Tick-Borne Encephalitis
Martin Haditsch
ABSTRACT
For a long time, tick-borne encephalitis (TBE) was perceived as
a risk only for the local population living in endemic areas.
There was very little specific awareness and hardly any knowl-
edge about this viral disease among doctors outside the endemic
areas. Thus TBE has been a neglected travel-associated health
risk.
World Tourism Organization statistics show that the Euro-
pean continent continues to be the main travel destination for
international travelers. Considerable parts of this continent,
especially those with the highest recent increases in interna-
tional tourism (i.e., the Baltic States) as well as parts of Asia are
proven TBE endemic areas (Figures 72-1 and 72-2). Thus it is
increasingly important to provide travelers to these areas with
current information on the risk of disease transmission and the
possibilities of prophylaxis in general, and vaccination options
in detail.
TBE is known under a variety of names, synonyms being
spring-summer-encephalitis, Central European encephalitis,
Far-East Russian encephalitis, Taiga encephalitis, Russian
spring-summer encephalitis, bi-undulating meningoencephali-
tis, diphasic milk fever, Kumlinge disease, Schneider′s disease,
and, in German-speaking areas, Früh-Sommer-Meningo-
Encephalitis (FSME) or early-summer meningoencephalitis—a
description that might be misleading, as will be shown later.
In its most severe course, the infection affects the central
nervous system (CNS), mostly as a meningoencephalitis leading
to persistent sequelae in up to 58% of patients. Prophylaxis is
focused on the avoidance of exposure and on vaccination.
Because many of the TBE endemic areas are (increasingly)
popular tourist destinations, it seems of utmost importance to
raise awareness among travelers and their health advisors,
primary care medicine practitioners, and infectious disease
specialists.
THE PATHOGEN
TBE is caused by a single-stranded ribonucleic acid (RNA) virus
that belongs to the family of the Flaviviridae and therefore
shows some similarities with other viruses in this family (e.g.,
West Nile virus and Japanese encephalitis [ JE] virus). The TBE
virus is fairly homogenous in endemic areas of Europe (Euro-
pean subtype). There are two additional subtypes within the
same group with few genetic differences: the recently identified
Siberian subtype (which genetically is quite closely linked to the
European subtype) and the Far Eastern subtype.
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72
VECTOR AND TRANSMISSION
TBE is transmitted by hard ticks and via consumption of raw
milk. By far the most frequent way of transmission to humans
is by bites of certain species of hard ticks (i.e., Ixodes ricinus and
Ixodes persulcatus) that previously have fed on infected reservoir
hosts (Figure 72-3). With some areas of overlap, I. ricinus (the
common castor-bean tick) mostly inhabits the western part, and
I. persulcatus (“Taiga tick”) mainly is found in the eastern part of
the endemic area that roughly stretches from the Alsace region
of France in the West to Hokkaido Island, Japan, in the East,
and from Scandinavia in the North to Italy, Albania, and Greece
in the South. According to old published data, the TBE virus
prevalence in the tick population in endemic areas may be as
low as 0.05% in Italy and 0.07% in Finland and as high as 26.6%
in some regions of Latvia.
One phenomenon contributing to an increasing prevalence
of TBE-infected tick populations is the fact that a vertical or
transovarian transmission (i.e., a TBE-infected female tick
infects her eggs before oviposition) takes place as well as from
an infected animal to a tick during a bite (or even from tick to
tick by cofeeding on the same blood pool). In contrast to other
blood-feeding insect vectors, ticks do not directly puncture
blood vessels but feed from a “feeding pool” produced by vaso-
active mediators and coagulation inhibitors released via the
tick′s saliva. The blood meal of an adult female and immature
blood-sucking nymphs may last up to 5 days, resulting in an
approximately 120-fold increase of the volume of an adult
female tick. Male ticks do not feed on blood at all but may
repeatedly feed on a small amount of tissue fluid during a rela-
tively short feeding period, which nevertheless may be sufficient
for the transmission of the TBE virus.
In addition to tick bites, another way of transmission is by
consumption of raw milk and products made from it. This mode
of transmission used to occur quite frequently in the Baltic
States (e.g., in Lithuania) and in Slovakia, but in 2008 there were
some cases of alimentary infection reported for the first time in
Austria. Another risk of exposure is laboratory work with this
virus.
EPIDEMIOLOGY
In the past, at least in central Europe, most cases were seen in
early summer. Later on, two peaks of this disease were described,
with the recognition of an additional peak in late summer. Tick
biting activity appears to be increased by humidity and tempera-
ture. Owing to recent climate changes observed in the whole
436 SECTION VII  •  Infections Associated with International Travel and Outdoor Activities

