Tick-borne encephalitis ( TBE)

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Tick-borne encephalitis ( TBE)

Post by Yvonne » Fri 7 Dec 2007 10:14

"TBE is endemic in regions of 27 European countries and we are discovering new risk areas every year. Vaccination is recommended to everyone living in or travelling to areas where it is endemic, children as well as adults.TBE/FSME vaccination is recommended within Europe for all people residing in or traveling to endemic areas."
(Michael Kunze MD, Vienna, 2007)

"Tick borne encephalitis (TBE) is a serious
acute central nervous system infection,
which may result in death or long term neurological sequelae in 35-58% of patients.
The fatality rate associated with
clinical infection is 0.5-20%."
WHO, State of the Art of New Vaccines: Research & Development 2003
http://www.who.int/vaccine_research/dis ... ndex2.html


"Even though TBE has already been described in 1931,
this dangerous form of encephalitis has been
underestimated for a long time."
(C. Kunz, MD, co-inventor of the first
Western-European TBE vaccine, Vienna)

TBE (tick-borne encephalitis) is a viral disease transmitted by ticks that attacks the nervous system and can cause both mild and severe illnesses, with permanent consequences such as concentration problems, paralysis and depression. Approximately every 100th case results in the death of the affected person.

High-risk areas
The Ixodes ricinus tick (common castor-bean tick) is prevalent across Europe. TBE endemic areas traverse Europe: from Croatia, Slovenia, Hungary, Switzerland and Austria, across Slovakia, the Czech Republic, Germany, Poland and Scandinavia (Sweden, Finland) to the Baltic States and Russia (and Siberia). Ticks live in forest clearings and meadows.

"TBE is endemic in regions of 27 European countries and
every year we detect new risk areas." (J. Süss, PhD, Jena

TBE virus is common in endemic foci in

Albania Austria Belarus
Bosnia Croatia Czech Republic
Denmark (Bornholm Island) Estonia Finland (SW Coast)
France Germany Greece
Hungary Italy Latvia
Liechtenstein Lithuania Norway
Poland Romania Russia
Serbia Slovakia Slovenia
Sweden Switzerland Ukraine

Not every tick transmits the dangerous TBE virus, but the rate of infestation in some high-risk areas can be great. In certain areas, one can find ticks at altitudes of up to 1,800 metres above sea level; infections of the TBE virus have been reported at altitudes of 1,300 metres.


Edit : change title
Last edited by Yvonne on Tue 30 Mar 2010 14:57, edited 1 time in total.
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Re: International prevention initiative on TBE

Post by cave76 » Fri 7 Dec 2007 16:55

Interesting site. Thanks---- at first glance it seems to be directed towards getting vaccinations to a greater percentage of people through the world.

My question----and not at all meant to be argumentative, since I don't know how I feel about vaccines at this point other than I won't take the flu shot OR another Hep B shot. :)

I've always lived in a 'rich' country, with the provincialism associated with that :( , it takes me a minute to realize that vaccines are very important for the poorer nations---- with poor health care and exposure to many diseases.

I don't want to throw vaccines out the window, metaphorically, for that reason.

Could other comment on this?

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Re: International prevention initiative on TBE

Post by Yvonne » Fri 19 Dec 2008 14:21

http://brain.oxfordjournals.org/cgi/con ... 22/11/2067

The clinical and epidemiological profile of tick-borne encephalitis in southern Germany 1994–98


