Tick-borne encephalitis (TBE) is a viral infectious disease involving the central nervous system, transmitted by the bite of several species of infected ticks. The disease most often manifests as meningitis, encephalitis or meningoencephalitis. Myelitis and spinal paralysis also occur. In about one third of cases sequelae, predominantly cognitive dysfunction, persist for a year or more. 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 has increased by almost 400% within the last three decades. Historically, TBE virus has been thought to be absent in the UK, but in 2020 Public Health England declared the first two TBE cases contracted within the country. 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.
Signs and symptoms
TBE virus infections are often asymptomatic, which means that the infected individual show no symptoms of disease. In clinical cases, the disease is most often biphasic. After an incubation period of approximately one week (range: 4–28 days) from exposure (tick bite), non-specific symptoms occur. These symptoms are fever, malaise, headache, nausea, vomiting, and myalgias that persist for about 5 days. Then, after approximately one week without symptoms, some of the infected develop neurological symptoms, i.e., meningitis, encephalitis, or meningoencephalitis. Myelitis also occurs with or without encephalitis. Tongue tremor has also been described as a characteristic neurological manifestation of TBE, occurring in more than 30% of patients during the neurological phase. Sequelae persist for a year or more in approximately one third of people who develop neurological disease. The most common long-term symptoms are headache, concentration difficulties, memory impairment, and other symptoms of cognitive dysfunction. Mortality depends on the subtype of the virus. For the European subtype, mortality rates are 0.5% to 2% for people who develop neurological disease. In dogs, the disease also manifests as a neurological disorder with signs varying from tremors to seizures and death. In ruminants, neurological disease is also present, and animals may refuse to eat, appear lethargic, and also develop respiratory signs.
Cause TBE is caused by tick-borne encephalitis virus, a member of the genus Flavivirus in the family Flaviviridae. It was first isolated in 1937 in the USSR by a team led by Lev A. Zilber. Three virus sub-types also exist:
European or Western tick-borne encephalitis virus (transmitted by Ixodes ricinus) Siberian tick-borne encephalitis virus (transmitted by I. persulcatus) Far-Eastern tick-borne encephalitis virus, formerly known as Russian spring summer encephalitis virus (transmitted by I. persulcatus). The former Soviet Union conducted research on tick-borne diseases, including the TBE viruses.
Transmission
It is transmitted by the bite of several species of infected woodland ticks, including Ixodes scapularis, I. ricinus and I. persulcatus, or (rarely) through the non-pasteurized milk of infected cows.
Milk Infection acquired through goat milk consumed as raw milk or fresh cheese (Frischkäse) has been documented in 2016 and 2017 in the German state of Baden-Württemberg. None of the infected had neurological disease. From 1980 to 2021, 384 confirmed cases of TBE in Europe were acquired through the consumption of raw milk or cheese. Countries that reported food-borne tick-borne encephalitis (FB-TBE) cases during this period included Slovakia, the Czech Republic, Poland, Hungary, Estonia, Germany, Croatia, Austria, Russia and Slovenia. Proven neuroinvasive disease was reported in 53 patients, with the described CNS syndromes including meningoencephalitis, meningitis, and meningoencephalomyelitis.
Diagnosis Detection of specific IgM and IgG antibodies in patients' sera, combined with typical clinical signs, is the principal method for diagnosis. The antibodies usually appear within six days after the onset of symptoms and are generally detectable once neurological signs appear. IgM antibodies may remain detectable for up to 10 months in both vaccinated individuals and those infected naturally. In more complicated situations, e.g., after vaccination, testing for the presence of antibodies in cerebrospinal fluid may be necessary. It has been stated that lumbar puncture should always be performed when diagnosing TBE and that pleocytosis in cerebrospinal fluid (CSF) should be added to the diagnostic criteria. The severity of TBE could be assessed using CSF calcium levels, according to recent studies of diagnostic markers for tick-borne encephalitis virus (TBEV). PCR (polymerase chain reaction) method is rarely used, since TBE virus RNA is most often not present in patient sera or cerebrospinal fluid at the time of neurological symptoms.
Prevention
Prevention includes non-specific (tick-bite prevention) and specific prophylaxis in the form of a vaccination. According to the CDC, non-specific tick-bite prevention for TBEV includes using insect repellent, wearing long-sleeved shirts and pants in high-risk areas, and treating clothing and gear with 0.5% permethrin. Tick checks, while useful for preventing some other tick-borne diseases such as Lyme disease, would not be expected to be effective in the prevention of tick-borne encephalitis, as the virus is transmitted within minutes of attachment by the tick. Tick-borne encephalitis vaccines are very effective and available in many disease-endemic areas and in travel clinics. Trade names are Encepur N and FSME-Immun CC. The vaccines are administered in two injections, given at least two weeks apart.
Treatment There is no specific antiviral treatment for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief although their long term effectiveness is debated. Tracheal intubation and respiratory support may be necessary.
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