Endemic areas of TBE 1100

Austria
Regions of single cases of TBE
1000 Lithuania

900
North 800
Baltic Finland

TBE increase (%)

Sea
Sea
700 Poland
Atlantic 600 Germany
Ocean ? Estoria
? ? 500
? ? 400
Average
Sweden
? ? Black Sea Switzerland
300 Latvia
Czech Republic
200 Slovakia
Mediterranean Sea
100
1974–1983 1984–1993 1994–2003
Figure 72-1  Geographic distribution of tick-borne encephalitis.
(Data from the International Prevention Initiative on
Figure 72-2  Tick-borne encephalitis cases reported in Europe,
Tick-Borne Encephalitis. Available at: www.tbe-
1974 to 2003. (Data from Kunze U, Baumhackl U,
prevention.info/m-6870.php.)
Bretschneider R, et  al: The golden agers and tick-borne
encephalitis. Conference report and position paper of the
International Scientific Working Group on Tick-Borne
Encephalitis, Wien Med Wochenschr 155 [11-12]:289-94,
2005.)

Larva Nymph Adult Adult Engorged

male female adult female
Ticks

Humans

Mammals

Raw milk (from cows, sheep, goats)

Tick removal

Figure 72-3  Transmission of tick-borne encephalitis virus.

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 CHAPTER 72  •  Tick-Borne Encephalitis 437

region, currently at least five new phenomena have been outdoors (e.g., collecting mushrooms, playing golf, camping and
observed: picnicking, Nordic walking, hiking, trekking). This particularly
is true for older and retired people, who, if they acquire a TBE
• In addition to the steady growth of the geographic risk
infection, tend to develop more severe symptoms.
area at the same latitude accompanied by a confluence of
As is the case with other infections, epidemiologic data
scattered foci to bigger endemic regions, there has been
reported officially depend on a variety of factors including the
movement of the TBE endemic area boundary northward,
awareness within the healthcare system caring for a patient, the
with the eruption of highly active foci in Scandinavia, for
availability of adequate diagnostic tools, the notification systems
instance. In addition, the areas of risk include higher
of regional, national, and international health authorities, and
altitudes.
the adherence of those who should report. The low awareness
• In some areas the two peaks of reported clinical cases have
of TBE in nonendemic countries is likely to result in an under-
merged into one broader peak occurring in July and
diagnosis of clinical cases, and this is the most probable explana-
August.
tion for the difference between the estimated attack rates in
• In some areas, most likely as a result of warmer tempera-
tourists and the numbers reported.
tures, the typical seasonal pattern with transmission-free
On a person-based calculation, the highest incidence pub-
intervals has vanished. Transmission seasons have
lished (98 per 100,000) is that of forestry workers in Austria. As
expanded, and, in some regions, year-round transmission
with other infectious diseases, not every infection results in
is occurring.
specific clinical symptoms. The risk of symptomatic disease after
• The tick populations in some areas have substantially
a single tick bite in an endemic area varies from 1 : 200 to
increased, probably because of climate changes that have
1 : 1000. Actual epidemiologic data underline the importance of
caused increased rain, warm winters, and moist springs. As
the vaccination of travelers going to endemic areas, the risk of
a consequence, the tick bite season starts earlier, and
acquiring TBE in an endemic area being about the same as for
the development of the different stages is quicker. Tick
typhoid fever in nonvaccinated travelers going to India.
activity starts with a soil temperature of about 7° C, and
the relative humidity of at least 92% necessary for the
ticks’ survival is provided by more frequent episodes of CLINICAL FEATURES
rainfall.
TBE typically is a biphasic disease. About 1 week (2 to 28 days)
• In most TBE-endemic countries, people have achieved
after an infectious tick bite, most patients develop an influenza-
better living conditions. They have more leisure time,
like illness (ILI) for a few days (2 to 8 days) caused by the viremia
which, at least during the warm season, contributes to an
(Figure 72-4). For many patients, this remains the one and only
increase of exposure-prone outdoor activities. Further-
symptomatic period. After an asymptomatic interval of about
more, many families have shifted from living in apartments
1 more week (1 to 20 days), some patients develop a sudden
to having their own house with a garden, bushes, and trees,
increase in temperature that marks the beginning of the second
associated with an increased risk of tick bites.
stage. In this context, it seems noteworthy that TBE patients
These factors contribute to a higher risk of exposure to ticks. tend to have higher temperatures than patients with other forms
In most regions, the risk of exposure to TBE has shifted from of viral meningitis or meningoencephalitis.
being mainly an occupational risk (forestry workers, farmers) to The second phase is that of CNS involvement. The symp-
that of being a health risk among people spending leisure time toms are most frequently caused by meningoencephalitis: stiff

