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Bogovic P, Strle F. Tick-borne encephalitis: A review of epidemiology, clinical characteristics, and management. World J Clin Cases 2015; 3:430-441. [PMID: 25984517 PMCID: PMC4419106 DOI: 10.12998/wjcc.v3.i5.430] [Citation(s) in RCA: 299] [Impact Index Per Article: 29.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/23/2014] [Revised: 09/18/2014] [Accepted: 03/09/2015] [Indexed: 02/05/2023] Open
Abstract
Tick-borne encephalitis is an infection of central nervous system caused by tick-borne encephalitis virus transmitted to humans predominantly by tick bites. During the last few decades the incidence of the disease has been increasing and poses a growing health problem in almost all endemic European and Asian countries. Most cases occur during the highest period of tick activity, in Central Europe mainly from April to November. Tick-borne encephalitis is more common in adults than in children. Clinical spectrum of the disease ranges from mild meningitis to severe meningoencephalitis with or without paralysis. Rare clinical manifestations are an abortive form of the disease and a chronic progressive form. A post-encephalitic syndrome, causing long-lasting morbidity that often affects the quality of life develops in up to 50% of patients after acute tick-borne encephalitis. Clinical course and outcome vary by subtype of tick-borne encephalitis virus (the disease caused by the European subtype has milder course and better outcome than the disease caused by Siberian and Far-Easter subtypes), age of patients (increasing age is associated with less favorable outcome), and host genetic factors. Since clinical features and laboratory results of blood and cerebrospinal fluid are nonspecific, the diagnosis must be confirmed by microbiologic findings. The routine laboratory confirmation of the tick-borne encephalitis virus infection is based mainly on the detection of specific IgM and IgG antibodies in serum (and cerebrospinal fluid), usually by enzyme-linked immunosorbent assay. There is no specific antiviral treatment for tick-borne encephalitis. Vaccination can effectively prevent the disease and is indicated for persons living in or visiting tick-borne encephalitis endemic areas.
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Infektionen. NEUROINTENSIV 2015. [PMCID: PMC7175474 DOI: 10.1007/978-3-662-46500-4_32] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Abstract
In diesem Kapitel werden zunächst die für die Neurointensivmedizin wesentlichen bakteriellen Infektionen (Meningitis, spinale und Hirnabszesse, Spondylodiszitis, septisch-embolische Herdenzephalitis) abgehandelt, die trotz gezielt eingesetzter Antibiotika und neurochirurgischer Therapieoptionen noch mit einer erheblichen Morbidität und Mortalität behaftet sind. Besonderheiten wie neurovaskuläre Komplikationen, die Tuberkulose des Nervensystems, Neuroborreliose, Neurosyphilis und opportunistische Infektionen bei Immunsuppressionszuständen finden hierbei besondere Berücksichtigung. Der zweite Teil dieses Kapitels behandelt akute und chronische Virusinfektionen des ZNS sowie in einem gesonderten Abschnitt die HIVInfektion und HIV-assoziierte Krankheitsbilder sowie Parasitosen und Pilzinfektionen, die in Industrieländern seit Einführung der HAART bei HIV zwar eher seltener, aber mit zunehmender Globalisierung auch in unseren Breiten immer noch anzutreffen sind.
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Kumar G, Kalita J, Misra UK. Raised intracranial pressure in acute viral encephalitis. Clin Neurol Neurosurg 2009; 111:399-406. [DOI: 10.1016/j.clineuro.2009.03.004] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2008] [Revised: 03/10/2009] [Accepted: 03/11/2009] [Indexed: 12/12/2022]
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Mpaka M, Karantanas AH, Zakynthinos E. Atypical presentation of varicella-zoster virus encephalitis in an immunocompetent adult. Heart Lung 2008; 37:61-6. [DOI: 10.1016/j.hrtlng.2007.02.009] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2006] [Revised: 02/16/2007] [Accepted: 02/27/2007] [Indexed: 11/16/2022]
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Liu ML, Lee YP, Wang YF, Lei HY, Liu CC, Wang SM, Su IJ, Wang JR, Yeh TM, Chen SH, Yu CK. Type I interferons protect mice against enterovirus 71 infection. J Gen Virol 2005; 86:3263-3269. [PMID: 16298971 DOI: 10.1099/vir.0.81195-0] [Citation(s) in RCA: 125] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
In this study, the contribution of type I interferons (IFNs) to protection against infection with enterovirus 71 (EV71) was investigated using a murine model where the virus was administrated to neonatal Institute of Cancer Research (ICR) mice by either the intraperitoneal (i.p.) or the oral route. In i.p. inoculated mice, post-infection treatment of dexamethasone (5 mg kg(-1) at 2 or 3 days after infection) exacerbated clinical symptoms and increased the tissue viral titre. In contrast, polyriboinosinic : polyribocytidylic acid [poly(I : C); 10 or 100 microg per mouse at 12 h before infection], a potent IFN inducer, improved the survival rate and decreased the tissue viral titres after EV71 challenge, which correlated with an increase in serum IFN-alpha concentration, the percentage of dendritic cells, their expression of major histocompatibility complex class II molecule and IFN-alpha in spleen. Treatment with a neutralizing antibody for type I IFNs (10(4) neutralizing units per mouse, 6 h before and 12 h after infection) resulted in frequent deaths and higher tissue viral load in infected mice compared with control mice. In contrast, an early administration of recombinant mouse IFN-alphaA (10(4) U per mouse for 3 days starting at 0, 1 or 3 days after infection) protected the mice against EV71 infection. In vitro analysis of virus-induced death in three human cell lines showed that human type I IFNs exerted a direct protective effect on EV71. It was concluded that type I IFNs play an important role in controlling EV71 infection and replication.
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Affiliation(s)
- Ming-Liang Liu
- Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Yi-Ping Lee
- Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Ya-Fang Wang
- Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Huan-Yao Lei
- Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Ching-Chuan Liu
- Department of Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Shih-Min Wang
- Department of Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Ih-Jen Su
- Department of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Jen-Reng Wang
- Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Trai-Ming Yeh
- Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Shun-Hua Chen
- Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
| | - Chun-Keung Yu
- Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan 70101, Republic of China
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Abstract
Central nervous system (CNS) infections are diverse. CNS infections can cause significant morbidity and mortality and are markedly different from systemic infections. The closed anatomic space of the CNS, its immunologic isolation from the rest of the body, and the often nonspecific nature of the key manifestations present a challenge to the clinician. Early recognition and aggressive management are essential to patient recovery and prevention of long-term neurologic sequelae. This review discusses the major types of CNS infections and focuses on critical care management, with emphasis on current epidemiologic trends.
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Affiliation(s)
- W C Ziai
- Neurosciences Critical Care Division, Johns Hopkins Hospital, Meyer 8-140, 600 N. Wolfe Street, Baltimore, MD 21287, USA
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