Seven hundred and nine patients fell ill in southern Germany (Baden-Württemberg) after infection with the tick-borne encephalitis (TBE) virus between 1994 and 1998. Detailed clinical and epidemiological data on TBE were available for 656 patients. A biphasic course of the disease occurred in 485 patients (74%). TBE presented as meningitis in 320 patients (49%), as meningoencephalitis in 270 (41%) and as meningoencephalomyelitis in 66 (10%). Eight of the patients (1.2%) died from TBE. Four hundred and forty-five patients (68%) had noticed a tick bite and the first symptoms occurred, on average, 7 days later. The most frequent neurological symptoms were impairment of consciousness (31%), ataxia (18%) and paresis of the extremities (15%) and cranial nerves (11%). Laboratory investigations revealed leucocytosis in the peripheral blood in 224 out of 392 patients (74%), elevation of the erythrocyte sedimentation rate in 223 out of 245 (91%), increased C-reactive protein in 127 out of 155 (82%), pleocytosis in the CSF of all patients tested, damage of the blood–CSF barrier in 255 out of 322 (79%), abnormalities in EEG in 165 out of 214 (77%) and abnormalities in MRI in 18 out of 102 (18%). In general, adolescents up to 14 years of age had a more favourable course of the disease than adults. Of 230 patients who were re-examined at a later time, 53 (23%) had moderate or severe sequelae. Patients with sequelae presented more frequently (P < 0.001) with impaired consciousness (Glasgow Coma Scale < 7), ataxia, pareses of the extremities or cranial nerves, a need for assisted ventilation, abnormal findings in MRI, pleocytosis > 300 cells/µl and impairment of the blood–CSF barrier (total protein > 600 mg/l). In view of the severity of the illness and the high frequency of sequelae, active immunization against TBE is recommended for all subjects living in and travelling to areas of risk. Prevention of TBE by post-exposure prophylaxis with hyperimmunoglobulins is less effective and therefore should be performed only when absolutely necessary


Tick-borne encephalitis (TBE) is caused by an RNA virus belonging to the flavivirus family. Based on antibody adsorption experiments, peptide mapping and nucleotide sequencing, two subtypes of TBE virus have been identified and designated as western and eastern (Heinz and Kunz, 1981, 1982; Mandl et al., 1988, 1989; Pletnev, 1990). The western subtype is endemic in large parts of Northern, Central and Eastern Europe, while the eastern subtype can be found in the European and Asian regions of the Commonwealth of Independent States (former Soviet Union) (WHO, 1986; Anonymous, 1997). In Germany, TBE is prevalent in Baden-Württemberg, Bavaria and South Hessen (Roggendorf, 1996; Anonymous, 1997). During the years 1991 to 1998, at least 1230 cases of TBE were reported in Germany, with a mean incidence in Baden-Württemberg of 1.2 per 100 000 inhabitants per year and a case fatality rate of 1% (Kaiser, 1996). In a highly endemic focus in Baden-Württemberg a seroprevalence of 9% has been found (Kaiser et al., 1997a).

TBE typically takes a biphasic course. After an incubation period, usually between 7 and 14 days, the prodromal symptoms (uncharacteristic influenza-like illness with fever, headache, malaise and myalgia) are followed by CNS involvement. After an afebrile interval of ~1 week the second stage develops. TBE may manifest as isolated meningitis, meningoencephalitis or meningoencephalomyelitis (Duniewicz, 1976; Ackermann et al., 1986; Köck et al., 1992; Kaiser, 1995). Reports describing the clinical course and outcome of large series of patients with TBE are sparse.

In 1994 a dramatic increase in the number of TBE virus infections occurred in the area of Freiburg (southern Germany). At the time there was a lack of information regarding the risks associated with and the outcome of TBE virus infection in southern Germany, which includes Baden-Württemberg, an important tourist area. A prospective study to investigate the clinical course, prognosis and epidemiology of TBE in Germany was undertaken. Results of this study support a policy of active immunization against TBE for all subjects who stay in or travel to areas of risk and are likely to be exposed to ticks


The diagnosis of TBE is derived from epidemiological (a stay in an area of risk for TBE, facultative history of a tick bite) and clinical (biphasic course of disease and neurological symptoms with ataxia being most indicative for this infection) data, and the demonstration of TBE-specific IgM and IgG antibodies in serum. In general, there is intrathecal synthesis of TBE-specific IgM and/or IgG antibodies in the CSF, at the latest, 3 weeks after admission to hospital. Although this latter criterion is the most specific serological method of confirming the diagnosis, the presence of specific IgM antibodies in serum is generally considered to be adequate evidence of recent TBE (Roggendorf et al., 1981b). The patients of the present study were assumed to have been infected by the western subtype of TBE virus, as the eastern subtype has not yet been isolated from ticks or patients in Western Europe.

