What is tick-borne encephalitis?
Tick-borne encephalitis (TBE) is a type of viral encephalitis caused by a virus that is spread by ticks. Ticks are small parasites that survive by sucking blood from animals – including humans. Ticks are the main carriers of the virus. The virus is also found in small rodents and some larger animals such as deer, sheep and goats.
There are three different main types of TBE virus: the European (Western), the Siberian and the Far-Eastern (spring-and-summer encephalitis) types. The European type is mainly found in central, eastern and northern Europe. People get TBE mostly in spring, summer and early autumn.
How can you get TBE?
Humans can be infected following a tick bite from an infected tick. Ticks live in forests, woods, grasslands, riverside meadows, marshes, brushwood and shrublands. They usually live in the undergrowth, where they can easily get onto the clothes or skin of passers-by. Therefore walkers, for example, are at an increased risk of getting the disease. The highest risk is for people when hiking or camping in forested areas up to an altitude of about 1500 m.
Not all ticks carry the virus, but it can be present in up to 10% of ticks in some areas.
Occasionally, people have been infected after drinking untreated milk from animals such as goats. There is no direct person-to-person transmission.
TBE virus is endemic in many parts of Europe (Estonia, Slovenia, Latvia, Lithuania, Czech Republic, Austria, Sweden, Switzerland, Slovakia, Hungary, Poland, Finland, Germany, France, Croatia and Norway), Siberia, Far-Eastern Russia, northern China and Japan. In the past years, TBE virus has been detected for the first time in countries such as the Netherlands (2016) and UK (2019). It is predicted that the areas affected will grow due to global warming.
What are the symptoms of TBE?
Most people, who are infected with the TBE virus, show no symptoms at all. In those that do have symptoms (2-30%), they typically appear about one-two weeks after the bite. From those with initial symptoms, one third will develop neurological symptoms.
In the European type of TBE there are normally two phases to the illness. The first phase consists of flu-like illness with symptoms such as fever, headache and generalized body aches. It lasts around five days. There is then about a week with no symptoms, which is followed by the second phase of the illness, when the brain or nerves are involved. The severity of the second phase varies between patients. Some people have a very mild illness whilst others may have a severe illness. Older people tend to get a more severe illness than younger people or children.
The symptoms in the second stage are similar to other causes of encephalitis and meningitis (inflammation of the lining of the brain). These include neck stiffness, headache, nausea, impaired consciousness (from drowsiness to coma), poor coordination, tremor, personality changes and psychosis. Some patients will also get muscle pain or limb weakness (most often in the arms). In severe cases the muscles that control the breathing are affected and people may die.
Tick-borne Encephalitis (TBE)
Tick-borne encephalitis, or TBE, is a human viral infectious disease involving the central nervous system. TBE is caused by the tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae, and was initially isolated in 1937. Three virus sub-types are described: European or Western tick-borne encephalitis virus, Siberian tick-borne encephalitis virus, and Far eastern Tick-borne encephalitis virus (formerly known as Russian Spring Summer encephalitis virus, REVERSE).
The family Flaviviridae includes several tick-borne viruses affecting humans. These viruses are closely related to TBEV and Far-eastern TBE, and include Omsk hemorrhagic fever virus in Siberia, Kassandra Forest disease virus in India and its close relative, Alkhurma virus in Saudi Arabia. Lou ping ill virus (United Kingdom) is also a member of this family; it causes disease primarily in sheep and has been reported as the cause of a TBE-like illness in laboratory workers and persons with contact to sick sheep (e.g., veterinarians, butchers). In the USA and Russia, another tick-borne flavivirus, Powassan virus, is responsible of encephalitis in human.
Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system. The disease most often manifests as meningitis, encephalitis, or meningoencephalitis. Long-lasting or permanent neuropsychiatric consequences are observed in 10 to 20% of infected patients.
