic EEEV activity (Crans 1985, Howard 1985). Virus isolations from mosquitoes, especially from other than Cs. melanura, signal possible epidemic activity and elude appropriate warnings and recommendations for increased mosquito control activity (Crans 1985, Maxfield 1982, Howard 1985).
These techniques are time-consuming and costly. Again, often the turnaround time from field to laboratory results is too long for implementing effective EEE-preventative mosquito control. The key to a better system lies in the development of rapid field applicable techniques for detecting virus in birds and invertebrates. The ELISA and other tests are currently being developed for this purpose (Olson 1985).
Prevention and Control
Prevention of epidemics of EEEV has already been accomplished. The prevention of outbreaks in man is simply a matter of effective surveillance and appropriate mosquito control. Techniques for both are currently available, and refinements and new methods are being developed. Prevention of EEE in equines and domestic fowl by immunization has been available for decades and is routinely practiced by responsible owners. The recurrence of human and equine EEE in known endemic foci results from educational deficiencies and/or complacency by owners or public authorities, not from a lack of scientific knowledge of the epidemiology and control of the disease.Changing land use has significant impact on the occurrence of EEEV, in two ways. The initial epidemics of the 1930s in the northeast resulted from close contact between mosquitoes and people who lived near endemic foci. As this area was developed and the significance of wetlands in disease epidemiology was recognized, many of these breeding areas were filled or drained and the incidence of EEE dropped.
The corollary, which is exemplified in central Florida, is that as cultural development occurs, man and his domestic animals move into areas near previously unknown endemic foci and both contract the disease. EEE is an established veterinary problem in most of Florida (Bigler et al. 1976, Gibbs 1985). It is becoming a medical problem because development is spreading inland, closer to the freshwater marshes and swamps, which are endemic foci of EEEV.
Vaccines for humans are available but are used only to immunize virus laboratory technicians. Vaccines have proven to be very effective for preventing equine EEE, but recent evidence suggests that there are windows of susceptibility in current vaccination practices of foals (Gibbs 1985). Vaccines for equines are available through veterinarians and feed stores. Reared pheasants are often vaccinated routinely although there is some question of efficacy of these vaccines (Beaudette et al. 1952, Kissling 1958a, Snoeyenbos et al. 1978, Eisner and Nusbaum 1983, Sussman et al. 1958). Both of the problems with vaccines and vaccination protocols appear to be correctable.
EEE prevention by controlling wild birds is untenable. However, because passerine birds have a strong breeding site affinity (Emord and Morris 1984), and because the level of immunity of wild birds can influence the level of virus circulation (Dalrymple et al. 1972, Stamm 1958), immunization of wild birds through the use of feeding or watering stations may be a way to reduce EEEV activity in small foci.
Prevention and control of EEE has historically been addressed by the use of mosquito control programs. The efficacy of these programs is difficult to evaluate in most cases because mosquito control is often undertaken in response to an ongoing epizootic. Evidence that ongoing programs are effective is seen in the absence of epidemics of EEE since the advent of modern mosquito control in the 1940s. Two difficulties with mosquito control as a means of EEE control are that EEEV foci are in rural/suburban areas, and the mosquito breeding areas are often extensive and difficult to reach and treat by means other than aircraft.
Mosquito control decisions for EEE control in some states are linked to abundance of certain mosquito species, with or without concurrent virus isolations (Crans 1985, Maxfield 1982, Howard 1985. The indicator species in New York and Massachusetts is Cs. melanura and in New Jersey Cs. melanura and Ae. sollicitans. Diurnal resting shelters have proven to be an excellent monitoring technique for all physiologic states and both sexes of Cs. melanura (Crans 1985, Morris et al. 1980, Moussa et al. 1966, Morris 1981). Miniature light traps are used to monitor host-seeking Cs. melanura and man-biting species (Maxfield 1982, Howard 1985, Sudia and Chamberlain 1962). Human-bait sweep collections are used to monitor Ae. sollicitans (Crans 1985).
One well-timed aerial adulticide over endemic swamps in early to mid-July in central New York has been effective in preventing EEE cases in adjacent uplands. This control effort is aimed at Cs. melanura and is accomplished within two weeks after peak emergence of large summer broods. The size of the summer brood tends to be clearly either large or small and the decision to spray is, therefore, usually clear-cut. Spraying can often be limited to the perimeter of large swamps where mosquito and bird densities are greatest (Emord and Morris 1984, Morris 1984, Howard et al. 1983).
The current preferred methods for mosquito control are the application of conventional insecticides and source reduction or habitat management. Societal demands for preserving natural wetlands means that source reduction will not likely be available in the 21st century. Also, societal pressure for greater controls on the use of, or for eliminating, agrichemicals vital to current mosquito control programs continues to increase. Tomorrow's challenge in EEE prevention via mosquito control will be substantial under these greater restrictions.
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Footnotes
1. This document is ENY-700-6-1, part of the Mosquito Control Handbook, published cooperatively by the Department of Entomology and Nematology, University of Florida; the Florida Medical Entomology Laboratory, Vero Beach; the Florida Department of Health and Rehabilitative Services, Office of Entomology Services (HRS-ES), Jacksonville; the Florida Mosquito Control Association (FMCS); the St. Lucie County Mosquito Control District; the Indian River Mosquito Control District; the Pasco County Mosquito Control District; Polk County Environmental Services; and the USDA Medical and Veterinary Entomology Research Laboratory, Gainesville, Florida. ENY-700-6-1 was revised January 1992; reviewed <pubdate>September 1998</pubdate>. The electronic edition of the Mosquito Control Handbook is provided by the Florida Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, 32611. Please visit the FAIRS Web site at http://hammock.ifas.ufl.edu.2. C.D. Morris, Assistant professor and extension medical entomologist at the Florida Medical Entomology Laboratory, IFAS-University of Florida, Vero Beach.
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