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Central Nervous System Infections
Published in Miriam Orcutt, Clare Shortall, Sarah Walpole, Aula Abbara, Sylvia Garry, Rita Issa, Alimuddin Zumla, Ibrahim Abubakar, Handbook of Refugee Health, 2021
Encephalitis is most commonly caused by viruses, including HSV-1 and -2, varicella zoster virus (VZV), CMV, measles, mumps and enterovirus. Other viruses based on geography include Japanese Encephalitis virus (East, South and South East Asia), West Nile Virus (parts of Africa, Europe, Asia and North America), equine encephalitis virus (USA, Central America and northern regions of South America), Nipah virus (Malaysia, Singapore and South Asia); rabies virus (worldwide; see WHO country risk; most deaths in Africa and Asia), Rift Valley fever virus (Eastern, Southern and Western Africa), tick-borne encephalitis virus (Eastern Europe and southern Russia) and yellow fever virus (tropical and subtropical regions of South America and Africa).
Encephalitis
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense (African sleeping sickness), Angiostrongylus cantonensis (rat lungworm), malaria, encephalitis due to flaviviruses: West Nile, dengue, Japanese encephalitis, Zika virus and tick-borne encephalitis should be considered in a traveller presenting with encephalitis. Less common is rabies encephalitis and Rickettsia. It is important to consider geographical differences, as West Nile virus may be the most common cause of encephalitis in the United States whilst Japanese encephalitis may be the most common cause of encephalitis worldwide. Tick-borne encephalitis virus (TBE) is a quite prevalent cause of encephalomyelitis in Europe and Russia.
Severe Tick-Borne Infections and Their Mimics in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Praveen Sudhindra, Gary P. Wormser
In the United States, Rocky Mountain spotted fever (RMSF), babesiosis, and Lyme carditis with advanced atrioventricular nodal block probably account for the majority of critical care admissions among tick-borne infections. Other infections such as human monocytic ehrlichiosis (HME), and encephalitis due to the deer tick virus (DTV)/Powassan virus (POWV) are also occasionally encountered in the CCU. Tularemia and Q fever can be transmitted by ticks but will not be discussed here since other routes of transmission predominate. Outside the United States, Crimean-Congo hemorrhagic fever and tick-borne encephalitis virus are important causes of severe illness.
Low prevalence of tick-borne encephalitis virus antibodies in Norwegian blood donors
Published in Infectious Diseases, 2021
Åshild Marvik, Yngvar Tveten, Anne-Berit Pedersen, Karin Stiasny, Åshild Kristine Andreassen, Nils Grude
Tick-borne encephalitis (TBE) is one of the most important tick-borne diseases in Europe and Asia [1–4]. The causative agent, tick-borne encephalitis virus (TBEV), is neurotropic and consists of three subtypes described according to their main distribution area: European (TBEV-Eu), Far-Eastern (TBEV-FE) and Siberian subtype (TBEV-Sib) [5]. Three other subtypes of TBEV, TBEV Baikalian (TBEV 886-84), TBEV 178-179 and TBEV Himalayan have also been suggested [6–9]. TBE is a zoonotic disease and transmission to humans is mainly due to tick bites and only a minor extent due to the alimentary route through infected dairy products [1,4,10]. Ticks and small rodents constitute the reservoirs for TBEV. Ixodes ricinus is the principal vector for TBEV-Eu and occurs in large parts of Europe. Ixodes persulcatus, the vector for the Far-Eastern and Siberian subtypes, occurs in Eastern Europe, Siberia and far east including Japan [2]. Thus, in Europe, human disease caused by TBEV-Eu predominates [2,3,11].
Post-exposure prophylactic vaccine candidates for the treatment of human Risk Group 4 pathogen infections
Published in Expert Review of Vaccines, 2020
James Logue, Ian Crozier, Peter B Jahrling, Jens H Kuhn
Finally, tick-borne encephalitis virus (TBEV; Flaviviridae: Flavivirus) is generally transmitted by ixodid ticks in Western (Ixodes ricinus) and Eastern (Ixodes persulcatus) Europe. The virus is maintained by over 100 species of wild animals, including voles, deer, and domestic animals such as sheep [122–124]. Although patients infected with TBEV normally only present with an initial, nonspecific febrile phase, 20–30% of patients progress to a second stage of disease with CNS signs (meningitis, encephalitis, or both). Lethality is generally 1–2%, but 30–60% of patients develop chronic neuropsychiatric sequelae [125,126]. Three different vaccines for pre-exposure disease prevention (IPVE, FSME-IMMUN, and Encepur) are generally available in endemic regions [127]. However, fears over the potential of antibody-dependent disease enhancement or increased viral infectivity caused by ‘sub-optimal’ concentrations of virus-specific antibodies have hampered further vaccine development [128]. For this reason and the potential of other adverse effects [129], none of these vaccines are licensed by the US FDA. Vaccine use is neither recommended by the US Centers for Disease Control and Prevention (CDC) nor the WHO except for high-risk individuals, such as laboratory workers or workers with high exposure to potentially infected host ticks [130,131]. Multiple studies into the use of antibody treatments as PEP have produced promising results in laboratory mice with no disease enhancement [132,133].
Rapid travel to a Zika vaccine: are we heading towards success or more questions?
Published in Expert Opinion on Biological Therapy, 2018
Carl Britto, Christina Dold, Arturo Reyes-Sandoval, Christine S. Rollier
Antibody-dependent enhancement (ADE) is an immunological event which potentiates DENV infection in individuals with a sub-protective DENV-specific antibody threshold [61]. It was first observed in 6–12 month-old infants in whom an unexpected number of severe dengue syndrome cases occurred, when maternal derived-antibodies waned below neutralizing levels [62,63]. Evidence of ADE induced via vaccination came from a phase III clinical trial: young DENV-infected vaccine recipients had an increased risk of DENV-related hospitalization more than one year after vaccination as compared with placebo controls. It was postulated that vaccination of DENV-naïve individuals induced poorly neutralizing anti-DENV antibodies, which translated to an increased risk of severe dengue disease via the mechanism of ADE [64]. A recent publication studying well characterized cohort of children from a DENV endemic region in Nicaragua revealed that the correlate of risk for severe disease (DENV-Ab titer 1:21–1:80) was independent from the correlate of protection (DENV-Ab titers at and above 1:80–1:320) against symptomatic DENV infection [62]. Notably, the Japanese encephalitis virus, tick-borne encephalitis virus and yellow fever virus vaccine platforms have not raised this concern.