Dr. Murai Éva - Gubányi András szerk.: Parasitologia Hungarica 29-30. (Budapest, 1997)

PATHOLOGY Prior to invading the central nervous system, the virus undergoes intensive replication in muscle and fibroblast cells. Subsequently it enters the central nervous system primarily by the haematogenic route. During its replication in the nerve cells, it damages the neurons, then gets out into the extracellular space. In the meantime, intensive glial proliferation commences. The process is accompanied by the development of cerebral oedema. The inflammatory reaction involves primarily the meninges and the perivascular cells and much less often the nerve roots and ganglions. Virus multiplication causes irreversible damage to the grey matter of the brain stem and medulla oblongata, and to motor neurons in the anterior horn of the cervical spinal cord. The encephalitic symptoms arise as a consequence of virus invasion and immunopathological events that give rise to the following changes: (1) nerve cell necrosis and consequent neuronophagia; (2) inflammatory reaction around the blood vessels, with serous exudation and cellular infiltration of the meninges and nervous tissue, followed by (3) spongiform focal necrosis which may be the result of anoxic or vascular lesions. DIAGNOSIS The diagnosis of TBE can be suggested on the basis of a relevant history and the signs indicative of encephalitis. Examination of the cerebrospinal fluid (CSF) is obligatory in all cases when TBE is suspected. The CSF usually shows lymphocytic pleocytosis of around 100 and a mostly moderate elevation of the protein level. The glucose concentration of the CSF may be variable. CSF taken at the onset of the first symptoms may be characterised by the predominance of granulocytes; however, if lumbar puncture is repeated 12 hours later, already lymphocytes will be the dominant cell type in the CSF. The CSF findings will start to improve in 5-10 days. A misleading picture may arise if TBE occurs in association with Lyme borreliosis. Considering that both infections are transmitted by the same vector, Ixodes ricinus, chances of a combined infection are high. At a TBE symposium held in Baden in 1979 (i.e. 4 years after the first description of Lyme borreliosis), several cases of atypical course, mostly accompanied by chronic meningitis and facial palsy, were reported (Kunz 1981). It may be guessed that the unusual clinical picture observed in these cases resulted from Borrelia infection. Since Borrelia antibodies take much longer time to develop than those produced against TBE virus (Lakos 1991), Borrelia infection may remain undetected. Protracted meningitis, the steadily rising protein level of the CSF, and the symptoms failing to abate and still fluctuating after 2-4 weeks should raise the suspicion of Lyme borreliosis, and serological tests should be extended in that direction or testing should be repeated. There are no other routine laboratory deviations typical of TBE. Several authors have observed leukopenia and thrombocytopenia as well as mild hepatitis (LotricFurlan and Strle 1995). These three abnormalities, which can perhaps be regarded as unusual, are typical first of all of ehrlichiosis. The chance of a dual infection is at least 10% (Lakos 1997). Accurate microbiological diagnosis can be established primarily by serological methods, as virus isolation is expensive, labour intensive and slow. In Hungary, such investigations are carried out at the Virological Department of the National Institute of Hygiene. The most commonly used test is indirect immunofluorescence. In some cases the haemagglutination