The number of reported cases has been increasing in most countries.TBE is posing a concerning health challenge to Europe, as the number of reported human cases of TBE in all endemic regions of Europe have increased by almost 400% within the last three decades.
The tick-borne encephalitis virus is known to infect a range of hosts including ruminants, birds, rodents, carnivores, horses, and humans. The disease can also be spread from animals to humans, with ruminants and dogs providing the principal source of infection for humans.
Fact-sheet about tick-borne encephalitis (TBE)
Tick-borne encephalitis (TBE) is a human viral infectious disease involving the central nervous system, and occurring in many parts of Europe and Asia. The virus is transmitted by the bite of infected ticks, found in woodland habitats.
TBE is most often manifested as a two-phased illness. The first phase is associated with symptoms like fever, fatigue, headache, muscular ache and nausea. The second phase involves the neurological system with symptoms of meningitis (inflammation of the membrane that surrounds the brain and spinal cord) and/or encephalitis (inflammation of the brain).
Like other tick-borne infectious diseases, the risk from TBE can be reduced by using insect repellents and protective clothing to prevent tick bites. A vaccine is available in some disease endemic areas.
Tick-borne encephalitis (TBE) is an acute viral illness caused by two closely related viruses of the family Flaviviridae: the central European encephalitis (CEE) virus, found in many European countries, and the Russian spring-summer encephalitis (RSSE) virus, found predominantly in the Asian parts of the former Soviet Union. These viruses, which are endemic to forested areas, are transmitted by ticks. In addition to humans, they infect small mammals and, to a lesser extent, birds. In Asia, the disease is characterized by abrupt onset of fever, severe headache, nausea and vomiting and severe back pain often associated with focal epilepsy and flaccid paralysis, especially of the shoulder girdle. Such paralysis may be permanent. The central European form of the disease has a longer course, often with biphasic fever, but severe sequelae are less frequent. The initial febrile stage is normally not associated with disease of the central nervous system, but the second phase, following approximately 4-10 days after apparent recovery, is characterized by fever and meningoencephalitis. The case-fatality rate is approximately 20% for the Asian form of the disease and 1-5% for the European form.
TBE is endemic to most European countries, the Russian Federation and possibly China. It is the most important arthropod-transmitted viral disease in Europe, and in some countries it represents a major public-health problem. The disease has been known by several names, including RSSE, Far Eastern encephalitis and CEE.
CEE virus is found is every European country, with the exception of Belgium, Luxembourg, the Netherlands, Portugal, Spain and the United Kingdom, and is transmitted primarily by the tick Ix odes ricinus. RSSE virus is most prevalent in the eastern part of the former Soviet Union and is transmitted by the tick Ix odes persulcatus.
Flaviviruses are a large group of small, enveloped viruses responsible for a number of severe human diseases, including yellow fever, Japanese encephalitis, dengue hemorrhagic fever and TBE. TBE virus particles are roughly spherical in shape, 40-50nm in diameter, and contain a core, 20-30nm in diameter. The genome consists of single-stranded positive-sense RNA with a relative molecular mass of about 4×10(6). Three structural proteins and the caps id, membrane and envelope proteins are all encoded by the viral genome. The envelope glycoprotein induces neutralizing and haemagglutination-inhibition antibodies and is the most important antigen for providing protection from disease.
The first vaccine against TBE was prepared in 1941 in the brains of mice. Some 20 years later TBE vaccines derived from cell cultures (chicken embryo fibroblast cells) were developed and used for active immunization in humans in the former Soviet Union. Later, a purified, inactivated virus vaccine was developed which proved to be more immunologic than previous TBE vaccines.
The efficacy of these vaccines has been well documented. They have also been shown to protect mice from a lethal challenge with several TBE-virus isolates obtained over a period of more than 30 years from all over Europe and the Asian part of the former Soviet Union. In addition, it has been demonstrated that antibodies induced by vaccination of human volunteers neutralized all tested isolates.
