Tick-borne encephalitis (TBE) is a viral disease that affects the brain and nervous system. It spreads to humans mainly through the bite of an infected tick. The illness usually develops in two stages. The first stage causes mild, flu-like symptoms such as fever, tiredness, headache, and muscle pain. The second stage can be more serious, involving swelling of the brain and the membranes surrounding it. This can lead to conditions like meningitis (inflammation of the brain’s protective layers), encephalitis (inflammation of the brain itself), or meningoencephalitis (a combination of both). In severe cases, it can also cause myelitis (inflammation of the spinal cord) and paralysis.
There is no specific cure or antiviral medication for TBE. Treatment focuses on easing symptoms such as pain and fever and providing supportive care, especially for patients with nerve or brain involvement.
The best way to prevent TBE is through vaccination, which is available and recommended for people living in or visiting areas where the disease is common. Other protective steps include wearing long sleeves and pants, tucking pants into socks, using insect repellents with DEET, and avoiding areas with high tick activity such as tall grass and thick vegetation. After spending time outdoors, it is important to check your body and clothing for ticks and remove them promptly.
TBE symptoms can range from mild to severe. They may include headache, sensitivity to light, dizziness, trouble concentrating, and muscle weakness or paralysis. Some people experience long-lasting effects, such as memory problems or difficulty moving, which can continue for months or years after infection.
In rare cases, TBE can be life-threatening. Around 1% of patients with serious nervous system symptoms die from the infection, while many others may develop lasting neurological problems that can affect daily life.
Historical Background
Tick-borne encephalitis was first identified in the 1930s, following a series of outbreaks in Siberia, where thousands of cases were recorded among forest workers and farmers. During this period, scientists successfully isolated the virus responsible for the disease and identified its primary carrier, the Ixodes tick. These discoveries laid the foundation for understanding the link between the virus, its tick vector, and the environment in which transmission occurs.
Over the following decades, research expanded to other regions of Russia, Central Europe, and Scandinavia, where similar outbreaks were observed. By the mid-20th century, advances in virology enabled scientists to distinguish between different viral strains of TBE, including the European subtype, the Siberian subtype, and the Far Eastern subtype, each varying slightly in severity and geographic distribution.
As global travel and land use changed throughout the 20th century, the geographic range of TBE expanded. Forest clearing, agricultural activity, and climate variations influenced tick habitats, contributing to the viruses spreading into parts of Eastern and Western Europe, and northern Asia. Governments and public health authorities responded by improving diagnostic tools, establishing surveillance systems, and developing vaccines to protect at-risk populations. The first vaccines became available in the 1970s, significantly reducing infection rates in vaccinated areas such as Austria and the Czech Republic.
Epidemiology
Tick-borne encephalitis is now recognized as an endemic disease across much of Europe and Asia, meaning it occurs regularly in certain areas. Each year, an estimated 10,000 to 12,000 cases are reported worldwide, though the true number is likely higher due to underreporting and misdiagnosis in remote regions.
The highest rates of infection are recorded in Russia, Austria, the Czech Republic, Switzerland, Germany, and the Baltic states (Estonia, Latvia, and Lithuania). The virus is transmitted mainly by Ixodes ricinus in Europe and Ixodes persulcatus in Asia. The risk of infection increases during late spring to early autumn, when ticks are most active. Activities such as hiking, camping, forestry work, and farming in tick-endemic regions significantly increase exposure risk.
While TBE can affect people of all ages, older adults are more likely to experience severe illness and long-term complications due to reduced immune response. In contrast, children often develop milder symptoms, though they are not immune to neurological effects.
Vaccination programs have been instrumental in reducing disease incidence in countries where the vaccine is routinely recommended. For example, Austria achieved a sharp decline in cases after implementing widespread immunization campaigns. However, vaccine coverage remains uneven across Europe and Asia, leaving many populations still vulnerable
Causes and Transmission
Tick-borne encephalitis (TBE) is caused by the tick-borne encephalitis virus (TBEV), a member of the Flavivirus genus in the Flaviviridae family, which also includes viruses responsible for dengue fever, yellow fever, and Zika virus disease. TBEV is a neurotropic virus, meaning it primarily targets the central nervous system (CNS), leading to inflammation of the brain and its surrounding tissues in severe cases.
