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Tick-borne Encephalitis
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| What
is tick-borne encephalitis? |
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Tick
image of Ixodes species
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Tick-borne encephalitis, or TBE, is a human viral infectious disease involving
the central nervous system. The disease is most often manifest as meningitis
(inflammation of the membrane that surrounds the brain and spinal cord),
encephalitis (inflammation of the brain), or meningoencephalitis (inflammation
of both the brain and meninges). Although TBE is most commonly recognized
as a neurologic disease, mild febrile illnesses can also occur. Long-lasting
or permanent neuropsychiatric sequelae are observed in 10-20% of infected
patients.
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| What
causes tick-borne encephalitis? |
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TBE is caused by
tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae,
that was initially isolated in 1937. A closely related virus in Far Eastern
Eurasia, Russian spring-summer encephalitis virus (RSSEV), is responsible
for a similar disease with a more severe clinical course.
| How
is TBEV spread, and how do humans become infected? |
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Ticks act as both the vector and reservoir for TBEV. The main hosts are
small rodents, with humans being accidental hosts. Large animals are feeding
hosts for the ticks, but do not play a role in maintenance of the virus.
The virus can chronically infect ticks and is transmitted both transtadially
(from larva to nymph to adult ticks) and transovarially (from adult female
tick through eggs). TBE cases occur during the highest period of tick activity
(between April and November), when humans are infected in rural areas through
tick bites. Infection also may follow consumption of raw milk from goats,
sheep, or cows. Laboratory infections were common before the use of vaccines
and availability of biosafety precautions to prevent exposure to infectious
aerosols. Person-to-person transmission has not been reported. Vertical
transmission from an infected mother to fetus has occurred.
| Where
is the disease found? |
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TBE is an important
infectious disease of in many parts of Europe, the former Soviet Union,
and Asia, corresponding to the distribution of the ixodid tick reservoir.
The annual number of cases (incidence) varies from year to year, but several
thousand are reported annually, despite historical under-reporting of
this disease.
| What
are the symptoms of TBE? |
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The incubation period
of TBE is usually between 7 and 14 days and is asymptomatic. Shorter incubation
times have been reported after milk-borne exposure. A characteristic biphasic
febrile illness follows, with an initial phase that lasts 2 to 4 days
and corresponds to the viremic phase. It is non-specific with symptoms
that may include fever, malaise, anorexia, muscle aches, headache, nausea,
and/or vomiting. After about 8 days of remission, the second phase of
the disease occurs in 20 to 30% of patients and involves the central nervous
system with symptoms of meningitis (e.g., fever, headache, and a stiff
neck) or encephalitis (e.g., drowsiness, confusion, sensory disturbances,
and/or motor abnormalities such as paralysis) or meningoencephalitis.
In contrast to RSSE, TBE is more severe in adults than in children.
During the first
phase of the disease, the most common laboratory abnormalities are a low
white blood cell count (leukopenia) and a low platelet count (thrombocytopenia).
Liver enzymes in the serum may also be mildly elevated. After the onset
of neurologic disease during the second phase, an increase in the number
of white blood cells in the blood and the cerebrospinal fluid (CSF) is
usually found. Virus can be isolated from the blood during the first phase
of the disease. Specific diagnosis usually depends on detection of specific
IgM in either blood or CSF, usually appearing later, during the second
phase of the disease.
| Are
there any complications after recovery? |
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In approximately
two-thirds of patients infected with the TBE virus, only the early (viremic)
phase is seen. In the remaining third, patients experience either the
typical biphasic course of the disease or a clinical illness that begins
with the second (neurologic) phase. The convalescent period can be long
and the incidence of sequelae may vary between 30 and 60%, with long-term
or even permanent neurologic symptoms. Neuropsychiatric sequelae have
been report in 10-20% of patients.
| Is
the disease ever fatal? |
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Yes, but only rarely.
In general, mortality is 1% to 2%, with deaths occurring 5 to 7 days after
the onset of neurologic signs.
| How
is TBE treated? |
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There is no specific drug therapy for TBE. Meningitis, encephalitis, or
meningoencephalitis require hospitalization and supportive care based on
syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may
be considered under specific circumstances for symptomatic relief. Intubation
and ventilatory support may be necessary.
| Who
is at risk for TBEV infection? |
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In disease endemic
areas, people with recreational or occupational exposure to rural or outdoor
settings (e.g., hunters, campers, forest workers, farmers) are potentially
at risk for infection by contact with the infected ticks. Furthermore,
as tourism expands, travel to areas of endemicity broadens the definition
of who is at risk for TBE infection.
| How
can TBEV infections be prevented? |
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Like other tick-borne
infectious diseases, TBEV infection can be prevented by using insect repellents
and protective clothing to prevent tick bites. A vaccine is available
in some disease endemic areas (though not currently in the United States);
however, adverse vaccine-reactions in children limit the utility of the
product.
| Other
related viruses. |
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The family Flaviviridae
includes other tick-borne viruses affecting humans and these viruses are
closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus
in Siberia and Kyasanur Forest disease virus in India. Louping ill virus
(United Kingdom) is a member of this family; it cases disease primarily
in sheep, and has been reported as a cause of a TBE-like illness in laboratory
workers and persons at risk for contact with sick sheep (e.g., veterinarians,
butchers).
| Suggested
Reading |
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Dumpis, U., Crook,
D., Oksi, J. Tick-borne encephalitis. Clinical Infectious Diseases. 1999;
28:882-890.
Haglund, M., Forsgren,
M., Lindh, G., Lindquist, L. A 10-year follow-up study of tick-borne encephalitis
in the Stockholm area and a review of the literature - Need for a vaccination
strategy. Scandinavian Journal of Infectious Diseases. 1996; 28(3)217-224.
Kaiser, R., Holzmann,
H. Laboratory findings in tick-borne encephalitis. Correlation with clinical
outcome. Infection. 2000; 28(2)78-84.
Logar, M., Arnez,
M., Kolbl, J., Avsic-Zupanc, T., Strle, F. Comparison of the epidemiological
and clinical features of tick-borne encephalitis in children and adults.
Infection. 2000; 28(2)74-77.
Mikiene, A., Laiskonis,
A., Gunther, G., Vene, S., Lundkvist, A., Lindquist, L. Tick-borne encephalitis
in an area of high endemicity in Lithuania: disease severity and long-term
prognosis. Clinical Infectious Diseases. 2002; 35(6)650-658.
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