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Perspective
Eastern Equine
Encephalitis (EEE)
Arthropod-borne viruses,
i.e. arboviruses, are viruses that are maintained in nature
through biological transmission between susceptible vertebrate hosts by
blood feeding arthropods (mosquitoes, psychodids, ceratopogonids, and
ticks). Vertebrate infection occurs when the infected arthropod takes a
blood meal. The term 'arbovirus' has no taxonomic significance.
Arboviruses that cause human encephalitis are members of three virus
families: the Togaviridae (genus
Alphavirus),
Flaviviridae, and Bunyaviridae.
All arboviral encephalitides are zoonotic, being maintained in
complex life
cycles involving a nonhuman primary vertebrate host and a primary
arthropod vector. These cycles usually remain undetected until humans
encroach on a natural focus, or the virus escapes this focus via a
secondary vector or vertebrate host as the result of some ecologic change.
Humans and domestic animals can develop clinical illness but usually are
"dead-end" hosts because they do not produce significant viremia, and do
not contribute to the transmission cycle. Many arboviruses that cause
encephalitis have a variety of different vertebrate hosts and some are
transmitted by more than one vector. Maintenance of the viruses in nature
may be facilitated by vertical transmission (e.g., the virus is
transmitted from the female through the eggs to the offspring).
Arboviral encephalitides have a
global
distribution, but there are four main virus agents of encephalitis in
the United States: eastern equine encephalitis (EEE), western equine
encephalitis (WEE), St. Louis encephalitis (SLE) and LaCrosse (LAC)
encephalitis, all of which are transmitted by mosquitoes. Another virus,
Powassan, is a minor cause of encephalitis in the northern United States,
and is transmitted by ticks. A new Powassan-like virus has recently been
isolated from deer ticks. Its relatedness to Powassan virus and its
ability to cause disease has not been well documented. Most cases of
arboviral encephalitis occur from June through September, when arthropods
are most active. In milder (i.e., warmer) parts of the country, where
arthropods are active late into the year, cases can occur into the winter
months.
The majority of human infections are asymptomatic or may result in a
nonspecific flu-like syndrome. Onset may be insidious or sudden with
fever, headache, myalgias, malaise and occasionally prostration. Infection
may, however, lead to encephalitis, with a fatal outcome or permanent
neurologic sequelae. Fortunately, only a small proportion of infected
persons progress to frank encephalitis.
Experimental studies have shown that invasion of the central nervous
system (CNS), generally follows initial virus replication in various
peripheral sites and a period of viremia. Viral transfer from the blood to
the CNS through the olfactory tract has been suggested. Because the
arboviral encephalitides are viral diseases, antibiotics are not effective
for treatment and no effective antiviral drugs have yet been discovered.
Treatment is supportive, attempting to deal with problems such as swelling
of the brain, loss of the automatic breathing activity of the brain and
other treatable complications like bacterial pneumonia.
There are no commercially available human vaccines for these U.S..
diseases. There is a Japanese encephalitis vaccine available in the U.S. A
tick-borne encephalitis vaccine is available in Europe. An equine vaccine
is available for EEE, WEE and Venezuelan equine encephalitis (VEE).
Arboviral encephalitis can be prevented in two major ways: personal
protective measures and public health measures to reduce the population of
infected mosquitoes. Personal measures include reducing time outdoors
particularly in early evening hours, wearing long pants and long sleeved
shirts and applying mosquito repellent to exposed skin areas. Public
health measures often require spraying of insecticides to kill juvenile
(larvae) and adult mosquitoes.
Selection of mosquito control
methods depends on what needs to be achieved; but, in most emergency
situations, the preferred method to achieve maximum results over a wide
area is aerial spraying. In many states aerial spraying may be available
in certain locations as a means to control nuisance mosquitoes. Such
resources can be redirected to areas of virus activity. When aerial
spraying is not routinely used, such services are usually contracted for a
given time period.
Financing of aerial spraying costs during large outbreaks is usually
provided by state emergency contingency funds. Federal funding of
emergency spraying is rare and almost always requires a federal disaster
declaration. Such disaster declarations usually occur when the
vector-borne disease has the potential to infect large numbers of people,
when a large population is at risk and when the area requiring treatment
is extensive. Special large planes maintained by the United States Air
Force can be called upon to deliver the insecticide(s) chosen for such
emergencies. Federal disaster declarations have relied heavily on risk
assessment by the CDC.
Laboratory diagnosis of human arboviral encephalitis has changed
greatly over the last few years. In the past, identification of antibody
relied on four tests: hemaglutination-inhibition, complement fixation,
plaque reduction neutralization test, and the indirect fluorescent
antibody (IFA) test. Positive identification using these immunoglobulin M
(IgM) - and IgG-based assays requires a four-fold increase in titer
between acute and convalescent serum samples. With the advent of
solid-phase antibody-binding assays, such as enzyme-linked immunosorbent
assay (ELISA), the diagnostic algorithm for identification of viral
activity has changed. Rapid serologic assays such as IgM-capture ELISA
(MAC-ELISA) and IgG ELISA may now be employed soon after infection. Early
in infection, IgM antibody is more specific, while later in infection, IgG
antibody is more reactive. Inclusion of monoclonal antibodies (MAbs) with
defined virus specificities in these solid phase assays has allowed for a
level of standardization that was not previously possible.