The virus is maintained in nature through a complex ecological cycle involving ticks and small wild mammals, particularly rodents. Humans are considered accidental or “dead-end” hosts, meaning that while they can contract the infection, they do not play a role in spreading it further. The majority of human infections occur through tick bites, but in some cases, people can also become infected by consuming unpasteurized milk or dairy products from infected animals such as goats, sheep, or cows.
TBEV has several genetic subtypes, European, Siberian, and Far Eastern, each associated with particular geographic regions and levels of disease severity. The European subtype generally causes milder illness with a lower fatality rate, whereas the Far Eastern subtype is more virulent and has been linked to higher rates of severe neurological complications and death.
Tick Species Involved
The main carriers, or vectors, of TBEV are Ixodes ricinus and Ixodes persulcatus, two tick species that differ in their geographic distribution but play similar roles in maintaining the virus in the environment.
- Ixodes ricinus, also known as the sheep tick or castor bean tick, is found mainly in Central and Western Europe, including countries such as Austria, Germany, Switzerland, and the Czech Republic.
- Ixodes persulcatus, commonly referred to as the taiga tick, is widespread in Eastern Europe and northern Asia, including Russia, Mongolia, and parts of China and Japan.
These ticks are blood-feeding ectoparasites, meaning they live on the outside of a host and feed on its blood. They pass through three active life stages, larva, nymph, and adult and can feed on a different host at each stage. The nymphal stage is considered the most important for TBEV transmission to humans because nymphs are small, difficult to detect, and highly active during the spring and early summer, when outdoor recreational activities increase.
Ticks typically acquire the virus when feeding on infected small mammals, such as mice, voles, and shrews, which act as reservoir hosts. Once infected, ticks can retain the virus for their entire lifespan, allowing them to transmit it to new hosts, including humans, during subsequent feedings.
Transmission Cycle
The transmission cycle of TBEV in nature involves a three-way interaction between ticks, wildlife hosts, and environmental conditions. The virus persists in the ecosystem mainly through a continuous cycle of infection between small mammals and ticks.
- Reservoir Hosts: Small mammals, especially rodents, play a critical role in maintaining the virus. Although they carry TBEV in their bloodstream, they rarely show signs of illness. This silent infection allows the virus to persist in wildlife populations.
- Tick Infection: Ticks become infected when they feed on the blood of an infected animal. The virus then multiplies within the tick’s salivary glands, which allows for efficient transmission during the next feeding. Once infected, a tick remains capable of spreading the virus throughout its lifetime.
- Human Infection: Humans enter the cycle accidentally when bitten by an infected tick. Transmission typically occurs within minutes to hours after a tick attaches, as the virus is present in the tick’s saliva. Unlike some other tick-borne diseases, such as Lyme disease, which require prolonged attachment, TBEV can be transmitted relatively quickly.
- Environmental Influence: The activity of TBEV-carrying ticks depends heavily on temperature, humidity, and vegetation. Warmer, humid conditions favor tick survival and increase the risk of contact between humans and infected ticks. Seasonal peaks occur in late spring and early autumn, matching the period of maximum tick activity.
Other Modes of Transmission
In addition to tick bites, foodborne transmission can occur when humans consume unpasteurized milk or dairy products from infected animals, particularly goats. This route is relatively rare but has been documented in several European countries, including Austria, the Czech Republic, and Slovakia. Pasteurization effectively kills the virus, making properly processed dairy products safe.
The virus can also be passed between ticks through other mechanisms that help sustain its presence in tick populations:
- Transovarial transmission: Infected female ticks can pass the virus directly to their offspring through their eggs, ensuring that new generations of ticks begin life already carrying the virus.
- Co-feeding transmission: This occurs when multiple ticks feed close together on the same host. Even if the host does not have detectable levels of the virus in its blood, the virus can spread locally between ticks through their feeding sites.
These mechanisms allow the virus to persist even when host infection rates are low, ensuring the long-term stability of TBEV in natural environments.
Symptoms and Clinical Stages
Tick-borne encephalitis (TBE) develops in well-defined stages that reflect the virus’s progression from the bloodstream to the central nervous system. The clinical course can be divided into three main phases: the early symptomatic phase, the neurological phase, and, in some cases, a long-term post-encephalitic phase characterized by lasting effects.