Site of entry

Lymph flow Blood

Regional lymph nodes, spleen, liver, bone marrow

1st stage of illness

Nerves Blood

CNS 2nd stage of illness

Figure 72-4  Spread of tick-borne encephalitis virus in the body. (Data from Kaiser R: Tick-borne encephalitis in Germany and clinical course
of the disease, Int J Med Microbiol 291[suppl 33]:58-61, 2002.)

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438 SECTION VII  •  Infections Associated with International Travel and Outdoor Activities

neck, fever, headache, nausea, vomiting, photophobia, and

impairment of CNS functions (Figure 72-5). These result from
either direct destruction of CNS tissue (irreversible) or from an
inflammatory edema (reversible). The amount of CNS involved,
the mass of destruction, and its location determine the severity
of the clinical course. Some factors, such as the presence of
underlying diseases or conditions and older age are associated
with increased severity of the disease. In its most severe form,
TBE might involve all parts of the CNS—that is, causing
meningoencephalomyeloradiculitis.
Compared with some other vector-borne flaviviral infections,
there is no impairment of the clotting system, and symptoms of
a viral hemorrhagic fever have never been proven in a case of
TBE in Western Europe. According to incidence figures,
cases in travelers from nonendemic countries are likely to stay
undiagnosed or misdiagnosed, showing that the doctors
responsible for the workup of these cases lack awareness of
and experience in diagnosing this disease. The features of
differential diagnosis between TBE and Lyme disease are given
in Table 72-1.
DIAGNOSTIC APPROACH
Typically, a patient will not seek medical care until the second
stage of the disease—that is, with the onset of neurologic signs.
As in other cases of meningoencephalitis, diagnostics usually
include a neurologic examination, serologic tests (paired samples:
blood and cerebrospinal fluid [CSF]), radiology (computed
tomography [CT] and magnetic resonance imaging [MRI]), and
general laboratory screening tests (including a differential blood
count and general inflammation parameters). The typical results
are as follows:
• Besides specific neurologic signs attributable to the cere-
bral region involved, patients show unspecific neurologic
symptoms such as headache, stiffness of the neck, photo-
phobia, nausea with or without vomiting, and fever. The
area most frequently affected in terms of paralysis is the
shoulder girdle.
• The radiologic examination (CT or MRI) shows signs of
meningitis and randomly spread foci in the CNS tissue

2/3 of patients

Recovery

Long-term and sometimes

permanent neuropsychiatric
sequelae: 10%-20%
Residual paresis and
1/3 of patients atrophies: 3%-11%

Mortality: 0.5%-20%
(according to WHO)
Incubation Stage 1 Interval Stage 2

Figure 72-5  Clinical course of tick-borne encephalitis infection. (Data from Kaiser R: Tick-borne encephalitis in Germany and clinical course of
the disease, Int J Med Microbiol 291[suppl 33]:58-61, 2002.)