Virus isolation and identification have also been useful in defining
viral agents in serum, cerebrospinal fluid and mosquito vectors. While
virus isolation still depends upon growth of an unknown virus in cell
culture or neonatal mice, virus identification has also been greatly
facilitated by the availability of virus-specific MAbs for use in IFA
assays. Similarly, MAbs with avidities sufficiently high to allow for
specific binding to virus antigens in a complex protein mixture (e.g.,
mosquito pool suspensions) have enhanced our ability to rapidly identify
virus agents in situ. While polymerase chain reaction (PCR) has
been developed to identify a number of viral agents, such tests have not
yet been validated for routine rapid identification in the clinical
setting.
Mosquito-borne encephalitis offers a rare opportunity in public health
to detect the risk of a disease before it occurs and to intervene to
reduce that risk substantially. The surveillance required to detect risk
is being increasingly refined by the potential utilization of these new
technologies which allows for rapid identification of dangerous viruses in
mosquito populations. These rapid diagnostic techniques used in threat
recognition can shorten public health response time and reduce the
geographic spread of infected vectors and thereby the cost of containing
them. The Arbovirus Diseases Branch of NCID's Division of Vector-Borne
Infectious Diseases has responsibility for CDC's programs in surveillance,
diagnosis, research and control of arboviral encephalitides.
Eastern equine encephalitis (EEE) is also caused by a virus transmitted
to humans and equines by the bite of an infected mosquito. EEE virus is an
alphavirus
that was first identified in the 1930's and currently occurs in focal
locations along the eastern seaboard, the Gulf Coast and some inland
Midwestern locations of the United States. While small outbreaks of human
disease have occurred in the United States, equine epizootics can be a
common occurrence during the summer and fall.
It takes from 4-10 days after the bite of an infected mosquito for an
individual to develop symptoms of EEE. These symptoms begin with a sudden
onset of fever, general muscle pains, and a headache of increasing
severity. Many individuals will progress to more severe symptoms such as
seizures and coma. Approximately one-third of all people with clinical
encephalitis caused by EEE will die from the disease and of those who
recover, many will suffer permanent brain damage with many of those
requiring permanent institutional care.
In addition to humans, EEE virus can produce severe disease in: horses,
some birds such as pheasants, quail, ostriches and emus, and even puppies.
Because horses are outdoors and attract hordes of biting mosquitoes, they
are at high risk of contracting EEE when the virus is present in
mosquitoes. Human cases are usually preceded by those in horses and
exceeded in numbers by horse cases which may be used as a surveillance
tool.
EEE virus occurs in natural cycles involving birds and Culiseta
melanura, in some swampy areas nearly every year during the warm
months. Where the virus resides or how it survives in the winter is
unknown. It may be introduced by migratory birds in the spring or it may
remain dormant in some yet undiscovered part of its life cycle. With the
onset of spring, the virus reappears in the birds (native bird species do
not seem to be affected by the virus) and mosquitoes of the swamp. In this
usual cycle of transmission, virus does not escape from these areas
because the mosquito involved prefers to feed upon birds and does not
usually bite humans or other mammals.
For reasons not fully understood, the virus may escape from enzootic
foci in swamp areas in birds or bridge vectors such as Coquilletidia
perturbans and Aedes sollicitans. These species feed on both
birds and mammals and can transmit the virus to humans, horses, and other
hosts. Other mosquito species such as Ae. vexans and Culex
nigripalpus can also transmit EEE virus. When health
officials maintain surveillance for EEE virus activity, this movement out
of the swamp can be detected, and if the level of activity is sufficiently
high, can recommend and undertake measures to reduce the risk to humans.
Centers for Disease Control and Prevention, National Center for
Infectious Diseases, Division of Vector-Borne Infectious Diseases, 1300
Rampart Road, Colorado State University Foothills Research Campus, P.O.
Box 2087, Fort Collins, Colorado 80522, USA; telephone: (970)221-6400;
fax: (970)221-6476
Every effort has been made to
provide correct, complete and up-to-date pest management information for
New York State in this publication. Changes in pesticide regulations thus
occur constantly, and human errors are still possible. These
recommendations are not a substitute for pesticide labeling. Before using
any product, chemical, or pesticide, read carefully, understand, and
follow strictly any instructions on the product label. The above
information has been obtained from sources believed to be reliable.
Neither the Fair Harbor Community Association or any employee of
FairHarbor.com has verified the correctness of any information contained
herein.
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