Early Symptomatic Phase
The early phase of TBE generally appears 7 to 14 days after the bite of an infected tick, though the incubation period can range from 4 to 28 days depending on viral load and immune response. This stage reflects the viraemic phase, during which the virus spreads through the bloodstream but has not yet reached the brain or spinal cord.
Symptoms begin suddenly and resemble those of the flu or other viral infections. Common signs include:
- Fever (often high-grade)
- Fatigue and malaise (a general feeling of being unwell)
- Headache and muscle aches (myalgia)
- Chills and joint pain (arthralgia)
- Gastrointestinal upset, including nausea, vomiting, and sometimes mild abdominal pain
This initial stage typically lasts 2 to 4 days. Most individuals recover fully after this period, as their immune system clears the virus. In fact, about two-thirds of infected patients do not progress beyond this phase and may not even realize they had TBE, mistaking it for a short-lived viral illness.
During the early phase, laboratory findings are often non-specific. Blood tests may show normal or slightly elevated levels of white blood cells (leukocytes) and inflammatory markers such as C-reactive protein. The virus can be detected in blood or serum samples during this stage using polymerase chain reaction (PCR) testing, but once the immune system begins producing antibodies, viral levels in the blood rapidly decline.
Asymptomatic Interval
In cases that progress beyond the first stage, there is often a symptom-free interval lasting about 4 to 10 days. During this time, patients may feel completely recovered, unaware that the virus has begun to invade the central nervous system (CNS). This temporary recovery period is a hallmark of TBE and helps distinguish it from other viral infections that cause continuous illness.
Neurological Complications
Roughly 20–30% of infected individuals develop a second, more severe phase involving neurological complications. This stage occurs when the virus crosses the blood–brain barrier and causes inflammation in various parts of the CNS. Depending on the affected regions, patients may develop meningitis, encephalitis, or meningoencephalitis, each with distinct clinical presentations.
Meningitic Form
The meningitic form of TBE is characterized by inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It presents with classic signs of meningeal irritation, such as:
- Severe, persistent headache
- Neck stiffness (pain and resistance when bending the neck forward)
- Photophobia (sensitivity to light)
- Nausea and vomiting
This form is more common in children and younger adults and often has a favorable outcome with full recovery after a few weeks.
Encephalitic Form
The encephalitic form is more serious and involves inflammation of the brain tissue itself. Symptoms may include:
- Confusion, disorientation, and difficulty concentrating
- Behavioral changes or agitation
- Seizures or convulsions
- Speech and movement difficulties (such as slurred speech or tremors)
- Focal neurological deficits, including paralysis or facial weakness
This form tends to occur more frequently in older adults, who are at greater risk for complications and slower recovery.
Meningoencephalitic Form
In some patients, the infection causes both meningitis and encephalitis, a condition known as meningoencephalitis. This is considered the most severe presentation of TBE and can result in respiratory failure, loss of consciousness, or coma in extreme cases.
Myelitic Form
Occasionally, the virus extends to the spinal cord, producing myelitis. This can lead to muscle weakness, limb paralysis, or flaccid paresis (loss of voluntary muscle movement). Involvement of the brainstem or cranial nerves may cause swallowing difficulties, facial nerve paralysis, or impaired eye movement.
Long-term Effects
A significant portion of patients with neurological involvement experience persistent symptoms after recovery. These may include cognitive impairment, memory loss, and concentration difficulties.
Chronic headaches, fatigue, and muscle weakness are also common. In rare cases, long-term motor deficits such as paralysis can occur.
Rehabilitation therapies may aid recovery, but some sequelae can last months or years. Early diagnosis and treatment are crucial to reduce the risk of lasting damage.
Diagnosis of Tick-borne Encephalitis
Because the disease can mimic a variety of other infectious and non-infectious neurological conditions, accurate identification of the virus and exclusion of other potential causes are essential to ensuring appropriate patient management and treatment.
Clinical Assessment
The diagnostic process begins with a comprehensive clinical evaluation, focusing on the patient’s medical history, exposure risk, and symptom chronology. Physicians should inquire specifically about recent tick bites, outdoor activities in forested or grassy areas, or travel to endemic regions—primarily Central and Eastern Europe, Russia, and parts of Asia. In many cases, patients may not recall a tick bite, making exposure history an important but sometimes incomplete clue.
