2005: Visualization of Central European TBE infection in fatal human cases.

1: J Neuropathol Exp Neurol. 2005 Jun;64(6):506-12. Related Articles,
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Visualization of Central European tick-borne encephalitis infection in
fatal human cases.

Gelpi E, Preusser M, Garzuly F, Holzmann H, Heinz FX, Budka H.

Institutes of Neurology, Medical University of Vienna, Vienna, Austria.

Central European tick-borne encephalitis (TBE) is caused by a
flavivirus vectored by the Ixodes ricinus tick. In severe infections,
TBE presents as (myelo)meningoencephalitis with considerable mortality.
Characteristic neuropathologic changes feature a multinodular to patchy
polioencephalomyelitis accentuated in spinal cord, brainstem, and
cerebellum. Visualization of viral infection by immunohistochemistry
has not yet been achieved. We analyzed immunohistochemically the
distribution of viral antigens and its correlation with neuropathologic
changes, serological data, and disease duration in 28 brains of cases
with a clinical diagnosis of TBE and neuropathologically confirmed
(meningo)encephalomyelitis. In 20 brains (including 10 seropositives),
viral antigens were detectable. These cases were characterized by
relatively short clinical duration ranging from 4 to 35 days.
Immunoreactivity was most prominent in perikarya and processes of
Purkinje cells and large neurons of dentate nucleus, inferior olives,
and anterior horns. In addition, immunoreactivity was detected in
neurons of other brainstem nuclei, isocortex, and basal ganglia. There
was an inverse topographical association of severe inflammatory changes
with presence of viral antigens. Some cytotoxic T cells were in direct
contact with tick-borne encephalitis virus (TBEV)-infected neurons. We
conclude that 1) TBE viral antigens are immunohistochemically
detectable in brains of fatal cases with relatively short natural
clinical course; 2) TBE virus neurotropism preferentially targets large
neurons of anterior horns, medulla oblongata, pons, dentate nucleus,
Purkinje cells, and striatum; 3) topographical correlation between
inflammatory changes and distribution of viral antigens is poor; and 4)
immunologic mechanisms may contribute to nerve cell destruction in
human TBE.

PMID: 15977642 [PubMed - indexed for MEDLINE]

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