The frequent presence of signs of inflammation in serum (leucocytosis, elevation of the sedimentation rate and of C-reactive protein) is noteworthy, as it should not be forgotten that these findings, associated with headache, fever and meningism, are highly indicative of bacterial meningitis. Predominance of neutrophilic cells over lymphocytes in the CSF would also support such a presumptive diagnosis, and consequently most of the patients were treated with antibiotics, at least until the TBE serology was found to be positive. Combined infections with TBE virus and, for example, Borrelia burgdorferi sensu lato are very rare, but may result in a more severe course of disease (Oksi et al., 1993)

The range of the incubation period was similar in this study to the 4–28 days reported previously. The first clinical symptoms occurred most frequently 8 days after a tick bite, which is also in line with previously reported data (Harasek, 1974; Falk et al., 1981; Roggendorf et al., 1981a; Kunz, 1992). In two published cases of infections occurring during laboratory work with TBE virus, the symptoms of the prodromal stage started 9 and 10 days after the presumptive infection (Moritsch, 1962; Bodemann et al., 1980). After experimental infection of monkeys the first signs of illness also appeared on the ninth day (Verlinde et al., 1955). In conclusion, the most probable incubation period lies between 7 and 14 days.

The most obvious feature of TBE, not only in patients but also in experimentally infected monkeys, is ataxia, followed by paresis or paralysis of one or more limbs (Duniewicz, 1976; Köck et al., 1992; Gunther et al., 1997). These and other neurological symptoms of TBE can be explained by the affinity of the TBE virus for certain regions of the CNS. Post-mortem examination of the brain and spinal cord from patients with a lethal course of TBE and from monkeys that were infected experimentally with the TBE virus showed similar findings (Grinschgl, 1955; Verlinde et al., 1955; Moritsch and Krausler, 1957). The cerebral and spinal meninges usually show a diffuse infiltration with lymphocytes and sometimes leucocytes; the most extensive area of meningitis is around the cerebellum. The brain is oedematous and hyperaemic and microscopic lesions are present in almost all parts of the CNS, but particularly in the medulla oblongata, the pons, the cerebellum, the brainstem, the basal ganglia, the thalamus and the spinal cord. The lesions are localized in the grey matter and consist of lymphocytic perivascular infiltrations, accumulation of glia cells, necrosis of nerve cells and neuronophagia. In particular, Purkinje cells in the cerebellum and the anterior horn cells in the spinal cord are frequently attacked. Infiltration and rarefaction of cells are also noted in the mesencephalon and diencephalon. Changes in the cerebral cortex are almost invariably restricted to the motor area, with degeneration and necrosis of the pyramidal cells and lymphocytic accumulation and glial proliferation near the surface.

It was obvious from the present study that there was a high frequency of sequelae in patients with TBE. While there are numerous reports on the clinical picture of TBE, there is little information available on the convalescent phase or on the risk of contracting permanent damage. Apart from 63 patients in this study, whose data have been presented in detail elsewhere (Kaiser et al., 1997b), follow-up data for other patients with TBE have been published in only two studies, which were performed in Sweden. In the first study, which was done retrospectively, the frequency of sequelae was nearly 36% (40 out of 112 patients) (Haglund et al., 1996). In the second study, a prospective study of 85 patients with TBE and 64 patients with meningoencephalitis of other viral aetiology (controls), the frequency of sequelae was significantly higher (40%) in patients with TBE than in the controls (Gunther et al., 1997). The lower frequency of sequelae reported for patients in the present study (27%) probably reflects the selection of assessment criteria and the fact that mental disorders were not investigated intensively. The relatively high number of patients presenting with paresis on follow-up examination (47 out of 230, 20%) may exaggerate the true prevalence of sequelae. A majority of the patients (n = 420), not available for follow-up, were discharged from hospital without pareses. It might, therefore, be speculated that only 47 out of 656 patients had residual pareses (7%), which is in line with other reports (0.3–10%) (Holmgren et al., 1959; Ziebart-Schroth, 1972; Duniewicz, 1976; Ackermann et al., 1979; Falisevac and Beus, 1981; Jezyna et al., 1984; Köck et al., 1992). In these latter studies, the frequency of all sequelae at discharge from hospital ranged from 10 to 25%.