The illness often follows a biphasic pattern, which is one of its hallmark features. The first phase typically manifests 7 to 14 days after a tick bite, resembling a nonspecific viral infection with symptoms such as:
- Fever, fatigue, malaise, and headache
- Myalgia (muscle pain) and arthralgia (joint pain)
- Nausea or mild gastrointestinal discomfort
This initial phase usually lasts a few days and is followed by a symptom-free interval lasting about a week. The second phase then emerges, characterized by neurological involvement that may include:
- Meningitis (headache, photophobia, neck stiffness)
- Encephalitis (confusion, tremors, altered mental status)
- Meningoencephalitis (a combination of both)
In severe cases, particularly in adults, symptoms may progress to ataxia, dysarthria, cranial nerve palsies, or even spinal cord involvement (myelitis), leading to limb weakness or paralysis. Children more commonly experience milder meningitic forms, while adults are at higher risk for severe neurological deficits.
A neurological examination is crucial in this stage to assess reflexes, coordination, mental clarity, and signs of meningeal irritation. Clinicians must also document the timing of symptom onset meticulously to identify the biphasic course, which helps differentiate TBE from other viral encephalitides.
Laboratory Testing
Laboratory confirmation of tick-borne encephalitis (TBE) is essential to establish a definitive diagnosis, particularly because its clinical symptoms overlap with those of many other viral and bacterial infections of the central nervous system (CNS).
Serological Testing (ELISA and Neutralization Tests)
The enzyme-linked immunosorbent assay (ELISA) remains the cornerstone of laboratory diagnosis for TBE. This test detects TBEV-specific IgM and IgG antibodies in the patient’s serum or cerebrospinal fluid. IgM antibodies typically emerge at the onset of neurological symptoms, marking the transition from the viremic to the neurologic phase. Their presence indicates a recent infection, as they can persist for several weeks or even months after the acute phase. On the other hand, IgG antibodies develop shortly after IgM and may persist for years, reflecting either a past infection or immunity following vaccination.
However, the presence of antibodies alone does not always provide a clear distinction between infection and vaccination response, especially in individuals previously immunized against TBE or other flaviviruses. To address this challenge, virus neutralization tests (VNTs) are often employed as confirmatory assays. VNTs measure the functional ability of antibodies to neutralize the virus, offering higher specificity. These tests are particularly useful when ELISA results are ambiguous or when cross-reactivity with other flaviviruses, such as West Nile virus or Japanese encephalitis virus, is suspected. The combination of ELISA and VNT helps ensure both sensitivity and specificity in serological diagnosis.
Molecular Testing (PCR)
The polymerase chain reaction (PCR) technique can directly detect TBEV RNA in biological samples such as serum, whole blood, or CSF. This molecular method is most effective in the early viremic phase of the illness, typically before the onset of neurological symptoms when viral replication is at its peak. However, by the time neurological manifestations appear, the virus is often cleared from the bloodstream, and viral RNA levels decline sharply, making PCR results frequently negative during this stage.
Despite this limitation, PCR remains valuable for early-phase diagnosis, particularly in patients presenting before the immune response develops. In such cases, detecting viral RNA can confirm infection even before antibodies are detectable. Nonetheless, because most patients seek medical attention only after neurological symptoms arise, serological testing remains the primary and most reliable diagnostic tool for TBE.
Cerebrospinal Fluid (CSF) Analysis
Analysis of cerebrospinal fluid plays a critical role in confirming CNS involvement and differentiating TBE from other neurological infections. A lumbar puncture is performed to obtain CSF, which is then examined for signs of inflammation. Typical CSF findings in TBE include lymphocytic pleocytosis (an increased number of white blood cells), moderately elevated protein levels, and normal or slightly reduced glucose concentrations. This pattern is consistent with viral meningitis or encephalitis.
Furthermore, detecting TBEV-specific IgM and IgG antibodies in CSF provides strong evidence of intrathecal antibody production, confirming that the infection has spread to the central nervous system. This finding helps differentiate TBE from systemic viral infections that do not involve the CNS.
Differential Diagnosis
Differentiating TBE from other viral and bacterial neurologic infections is vital.
Other Viral Encephalitides
Several other viruses can cause encephalitis that mimics TBE. Herpes simplex virus (HSV) encephalitis, for example, frequently presents with fever, confusion, seizures, and focal neurological deficits. Unlike TBE, HSV encephalitis often affects the temporal lobes and can be confirmed by PCR testing of CSF, which detects HSV DNA with high sensitivity.