Table 72-1  Differential Diagnosis of Tick-Borne Encephalitis and Lyme Disease

TICK-BORNE ENCEPHALITIS (TBE) LYME DISEASE

Pathogen TBE virus Borrelia burgdorferi (bacterium)

Clinical Picture
Phase 1 Temperature ≤38° C Red rash (usually round or oval, erythema chronicum migrans)
Uncharacteristic influenza-like signs and symptoms Uncharacteristic influenza-like signs and symptoms
Lymphadenosis benigna cutis (rare form of benign recurrent
tumor)
Phase 2 Fever (temperature ≥40° C) Meningopolyneuritis (Garin-Bujadoux-Bannwarth)
Meningitis Facial paresis
Meningoencephalitis Cardiac arrhythmia
Meningomyelitis Myocarditis
Meningoencephalomyelitis
Phase 3 Acrodermatitis chronica atrophicans
Arthritis

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(encephalitis). Some of these abnormal signals are caused
by destruction, others by perifocal edema.
• In the differential blood count at this stage there is a shift
toward mononuclear cells in a usually decreased white
blood cell (WBC) count. C-reactive protein CRP and pro-
calcitonin PCT levels are low; lactate dehydrogenase
(LDH) levels may be elevated (in accordance with CNS
tissue destruction).
• CSF examination shows the typical picture of a viral
meningitis—that is, elevated cell count (mononuclear
cells) and protein, with a normal glucose level. The protein
elevation is partly a result of unspecific inflammatory
proteins and partly of the autochthonous production of
TBE-specific immunoglobulin (Ig).
• When checking paired samples serologically, the first
result indicating a recent infection is the detection of spe-
cific anti–TBE-virus IgM antibodies both in the serum and
in the CSF. These antibodies are often present at the time
of hospital admission, which, as mentioned previously,
usually is triggered by the appearance of neurologic signs
(i.e., in the second phase). The tests routinely used are
based on the enzyme-linked immunosorbent assay (ELISA)
technique. It is important to note that TBE antibodies may
cross-react with other flaviviruses in these test systems,
which is important particularly among travelers returning
from endemic areas of JE and dengue fever, or those previ-
ously vaccinated against JE and/or yellow fever (YF). In
case of inconclusive results, there are additional options
such as the neutralization test (NT) or polymerase chain
reaction (PCR) assays (which usually are limited to special-
ized laboratories).
TREATMENT
As with most other viral diseases, there is no specific therapy
available. Treatment therefore is symptomatic only and focused
on managing inflammation, pain, fever, and nausea as well as
convulsions in serious infections. The most severe TBE cases
may require intensive care, including parenteral nutrition and
auxiliary ventilation. The availability of a high-quality standard
of care may reduce the incidence and the amount of neurologic
sequelae and affects the survival rate. This should be recognized,
especially by nonvaccinated travelers heading to remote areas
within an endemic region.
PROGNOSIS
The outcome of the disease depends on the amount, location,
and function of the CNS structures destroyed. TBE viruses are
known to have a particular predilection for anterior horn cells
of the cervical spinal cord, thus leading to paresis of the upper
limbs, the shoulder girdle, and the head levator muscles and
having the potential to involve the respiratory muscles. The
incidence rate of sequelae after TBE varies from 35% to 58%.
The case-fatality rate (CFR) in central Europe is about 1% to
2%, whereas the CFR of the Siberian subtype (the Taiga strain,
which is closely related to the Far Eastern form) is said to be as
high as 20%, but there are doubts about whether this figure is
correct; it might be biased by the fact that only people who are
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CHAPTER 72  •  Tick-Borne Encephalitis 439
severely sick go to hospitals. On the other hand, there are inves-
tigations that show a higher virulence of the Siberian subtype
in mice compared with the other Far Eastern strains.
After an infection (whether symptomatic or asymptomatic)
TBE always leads to lifelong immunity.
PREVENTION
There is no chemoprophylaxis against TBE, so only the two
other methods of prevention are left: avoidance of exposure and
vaccination. In contrast to widespread beliefs, ticks do not pri-
marily live on trees, nor do they jump down on their victims.
Their usual habitats are areas with grass, meadows, bushes, and
small trees. The ticks increase their chances to attach to warm-
blooded animals (and humans) by sitting at the tips of the plants
analyzing their surroundings with a very complex organ
(so-called organ of Haller, located at their first pair of legs).
Although it is not understood in detail, temperature, CO2, and
butyric acid (which is also responsible for the smell of sweat)
seem to attract ticks and to trigger the attachment of ticks to
the skin, facilitated by a contact time of not more than 0.1
second.
Because ticks in TBE-endemic areas might also transmit
other diseases (Lyme borreliosis being the most common), the
avoidance of all tick exposure is crucial. This includes avoidance
of running or walking through high grasses or on narrow paths
with repeated unavoidable contact with grass and bushes, and
the use of insect repellents on exposed skin surfaces and impreg-
nating outer clothing. Products containing the chemical N,N-
diethyl-meta-toluamide (DEET) (in higher concentrations,
preferably >20%) are considered to be effective skin repellents
against ticks (and other arachnids, as well as insects). An insec-
ticide containing permethrin is recommended for the impregna-
tion of clothing. Several products are commercially available at
sporting goods stores, to be used according to package direc-
tions. Another consideration is the fact that the color of the
clothes has substantial impact on the attraction of ticks, light-
colored clothing being significantly less attractive than dark-
colored clothing. A summary of recommendations is provided
in Table 72-2.
First Aid
After an infected tick is attached to the skin, some time is
required until the transmission of a specific pathogen takes
place. The process involves the time it takes for the tick to select
the location for its bite, the penetration of the skin, the produc-
tion of a “feeding pool” in the case of the blood-sucking nymph
stages and adult females (adult males feed on tissue fluid only),
and the time for the influx of a sufficient amount of tick saliva
and/or regurgitated sucked blood to reach the minimal infec-
tious dose in the human host. Therefore it makes sense to
remove a tick as soon as possible to avoid an infection—even if
the bug is already firmly attached to the skin.
To be able to remove attached ticks in a timely fashion, the
whole body should be examined after outdoor activities. A thor-
ough inspection usually necessitates the help of a second person
(e.g., before showering or bathing). The removal of an attached
tick should be as atraumatic as possible. This can be managed
440 SECTION VII  •  Infections Associated with International Travel and Outdoor Activities