Large outbreaks of TBE, sometimes involving thousands of cases, continue to occur in endemic areas. In addition, certain special groups, such as forest workers, geologists, travelers to endemic areas and laboratory workers, are also at risk. In view of the need to immunize large numbers of people, requirements for inactivated TBE vaccine have been formulated. In drafting these requirements, account has been taken of the regulations and requirements for the manufacture and control of TBE vaccines that have already been established in several countries.
Tick-borne encephalitis virus – a review of an emerging zoonosis.
During the last 30 years, there has been a continued increase in human cases of tick-borne encephalitis (TBE) in Europe, a disease caused by tick-borne encephalitis virus (TBEV). TBEV is endemic in an area ranging from northern China and Japan, through far-eastern Russia to Europe, and is maintained in cycles involving Ixodid ticks (Ix odes ricinus and Ix odes supersaturate) and wild vertebrate hosts. The virus causes a potentially fatal neurological infection, with thousands of cases reported annually throughout Europe. TBE has a significant mortality rate depending upon the strain of virus or may cause long-term neurological/neuropsychiatric sequel in people affected. In this review, we comprehensively reviewed TBEV, its epidemiology and parthenogenesis, the clinical manifestations of TBE, along with vaccination and prevention. We also discuss the factors which may have influenced an apparent increase in the number of reported human cases each year, despite the availability of effective vaccines.
Tick-Borne Encephalitis Viruses
Tick-borne encephalitis virus (TBEV; family Flaviviridae, genus Flavivirus) is a complex of closely related arboviruses transmitted to humans and other vertebrates by infected Ix odes spp. ticks. The virions contain positive polarity single-stranded RNA (Smyrna) (∼ 11 kbps) enclosed in a core consisting of caps id protein surrounded by a lipid membrane containing envelope and membrane nitroglycerin. Three-dimensional structural analysis has revealed the mechanism of the pH-dependent fusion between viral and endometrial membranes during entry into cells. After fusion, viral RNA is translated, producing a poly protein of ∼ 3400 amino acids that is co-translation-ally processed into three structural and seven nonstructural proteins, the latter providing viral proteolytic and replicate functions. The mode of RNA replication is asymmetric and semi conservative and mediated by the interaction of 5′-and 3′-untranslated regions. Details of virion maturation have been resolved at the atomic level. These viruses circulate in the forests and on the sheep-rearing and goat-rearing hillsides of the Northern Hemisphere, using both viremic and nonvirulent transmission strategies. The specific biological characteristics of different TBEVs and related viruses and their evolution and dispersal directly reflect the ecological requirements of the tick and its protracted life cycle. Human disease control in endemic regions relies primarily on the use of vaccines.
Treatment of TBE?
Unfortunately, there is no specific treatment for TBE. For people who have severe disease they may need supportive treatment in hospital such as intensive care. However, most people will only need symptom control.
Consequences of TBE
Some people (less than 2%) may die from TBE. This is more common in the Far-Eastern type. Some people will recover completely. Still others may have long lasting problems such as paralysis (the inability to move your arms and/or legs), ataxia (difficulties with coordination, balance and speech), headache, tiredness, difficulty concentrating and poor memory. If children are affected, they may be left with long-term cognitive problems such as short-term memory, headache, fatigue and irritability.
Prevention of TBE
TBE can be prevented by avoiding the areas where the disease occurs, however, this may not be possible. If walking in affected wooded or rural areas, it is recommended to wear long trousers/sleeves to cover exposed skin, use an insect repellent that is effective against ticks, and inspect your skin for ticks regularly. The attached ticks need to be removed as soon as possible by using tweezers as close to the skin attachment as possible through steady pulling without jerking or twisting. Unpasteurized dairy products should also be avoided in these areas.
