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Toscana virus central nervous system infections in southern Italy.

ABSTRACT: Toscana virus was detected by reverse transcription-nested PCR in 5.6% of cerebrospinal fluid (CSF) samples from patients with meningitis and encephalitis during the summer in southern Italy. The central nervous system infections were associated with young adults and with a substantially benign clinical course. Presenting features and CSF findings are also discussed in the present report.

SUBMITTER: Di Nicuolo G

PROVIDER: S-EPMC1317182 | biostudies-literature | 2005 Dec

REPOSITORIES: biostudies-literature

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Toscana virus central nervous system infections in southern Italy.

Di Nicuolo Giuseppe G Pagliano Pasquale P Battisti Sonia S Starace Maria M Mininni Vera V Attanasio Vittorio V Faella Francesco Saverio FS

Journal of clinical microbiology 20051201 12

Toscana virus was detected by reverse transcription-nested PCR in 5.6% of cerebrospinal fluid (CSF) samples from patients with meningitis and encephalitis during the summer in southern Italy. The central nervous system infections were associated with young adults and with a substantially benign clinical course. Presenting features and CSF findings are also discussed in the present report. ...[more]

PMID: 16333126

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Project description:BackgroundVentriculitis, a dreaded complication of brain abscess, meningitis, and various neurosurgical procedures, has attracted limited attention in the medical literature.MethodsThis is a retrospective, single-center study. We screened the medical files of all patients who had a brain imaging report that included the word "ventriculitis" during years 2005-2019. Only patients with clinical, microbiological, and imaging features of ventriculitis were included. Data were collected through a standardized questionnaire.ResultsNinety-eight patients fulfilled inclusion criteria: 42 women and 56 men, and the median age was 60 years (interquartile range, 48-68). The primary mechanism for ventriculitis was classified as follows: brain abscess (n = 29, 29.6%), meningitis (n = 27, 27.6%), intraventricular catheter-related (n = 17, 17.3%), post-neurosurgery (n = 13, 13.3%), and hematogenous (n = 12, 12.2%). The main neuroimaging features were intraventricular pus (n = 81, 82.7%), ependymal enhancement (n = 70, 71.4%), and intraventricular loculations (n = 15, 15.3%). The main pathogens were streptococci (n = 44, 44.9%), Gram-negative bacilli (n = 27, 27.6%), and staphylococci (n = 15, 15.3%). In-hospital and 1-year mortality rates were 30.6% (n = 30) and 38.8% (n = 38), respectively. Neurological sequelae were reported in 34 of 55 (61.8%) survivors, including cognitive impairment (n = 11), gait disturbances (n = 9), paresis (n = 7), behavior disorder (n = 6), and epilepsy (n = 5). On multivariate analysis, age >65 years, Glasgow Coma Scale score <13 at initial presentation, status epilepticus, hydrocephalus, and positive cerebrospinal fluid culture were associated with 1-year mortality. We built a scoring system to stratify patients with ventriculitis into low risk (12.5%), intermediate risk (36.5%), and high risk (71.4%) of death.ConclusionsVentriculitis is a severe complication of brain abscess, meningitis, or neurosurgery, with an in-hospital mortality rate of 30% and neurological sequelae in 60% of survivors.

Project description:Rabies remains a major public health concern in many developing countries. The precise neuropathogenesis of rabies is unknown, though it is hypothesized to be due to neuronal death or dysfunction. Mice that received intranasal inoculation of an attenuated rabies virus (RABV) strain HEP-Flury exhibited subtle clinical signs, and eventually recovered, which is different from the fatal encephalitis caused by the virulent RABV strain CVS-11. To understand the neuropathogenesis of rabies and the mechanisms of viral clearance, we applied RNA sequencing (RNA-Seq) to compare the brain transcriptomes of normal mice vs. HEP-Flury or CVS-11 intranasally inoculated mice. Our results revealed that both RABV strains altered positively and negatively the expression levels of many host genes, including genes associated with innate and adaptive immunity, inflammation and cell death. It is found that HEP-Flury infection can activate the innate immunity earlier through the RIG-I/MDA-5 signaling, and the innate immunity pre-activated by HEP-Flury or Newcastle disease virus (NDV) infection can effectively prevent the CVS-11 to invade central nervous system (CNS), but fails to clear the CVS-11 after its entry into the CNS. In addition, following CVS-11 infection, genes implicated in cell adhesion, blood vessel morphogenesis and coagulation were mainly up-regulated, while the genes involved in synaptic transmission and ion transport were significantly down-regulated. On the other hand, several genes involved in the MHC class II-mediated antigen presentation pathway were activated to a greater extent after the HEP-Flury infection as compared with the CVS-11 infection suggesting that the collaboration of CD4(+) T cells and MHC class II-mediated antigen presentation is critical for the clearance of attenuated RABV from the CNS. The differentially regulated genes reported here are likely to include potential therapeutic targets for expanding the post-exposure treatment window for RABV infection.

Dataset Information

Toscana virus central nervous system infections in southern Italy.

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Toscana virus central nervous system infections in southern Italy.

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