Table 72-2  General Preventive Measures

INTERVENTION MEASURE COMMENT

Behavior Avoid tick-infested areas Whenever possible

Clothing
Use of repellents
Early detection
Early removal of ticks
Light-colored clothing that covers arm and legs
(long-sleeved shirts, tight at the wrists; long
pants, tight at the ankles and tucked into the
socks), shoes covering the entire foot
Apply adequate repellent (with proven activity
against ticks) to exposed skin and to outer
clothing
Adults should check daily, children should be
checked more frequently (i.e., after each episode
of potential exposure [could result in two or three
checks per day])
Remove tick as soon as possible by using fine
tipped tweezers or special cards (resembling
carved credit cards); grasp the tick firmly as close
to the skin as possible and simply tear it out
without squeezing or rotating the tick
Dark clothing is more attractive for ticks (which
in addition are more difficult to identify against
a dark background)
DEET* in higher concentrations and permethrin
are proven to act against ticks; allow clothing
to dry before wearing
The checks should especially focus on
waistbands, sock tops, underarms, other moist
areas (in children: check the head and behind
the ears); even adults may need the help of a
second person to check the whole body
Don’t suffocate the tick (do not use oil, cream,
nail polish, water); don’t burn the tick; don’t
apply “traditional recipes”; don’t wait for
medical services when not promptly
available—remove the tick yourself