The best protection against TBE is given by the vaccine which is available mainly in countries from Western Europe. It is an inactivated vaccine, does not contain live organisms and cannot cause the disease against which it protects. In some countries, (e.g. Austria) the vaccination was included in the national vaccination programmers and resulted in huge reduction of TBE cases. Internationally, there isn’t a consensus regarding the risk of TBE in travelers. However, according to the World Health Organization, the vaccine is recommended to at risk- travelers (travelers exposed outdoors in rural endemic areas between April to November).
Members of the Genus Flavivirus: Tick-Borne Encephalitis VIRUSES
Tick-borne encephalitis viruses constitute a complex of approximately a dozen flaviviruses, several of which are important zoophytic pathogens including tick-borne encephalitis virus in Eurasia (European, Far Eastern, and Siberian sub-types), Omsk hemorrhagic fever virus in Siberia; Kassandra Forest disease virus in India and recently in the Middle East, Powassan/deer tick virus in the northeastern region of North America, and Lou-ping ill virus in continental Europe and the British Isles (Table 29.1). Infected animals (including dogs and livestock such as cattle, sheep, and goats) are important in the spread of these viruses to humans because they serve as amplifying hosts for ticks; animals also may transmit some of these viruses to humans via raw milk (Fig. 29.7).
The epidemiology of tick-borne flaviviruses is more complex than that of their mosquito-borne counterparts, as ticks serve both as reservoirs of infection and as virus vectors. Unlike mosquitoes, the Ix odes tick vectors can live for several years, often longer than the generational time of their rodent reservoir hosts. Ticks are typically active from spring through autumn in temperate climates. Ticks develop successively through stages (larva to nymph to adult) and a blood meal is required at each stage. Tick-borne flaviviruses are passed from one developmental stage to another (trans-distal transmission), from one generation of tick to the next (transovarial transmission), and from infected to uninfected cofeeding ticks (nonviremic transmission) through the host integument. Larvae and nymphs generally feed on small mammals such as rodents, whereas adult ticks prefer larger animals, especially deer and wild boar.
The tick-borne encephalitis viruses all cause encephalitis in humans with the exception of Omsk hemorrhagic fever virus, which causes hemorrhagic fever in humans (as its name implies) in the absence of encephalitis. Kassandra Forest disease virus and its close relative Alkhuma virus, which is present in Saudi Arabia and Middle East, also cause hemorrhagic fever in humans but with accompanying encephalitis. Omsk hemorrhagic fever virus is also different from other tick-borne encephalitis viruses in that its principal tick vector is Dermacentor reticulated rather than Ix odes ticks. Electroencephalograms has been described in horses experimentally infected with Powassan virus, but similar disease has not been documented in naturally infected horses in North America.
Although expensive to produce, inactivated-virus vaccines for use in humans are available to prevent tick-borne encephalitis in Europe and eastern Asia.
LOUPING ILL Virus
Lou ping ill is an infectious electroencephalograms of sheep (syn. o vine electroencephalograms, trembling-ill) that occurs in the British Isles and the Iberian Peninsula. It is a typical member of the tick-borne virus complex, with a life cycle that involves transmission to sheep by the tick, Ix odes ricinus, with occasional involvement of horses, cattle, deer, and grouse. Horses in enzymatic areas sporadically develop electroencephalograms that resembles that caused by West Nile virus. Lou-ping ill occurs in spring and summer. Infected sheep develop a prolonged viremia and a biphasic febrile response, the second peak of which coincides with the development of nervous system dysfunction, including ataxia, tremors, hyper excitability, and paralysis. The disease gains its name from the peculiar leaping gait of ataxic sheep. Few animals that develop neurologic signs survive, and most of those that do suffer permanent neurology deficits. Control of the disease involves immunization of lambs with an inactivated vaccine, use of acaricides on susceptible sheep where allowed, and environmental control of ticks. Lou-ping ill virus is zoophytic, being transmitted to humans by ticks, or occupationally by contact with infected sheep and sheep tissues. The human disease is biphasic: the first phase is influenza-like, and the second phase is characterized by meningoencephalitis that usually resolves, without complications, in 4–10 days.