West Nile virus and Japanese encephalitis virus infections also share overlapping symptoms with TBE, such as fever, meningitis, and altered mental status. These viruses belong to the same Flaviviridae family, making serological cross-reactivity a diagnostic challenge. Confirmatory neutralization assays are often required to differentiate between these infections, especially in regions where multiple flaviviruses co-circulate. Enteroviral infections can also produce meningitic symptoms but typically follow a shorter course and lack the biphasic illness pattern that characterizes TBE.
Bacterial and Tick-borne Co-infections
Tick bites can transmit multiple pathogens, making co-infection a possibility in endemic regions. Lyme neuroborreliosis, caused by Borrelia burgdorferi, is an important differential diagnosis. Unlike TBE, it often presents with cranial nerve palsies, radiculitis, and progressive neuropathy rather than acute encephalitis. Diagnosis is confirmed by detecting Borrelia-specific antibodies or DNA in CSF.
Other tick-borne diseases such as rickettsial infections and anaplasmosis may occasionally produce neurological manifestations but are usually accompanied by systemic symptoms, including rash, cytopenias, or hepatosplenomegaly. Recognition of these distinguishing features helps rule out these conditions during clinical evaluation.
Autoimmune and Other Non-Infectious Causes
In addition to infectious diseases, autoimmune encephalitides should be considered in the differential diagnosis of TBE, particularly when infectious agents are not detected. Anti-NMDA receptor encephalitis is a key example; it may present with psychiatric symptoms, seizures, and movement disorders that resemble viral encephalitis. The diagnosis is established through autoantibody testing of serum or CSF.
Other non-infectious causes such as multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM) can produce CNS inflammation and neurological deficits similar to TBE. MRI findings are helpful in distinguishing these demyelinating disorders, as they reveal characteristic lesions in white matter regions. Additionally, toxic, metabolic, or drug-induced encephalopathies must be excluded through detailed medical history, metabolic panels, and exposure assessments.
Treatment Approaches
Treatment for tick-borne encephalitis (TBE) centers on symptomatic management and supportive care, as there is currently no specific antiviral therapy proven effective against the tick-borne encephalitis virus (TBEV).
Supportive Care
For patients with mild to moderate forms of tick-borne encephalitis, typically those presenting with fever, headache, fatigue, and mild meningitic symptoms, supportive care remains the cornerstone of treatment. Because the disease is viral in nature, antibiotics have no therapeutic role unless there is a secondary bacterial infection.
Symptomatic management begins with controlling fever and pain. Acetaminophen (paracetamol) or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen are commonly administered to reduce fever, relieve headache, and ease muscle aches. Care must be taken to avoid excessive dosing, especially in patients with liver or kidney impairment.
Adequate hydration is equally important. Patients are encouraged to maintain oral fluid intake to compensate for fever-related fluid loss, though intravenous fluids may be required if oral hydration is insufficient. Rest is vital during the acute phase to reduce metabolic stress and support immune function.
In cases where patients experience agitation, anxiety, or insomnia, mild sedatives or anxiolytics may be prescribed to promote comfort and rest. Anti-inflammatory agents can also help manage systemic discomfort, although their use should be carefully balanced against potential side effects.
Hospital Management
Patients exhibiting neurological complications such as encephalitis, meningoencephalitis, or myelitis, require hospital admission for close monitoring and advanced supportive interventions. The management of these cases focuses on maintaining homeostasis, respiratory function, and intracranial stability, while minimizing secondary complications.
Intravenous fluid therapy is routinely administered to correct dehydration and electrolyte imbalance, particularly in patients unable to maintain adequate oral intake. Electrolyte levels are closely monitored, as imbalances can exacerbate neurological symptoms or trigger seizures.
For patients with respiratory compromise, decreased consciousness, or brainstem involvement, mechanical ventilation may be required to sustain oxygenation and prevent respiratory failure. Continuous monitoring in an intensive care unit (ICU) allows for rapid intervention in the event of seizures, increased intracranial pressure, or cardiovascular instability.
Seizure management is an essential component of hospital care. Anticonvulsants, such as benzodiazepines or phenytoin, are administered as needed to control or prevent recurrent seizures. In cases of raised intracranial pressure, measures such as head elevation, osmotic diuretics (e.g., mannitol), or controlled hyperventilation may be used to reduce cerebral edema.