*DEET, N,N-diethyl-meta-toluamide.

by using a pair of fine-tipped tweezers. The recommended
method for tick removal is to pick the part of the tick closest to
the skin and to tear it off without rotation and without squeezing
the body, which could result in an increased influx of pathogens
(see Figure 72-3). The tick should also not be drowned (e.g., by
bathing), suffocated (by putting a drop of glue, nail polish, or
oil on the tick), or burned (with a match or a cigarette), because
an increased burden of infectious particles may be released into
the bite wound while the tick is struggling. Another misconcep-
tion is that if a black dot remains in the wound, it is the head;
rather, it is some part of the biting apparatus only. Because of
the anatomy of the tick, the salivary glands containing the TBE
virus are removed by removing the body as described here, and
any remaining mouth parts are of no significant contribution to
the time span of possible virus transmission.
Vaccination
In former times, postexposure prophylaxis (PEP) by using TBE
hyperimmune globulin within 96 hours for passive immuniza-
tion after a tick bite was practiced. However, TBE hyperim-
mune globulin is no longer available, and standard lots of
commercially available human immune globulin are untested
as PEP and unlikely to contain a sufficient level of specific anti-
bodies to protect against this infection.
Immunization against TBE before exposure is advised for
persons living in or traveling to TBE-endemic areas, and the
vaccine is currently available year round without any seasonal
restrictions in many countries (but is not yet licensed in the
United States).
The vaccine products that are registered in some western
countries are branded as FSME-IMMUN and Ticovac (Baxter;
originally developed by the Immuno AG, Vienna, Austria) and
Encepur (Novartis; originally developed by the Chiron Behring
GmbH and Company KG, Marburg, Germany). Both vaccines
use very closely related inactivated TBE virus strains as antigens
that elicit protective antibodies against all known subtypes of
the TBE virus and are registered for intramuscular administra-
tion. Reported adverse events are mainly local side effects, with
the likelihood of serious side effects such as neuritis being
extremely low (neuritis occurs in less than 1 : 1,000,000 vaccin-
ees). Neurologic disorders in general did not occur more often
in the vaccinees than in the unvaccinated population. Standard
and rapid immunization schedules are established, and virtually
all lead to a strong immune response.
The topic of the booster dose interval is controversial. The
intervals recommended by the companies are not always identi-
cal to those recommended by national vaccination boards or
those listed on Internet websites (frequently used by travelers as
a basic source of information). In case of a history of a probable
TBE infection or irregular vaccination schemes, serologic
testing to check or prove immunity should be stressed.
Data from 2004 show that about 60 million travelers visit
TBE-endemic parts of Europe each year. Among these travelers,
according to World Tourism Organization (WTO) data, there
is an increasing trend to travel to those countries with an excep-
tionally high risk of TBE. Calculations show that for nonvac-
cinated travelers, the risk of acquiring TBE in a highly endemic
area is not less than the risk of contracting typhoid fever in India
(and typhoid fever vaccination on a regular basis for travelers
heading to this destination is recommended).
Travelers tend to explore and enjoy their destinations, which
usually includes some outdoor exposure. Furthermore, the curi-
osity to sample authentic regional food in some areas might
expose travelers to TBE via raw milk and dairy products. In
addition to advice for recreational travelers whose stated purpose
in going to a TBE-endemic area is to participate in outdoor
activities, education about the risks of TBE and prevention of
transmission and discussion about the availability of vaccines to
prevent disease should be offered by healthcare practitioners to
families, scout groups, school classes, and students on exchange
programs.