The predictive value of selected clinical and laboratory parameters concerning the prognosis was examined. The most striking signs of an unfavourable course of disease was the rapid development of unconsciousness (GCS <7) as well as paresis of the limbs and lower cranial nerves. Individual patients with meningoencephalomyelitis, who were initially admitted to hospital without paresis, showed paralysis and respiratory insufficiency within 24–48 h. In other patients, severe ataxia at presentation was associated with long-lasting disability after discharge from hospital. In general, the rapid evolution of severe symptoms was very likely to lead to a bad prognosis, especially in patients with meningoencephalomyelitis. Of the laboratory parameters, only the findings in MRI, cell count and total protein in the CSF correlated with the global outcome of disease.

The more favourable course and better outcome of TBE in adolescents than in adults documented in this study agrees with the findings of various other authors. Of 363 children up to 14 years of age, whose history was published between 1962 and 1993, 284 (78%) suffered from meningitis, 76 (21%) from meningoencephalitis and three (1%) from encephalomyelitis (Moritsch, 1962; Harasek, 1974; Falk and Lazarini, 1981; Messner, 1981; Helwig et al., 1983; Rakar, 1993; Cizman et al., 1999). Most of the children, even the three children with encephalomyelitis who were reported by Harasek and Messner, had a favourable outcome (Harasek, 1974; Messner, 1981). Only Rakar reported on sequelae in 6 out of 160 children (paresis, seizures, emotional disturbance), who were studied between 1978 and 1992 in Slovenia (Rakar, 1993). Owing to the rarity of sequelae, the histories of children with an unfavourable prognosis have been presented mostly as individual reports. Roggendorf and colleagues mentioned a 12-year-old child with severe meningoencephalitis who was discharged from hospital after 9 months with epileptic seizures (Roggendorf et al., 1981a). Failure to recognize abdominal symptoms as criteria of the prodromal stage of TBE occurred in the only fatal case of TBE in adolescents so far reported in the literature (Messner, 1981). An 11-year-old boy who lived in an area of risk but had no history of a tick bite and presented with symptoms of vomiting, diarrhoea and marked abdominal pain was operated on under general anaesthesia for suspected appendicitis, but the appendix was normal. Three days later brainstem encephalitis and respiratory insufficiency evolved and 10 days later the boy died. Autopsy showed brainstem haemorrhage and general sinus thrombosis. The general anaesthesia and the stress of the surgical intervention were discussed as contributing factors in the lethal course of the disease in this adolescent. In 1992, Grubbauer and colleagues reported on the youngest child so far (3.5 months of age) with severe meningoencephalitis resulting from TBE, which led to an epileptic state and required neurointensive care with intubation and assisted ventilation (Grubbauer et al., 1992). A 1 year follow-up examination showed no abnormalities. The authors recommended active immunization after the first year of life and prophylactic treatment with hyperimmunoglobulin after a tick bite (post-exposure prophylaxis) in endemic areas. However, between 1981 and 1993 this post-exposure prophylaxis was associated with an unfavourable course of disease in at least five children between 1 and 14 years of age (C. Laub and G. Wündisch, unpublished data). MRI of four of these children revealed enhancement of the thalamus (Waldvogel et al., 1996), but similar findings were also demonstrated in five of the nine children of this study. These data and the findings from a further 13 adults who had
abnormalities in MRI but had not received post-exposure prophylactic treatment suggest that a causal association between prophylaxis and abnormalities in MRI is rather unlikely. The proof of a causal relationship between post-exposure prophylaxis and a more severe course of TBE in adolescents up to 14 years of age is rather difficult since individual children had received high doses of corticosteroids, antibiotics and antiviral drugs and in all children an unobserved—and possibly causal—earlier tick bite could not be excluded. Due to the risk of a causal relationship between the administration of hyperimmunoglobulin and a severe course of disease, this prophylaxis after a tick bite is not recommended in adolescents up to 14 years of age (Arras et al., 1996). Indeed, in most children and adolescents the natural course of TBE is associated with a favourable outcome, and only in a minor proportion of these patients is the long-term prognosis bad.
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Re: International prevention initiative on TBE

