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Cytomegalovirus infection may play a role, not only in intrahepatic neonatal cholestasis, as was suggested earlier, but also in extrahepatic biliary atresia. The pathogenetic mechanism for this link remains to be established.

A total of 149 patients with clinical symptoms of acute viral meningo-encephalitis were enrolled in this study from June 1991 to December 1993. Tick-borne encephalitis (TBE) was diagnosed in 85 of the 149 patients (males 54%, median age 42 years (range 15-78)). The initial clinical appearance of TBE was classified as mild (mainly meningeal; (n = 47), moderate (n = 31) or severe (n = 7), more or less encephalitic. The most common acute symptoms of encephalitis were ataxia (26%), altered consciousness (20%), decreased concentration or memory (9%), irritable response to light and sound (28%), tremor (9%) and dysphasia (9%). Spinal nerve paralysis (11%) occurred in all three clinical stages and did not correlate with the severity or duration of encephalitis. The duration of hospitalisation, the time on the sick-list and the time to recovery were significantly longer in TBE patients. All patients survived, but many patients with TBE suffered an extended period of neurological dysfunction. Of patients with TBE 80% (68/85) showed persisting symptoms of CNS dysfunction on follow-up at week 6, compared with 55% (35/64) of the patients with aseptic meningitis of other aetiology. The corresponding figures after 1 year were 40% (33/83) and 20% (13/64). One year after TBE 13 (28%) patients with initially mild, meningeal symptoms had decreased memory and decreased concentration capacity, dysphasia or ataxia. Spinal nerve paralysis persisted after 1 year in 5 of 9 patients with TBE. In conclusion, TBE in Sweden is associated with a significant morbidity and a post-TBE syndrome existed after 1 year in more than one third of the patients.

143 people treated for tick-borne encephalitis (TBE) were included in a retrospective follow-up study. Sequelae and epidemiological characteristics in 114 individuals were analysed. The case fatality rate and the prevalence of residual paresis were low, 1.4 and 2.7%, respectively. However, 40 (35.7%) individuals were found to have a postencephalitic syndrome after a median follow-up time of 47 months, and a majority (77.5%) of these were classified as moderate to severe. Various mental disorders, balance and co-ordination disorders and headache were the most frequently reported symptoms. Increasing age was correlated to a longer duration of hospital stay, longer convalescence and increased risk of permanent sequelae. Results from a neuropsychiatric questionnaire showed marked differences between the subjects with sequelae compared to controls. 57% had noticed a tick bite before admission, and 48% were aware of at least one person in their environment who previously had contracted TBE. 79% were permanent residents or visited endemic areas often and regularly. In conclusion, we have found that TBE in the Stockholm area has a low case fatality rate, but gives rise to a considerable number of different neurological and mental sequelae, which justifies vaccination of a defined risk population in endemic areas.

A herpes simplex virus type 2 (HSV 2) etiology was sought in 93 consecutive cases of herpes simplex encephalitis (HSE) in immunocompetent post neonate patients. Antibodies to HSV 2 glycoprotein G antigen were determined by an enzyme-linked immunosorbent assay (ELISA) and HSV 2 DNA in cerebrospinal fluid (CSF) by a nested polymerase chain reaction (PCR) assay with primer pairs in the glycoprotein G gene. Evidence of HSV 2 infection was found in 6 patients; HSV 2 DNA was demonstrated in CSF and the intrathecal HSV 2 antibody response confirmed the findings. Five of the 6 patients with HSV 2 encephalitis presented a clinical picture, CSF, EEG, and CT findings characteristic of severe HSE. An atypically mild clinical course was seen in one patient. HSV 2 should be considered as an etiological agent in the viral diagnosis of HSE. With a combination of nested PCR assays for HSV 1 (primer pairs in the glycoprotein D gene) and HSV 2 in 10 microliters of CSF with no other preparation than freeze-thawing, HSV 1 or HSV 2 DNA was detected in 88 out of 93 (95%) of the first CSF specimens collected after the onset of neurological HSV disease. These findings extend and confirm previous results with PCR as a rapid and sensitive tool for early diagnosis of HSE.

Moderate or severe outcomes were reported in 11% of children with congenital CMV identified through population screening, all by 1 year; all impairment detected after this age was mild. Nonprimary infections contributed substantially to the burden of childhood congenital CMV disease.

The lack of demonstrable HSV DNA in CSF, the lack of acute CSF signs and the lack of signs of neural and glia cells destruction indicate that a direct viral cytotoxicity is not the major pathogenic mechanism in relapse. Instead, the pronounced CSF proinflammatory immunological response and the relative lack of CSF anti-inflammatory cytokine IL-10 response suggest immunologically-mediated pathogenicity.

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