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 CHAPTER 72  •  Tick-Borne Encephalitis 441

ADDITIONAL RESOURCES
ACKNOWLEDGMENTS
Centers for Disease Control and Prevention (CDC): Tick-borne encephalitis.
I want to thank the companies of Baxter and Novartis for pro- Available at: www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/TBE.htm.
viding information material including data and graphics. In par- Good basic information on many aspects of this infectious disease.
ticular, Dr. Dieter Gniel was very helpful in sharing his vast Centers for Disease Control and Prevention (CDC): Travelers’ health.
Available at: www.cdc.gov/travel/yellowbook/2010/chapter-5/tick-borne-
experience on TBE.
encephalitis.aspx. One of the reference sites on infectious diseases for U.S.
doctors.
International Scientific Working Group on Tick-Borne Encephalitis: Pre-
EVIDENCE vention information. Available at: www.tbe-prevention.info. Site providing
information focused on tick bite and TBE prevention.
Centers for Disease Control and Prevention (CDC): Tick-
International Scientific Working Group on Tick-Borne Encephalitis: Tick
borne encephalitis among U.S. travelers to Europe and victims information. Available at: www.tick-victims.info. Information on
Asia—2000-2009, Morb Mortal Wkly Rep 26:59(11):335-338, the disease focused on clinical aspects provided by tick victims as well as by people
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to identify cases of TBE among U.S. travelers. Five cases were victims”).
identified by IgM serum antibodies and confirmed as TBE by International Scientific Working Group on Tick-Borne Encephalitis
plaque-reduction neutralization tests: four patients had traveled to website. Available at: www.isw-tbe.info. Information on TBE by the Inter-
Europe or Russia and had a biphasic illness followed by nearly national Scientific Working Group on Tick-Borne Encephalitis.
complete recoveries. The fifth patient had traveled to China and had World Health Organization (WHO): The vector-borne human infections
of Europe: their distribution and burden on public health. Available
a monophasic illness with severe encephalitis and neurologic sequelae.
at: www.euro.who.int/__data/assets/pdf_file/0008/98765/e82481.pdf. A
Czupryna P, Moniuszko A, Pancewicz SA, et al: Tick-borne WHO Internet site dedicated to European infectious diseases.
encephalitis in Poland in years 1993-2008—epidemiology and World Health Organization (WHO): Tick-borne encephalitis. Available
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at: www.who.int/biologicals/areas/vaccines/tick_encephalitis/en/. WHO
TBE in this region of Europe were analyzed. In this group of
site explaining prophylaxis and vaccination.
patients, the initial disease presented with meningitis in 41%,
Zuckerman JN, Jong EC, eds: Travelers vaccines, ed 2, Shelton, Conn., 2010,
meningoencephalitis in 51%, and meningoencephalomylelitis in 8%. Peoples Medical Publishing House. This book includes a chapter on TBE,
Ataxia in 14% and pareses in 9% were the most common mostly focused on travel medicine aspects.
neurological abnormalities that developed. Upon discharge, 23% had
neurological and 44% had psychiatric sequelae.
Schoendorf I, Ternak G, Oroszlan G, et al: Tick-born
encephalitis (TBE) vaccination in children: advantage of the
rapid immunization schedule (i.e., days 0, 7, 21). Hum Vaccin
4:42-47, 2007. A clinical study involving 294 children aged 1-11
years old vaccinated with a pediatric formulation of TBE vaccine
(Encepur children) according to the conventional schedule on days 0,
28, and 300, the modified conventional schedule on days 0, 21, and
300, or the rapid schedule on days 0, 7, and 21. The rapid
immunization schedule in children stimulated rapid protection and
stable titers for at least 300 days after vaccination.
Weinberger B, Keller M, Fischer KH, et al: Decreased
antibody titers and booster responses in tick-borne encephalitis
vaccinees aged 50-90 years. Vaccine 28:3511-3515, 2010. Cases
of vaccine failures (clinical and serological evidence of TBE infection
despite adequate immunization) have been reported predominantly in
older persons. The immune-responsiveness to TBE vaccinations for
age groups 50-59, 60-69, and >69 years were compared to a control
group aged below 30 years. The antibody titers and booster responses
measured for each group suggest that responsiveness of the immune
system to vaccination is already impaired at the age of 50 compared
to the control group. Booster intervals of 3 years are currently
recommended for persons = or >60 years in Austria, but might be
beneficially applied to persons = to or >50 years.

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