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Chapter 6: TBE in children

somewhat lower extent (11%) over the long- In contrast to somatic residua and epilepsy,
17
term after childhood TBE. which of course are rare but more easily
diagnosed, neurodevelopmental/cognitive
Long-term sequelae of a somatic nature have problems may elude diagnosis due to young
been more infrequently reported in childhood children’s difficulties in verbalizing their
TBE. However, such cases occur and should problems and for their parents to recognize
not be forgotten. Fritsch et al. reported severe them. Hence, an opportunity exists to
neurologic residua (hemiparesis and epilepsia) advocate for structured follow-up of children
at a rate of 1.7% in their large pediatric diagnosed with TBE so that early actions can
1
cohort. Others have also reported on be taken (for example, to explain why the
neurologic sequelae, mainly hemiparesis, in child may not function as usual, to initiate
children with TBE. 13,17,21,25 However, the educational support, to start medication for
frequency of paralysis and paresis in pediatric attention deficit, etc.).
TBE is only reported up to approximately 2%,
which is lower than the rate seen in adults
2,4,13,16,19,21,25,
(approximately 10% of patients).
32 Immune response against TBE in
While rare, such neurologic residua
constitute a significant handicap in those children
affected, disrupting quality of life for many
years. That TBE in childhood can be associated Children (from the age of 1 year), as well as
with altered cerebral electrophysiologic adults, have been shown to elicit protective
processes, i.e., pathologic EEGs and develop- immunity to TBEV (i.e., response to the viral E
ment of epilepsia, 1,13,17,20,21 is further sub- protein) by immunization with the 2 vaccines
stantiated by a report by Mukhin et al. Rather available in the EU. These vaccines are based
treatment-resistant epilepsia partialis on the European TBEV strains Neudörfl (FSME-
continua was seen in 10 children (predomi- IMMUN® Junior) and K23 (Encepur® Children),
35
nantly boys) days to years after TBE. This (see Chapter 12 for more details). The field
cohort also suffered from oculomotor dys- effectiveness in children less than 15 years of
function, varying degree of paresis, dysarthria, age is reported to be 97% after immunization
26
cerebellar signs, and cognitive dysfunction. with the 2 vaccines; however, it should be
noted that the vaccine based on the Neudörfl
To conclude, pediatric TBE carries a high risk strain had a higher market share at the time of
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for subjective complaints (residual symptoms) the study (>96%). That TBE vaccination has
which to some extent can be objectively been effective has also been demonstrated by
assessed by using structured questionnaires the nearly complete disappearance of TBE in a
and interviews. 23,24,29 The early findings by highly endemic area with implementation of a
20
4
Schmolck et al. suggesting that TBE in general vaccination program. Among the
childhood can be associated with neuro- many publications on immunization in
developmental/cognitive difficulties have now children, it is important to note that the
been verified. 17,24,30 While larger studies may vaccines marketed within the EU have been
be required to determine the incidence of shown to be safe and effective in eliciting
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these sequelae, the individual child’s long- antibody titers , that the booster interval can
38
term disease burden cannot be neglected. 31 be expanded , and that rapid immunization
schedules have worked well. 38 However,
primary TBE vaccination (i.e., the first 3 doses)
preferably should be accomplished with the

same vaccine because of differences in each
vaccine’s immunologic properties. 39,40

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