Post by Yvonne » Sun 21 Dec 2008 16:19

http://priede.bf.lu.lv/grozs/LU/LU_Bio_ ... ormane.pdf

Tick-borne encephalitis – pathogen, vectors and epidemiological situation in Latvia 2002 - 2003
Tick-borne encephalitis (TBE) morbidity in Latvia declined signifi cantly in 2002 compared to the
previous decade, although in 2003 the number of TBE cases rose again. Ixodes ricinus tick activity
observations in nature as well as from the records on seasonal tick numbers removed from patients
in the Vaccination service for TBE virus (TBEV) tests pointed to a sharp rise in nymph numbers.
TBEV prevalence shown with ELISA in ticks removed from humans was four times higher than in
fi eld collected ticks, but the total TBEV prevalence level decreased in 2003. Investigations of TBEV
by RT-PCR was performed by means of two methods, targeting 5'NCR (non-coding) or NS5 (nonstructural)
sequences of the TBEV
gene. The initial results of the newly adapted methods confi rmed the validity of the developed RT-PCR and pointed at the necessity to improve and standardise the
system of sampling, storage and transporting. Observations identifi ed TBE as a continuing public
health problem in Latvia requiring further research.


Tick-borne encephalitis virus (TBEV) is a RNA fl avivirus of the Flaviviridae family
causing tick-borne encephalitis, a severe neurological disease in Eurasia (Kaiser 2002).
Epidemiologically signifi cant TBEV vectors are hard-bodied (Ixodidae) ticks among
which Ixodes ricinus and I. persulcatus are common carriers of the disease in Latvia.
Three subtypes of the TBEV are known until now: Western subtype (W-TBEV), Far-
Eastern subtype (FE-TBEV) and Siberian subtype. All known TBEV isolates from Europe
belong to the W-TBEV subtype, while isolates from eastern Russia, China and Japan
belong to the FE-TBEV subtype. The recently discovered Siberian subtype includes only
three isolates – 'Vasilchenko', 'Aina' and 'Latvia 1-96'. All three subtypes are antigenically
and phylogeneticlly closely related (Lundkvist et al. 2001). I. ricinus is known to be main
transmitter for the W-TBEV subtype, and I. persulcatus for the FE-TBEV and Siberian
The severity and clinical course of tick-borne encephalitis are dependent on the TBE
virus subtype causing the disease. The FE-TBEV subtype is characterised by more serious
Acta Universitatis Latviensis, Biology, 2004, Vol. 676, pp. 27– 676 37
damage of the central nervous system and a two-fold higher lethality in comparison with
the W-TBEV subtype (Oschmann et al. 1999). Latvia belongs to the regions where all
three virus subtypes are found (Mavchoutko 2000; Süss 2002).
I. ricinus has two activity peaks for both epidemiologically most signifi cant
developmental stages – adults and nymphs, this species is spread in the whole territory
of Latvia but is rarer in its eastern regions where I. persulcatus dominates (Bormane
1999). I. persulcatus adults have only one activity peak in the spring. The majority of
TBE cases each year occur in I. ricinus habitat regions of Latvia. Rather sharp annual
changes were typical for TBE morbidity in Latvia: the highest peaks of TBE cases were
registered in 1994 and 1995 (accordingly 1366 and 1341) while in 2002 there were 153
cases. However, in 2003, according to the statistical records, TBE morbidity rise again
and 365 TBE cases were registered.

TBE virus is about 50 nm total diameter and has an infectious genomic single-stranded
RNA. The length of the genome is about 11 000 nucleotides (10 927 - 11141 depending on
the strain). TBEV has three main structural proteins: immunogenic envelope glycoprotein
E, membrane-associated protein M and capsid protein C. Protein C, together with genomic
RNA, forms the nucleocapsid; the protein coat consists mainly of glycoprotein E, and in
mature virus particles – of protein M. Gene sequences coding structural proteins (E, M
and C) are located in the fi rst fourth of the TBEV genome, the rest is occupied by nonstructural
gene sequences (NS). Non-coding regions (NCR) limit the TBEV genome at
the 5'- and 3'-terminations (Oschmann et al. 1999). Genetic analysis of E glycoprotein
coding gene sequences has been used to determine TBEV subtypes.
The methods used world-wide for diagnosis of TBEV have been direct tests (RT-PCR
reverse transcription polymerase chain reaction, electron microscopy, virus culture) and
indirect tests for antibody detection – ELISA, immunoblot, hemagglutination inhibition
test (HIT), virus neutralization test (NT) and complement-fi xation reaction (CFR)
(Oschmann et al. 1999).
and IgM antibodies in human sera and cerebrospinal fl uid, as well as to determine TBEV
prevalence in questing Ixodes ticks collected from vegetation and in, to a more or less
extent, engorged ticks removed from patients.
A recent development has been direct virus detection in ticks and human blood sera by
RT-PCR by use of two methods: amplifi cation of the non-coding (5'NCR) gene fragment
and amplifi cation of the non-structural (NS5) gene fragment. RT-PCR methods are known
to be among the most sensitive tools of TBE virus detection (Schrader, Süss 1999). The
aim of the present work was to assess the importance of the most signifi cant factors likely
affecting TBE morbidity in the period of 2002 - 2003 as well as to develop a direct and
more sensitive PCR-based TBEV test method.
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Re: International prevention initiative on TBE

Post by lou » Mon 5 Jan 2009 19:11

The interesting thing is that the U.S. has a flavivirus (in the same group as TBE), found in ticks that carry borrelia, and no one is looking to see if any of the patients in that country have these coinfections. How backward is this?

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Re: International prevention initiative on TBE

Post by LymeEnigma » Tue 6 Jan 2009 3:40

lou wrote:The interesting thing is that the U.S. has a flavivirus (in the same group as TBE), found in ticks that carry borrelia, and no one is looking to see if any of the patients in that country have these coinfections. How backward is this?
Half of what the U.S. does to deal with tick-borne illness is backward....

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Re: International prevention initiative on TBE

Post by Yvonne » Sun 18 Jan 2009 15:39

Statement on tick-borne encephalitis :

http://www.phac-aspc.gc.ca/publicat/ccd ... ex-eng.php
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Re: International prevention initiative on TBE

Post by Yvonne » Sun 25 Oct 2009 16:25

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Re: International prevention initiative on TBE

Post by Yvonne » Fri 11 Dec 2009 14:37

Expert Rev Anti Infect Ther. 2009 Dec;7(10):1251-60.

Tick-borne encephalitis in children: an update on epidemiology and diagnosis.

Arnez M, Avsic-Zupanc T.

Department of Infectious Diseases, University Medical Centre Ljubljana, Japljeva 2, Ljubljana 1525, Slovenia. maja.arnez@kclj.si

Tick-borne encephalitis is an infection of the CNS caused by a tick-borne encephalitis virus transmitted by ticks. It is more common in adults than in children. During the last 30 years, the incidence of the disease increased continuously in almost all endemic European countries except Austria. Many factors are responsible for the increased incidence. However, in Austria, the incidence of tick-borne encephalitis decreased dramatically since the introduction of a well-organized vaccination campaign against tick-borne encephalitis. The diagnosis of tick-borne encephalitis is based on clinical criteria and laboratory confirmation of infection. Other tick-borne diseases, such as Lyme borreliosis and human granulocytic anaplasmosis, should be considered in children with tick-borne encephalitis since endemic areas for all three diseases overlap.

PMID: 19968516 [PubMed - in process]
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Re: International prevention initiative on TBE

Post by Yvonne » Tue 29 Dec 2009 10:09


Neurologic, Neuropsychologic, and Electroencephalographic Findings After European Tick-Borne Encephalitis in Children

Tick-borne European early summer meningoencephalitis is believed to be a benign disease in childhood. The causative RNA virus is from the same family as the West Nile virus, and the respective clinical presentations have many similarities. We studied 19 German children who had suffered from tick-borne encephalitis virus meningitis or meningoencephalitis in an endemic area and compared them with 19 matched controls. Epidemiologic data were consistent with known features of tick-borne encephalitis infection in southern Germany. None of the children studied had severe neurologic or neuropsychologic sequelae. One child developed significant clinical depression shortly after the illness. Electroencephalograms (EEGs) from children with tickborne encephalitis were significantly slower on follow-up than control EEGs. After tickborne encephalitis, children had a higher likelihood of having an impairment of attention and psychomotor speed. Using the Touwen neurologic examination, after tick-borne encephalitis, children had lower scores than control children on 4 of the 10 subsystems. Owing to the small sample size, it was difficult to identify risk factors for and predictors of adverse outcomes.
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