The role of corticosteroids, such as dexamethasone, in TBE management remains controversial. Although they are sometimes used to alleviate cerebral inflammation and edema, evidence supporting their efficacy is limited. Most experts recommend that corticosteroid therapy be considered only in severe cases where inflammation contributes significantly to neurological deterioration, and under close supervision by specialists.
Prevention and Vaccination
Preventing tick-borne encephalitis (TBE) requires a two-pronged approach: reducing exposure to infected ticks and building immunity through vaccination.
Tick Bite Prevention Strategies
Ticks are most active during warmer months, especially between April and October, and are commonly found in wooded, bushy, and grassy areas where humidity is high. These environments provide ideal conditions for their survival and increase the likelihood of contact with humans and animals. Thus, individuals spending time outdoors, whether hiking, camping, or working, must adopt practical protection methods.
Wearing long-sleeved shirts, long pants tucked into socks, and closed shoes provides a physical barrier that reduces the chance of tick attachment. Light-colored clothing is preferable because it makes spotting ticks easier before they can bite. Applying insect repellents is another critical measure: repellents containing DEET (N,N-Diethyl-meta-toluamide), picaridin, or IR3535 can be applied directly to exposed skin, while permethrin can be used to treat clothing and gear, offering long-lasting tick repellency.
After outdoor activities, it’s essential to perform full-body tick checks, paying special attention to warm, hidden areas such as the scalp, behind the ears, under the arms, around the waist, and behind the knees. Bathing or showering within two hours of returning indoors can help wash off unattached ticks. Any tick found attached should be removed promptly using fine-tipped tweezers, gripping the tick close to the skin and pulling steadily upward without twisting. The site should then be cleaned with soap and water or an antiseptic. Prompt removal reduces the likelihood of virus transmission, as TBE virus transmission typically occurs soon after the bite, unlike Lyme disease, which requires a longer feeding period.
Maintaining short grass in yards, removing leaf litter and tall weeds, and creating gravel or woodchip barriers between lawns and wooded areas reduce tick habitats near homes. Pet owners should use veterinarian-approved tick prevention products for dogs and cats, as they can carry ticks indoors. Collectively, these personal and environmental precautions can significantly minimize human exposure to infected ticks.
Available Vaccines
Vaccination provides reliable and long-term protection against TBE, especially for people living in or traveling to high-risk regions. Unlike preventive measures that rely on behavior, vaccines build immunity by stimulating the body’s defense system against the virus. Several safe and effective inactivated TBE vaccines are available, primarily in Europe and parts of Asia, where the disease is endemic.
Two of the most widely used vaccines are FSME-IMMUN® (manufactured by Pfizer) and Encepur® (produced by Bavarian Nordic). Both vaccines are approved for adults and children aged one year and above. They are given as part of a multi-dose schedule: typically, two or three initial doses spaced over several months establish primary immunity, followed by booster doses every three to five years to maintain protection. The timing may vary slightly between vaccine brands.
These vaccines have demonstrated high efficacy, offering up to 95–99% protection after full immunization. They are generally well-tolerated, with side effects limited to mild redness, soreness, or swelling at the injection site. Occasionally, individuals may experience transient fatigue, headache, or mild fever, symptoms that typically resolve without treatment. Importantly, TBE vaccination protects only against the tick-borne encephalitis virus; it does not provide immunity against other tick-borne infections such as Lyme disease, anaplasmosis, or babesiosis, which may coexist in the same tick populations.
Vaccination is strongly recommended for people living in or traveling to endemic areas during tick season. This includes forestry workers, hikers, campers, and residents in rural regions of Central and Eastern Europe.
Pregnant women and individuals with severe allergies should consult healthcare providers before vaccination. Immunization programs are sometimes offered free of charge or subsidized in high-incidence zones.
Risk Factors and Vulnerable Populations
Several factors influence the likelihood of contracting tick-borne encephalitis (TBE). These include specific environmental conditions and inherent risks associated with certain occupations.
Environmental Risk Factors
TBE risk is highest in areas where the primary tick vectors, mainly Ixodes ricinus and Ixodes persulcatus, thrive. These ticks prefer deciduous and mixed forests with dense undergrowth.
Seasonality also affects risk. The peak period for tick activity is from April to November, which aligns with warmer temperatures and higher humidity.
Rural areas with abundant wildlife, such as rodents and deer, create suitable habitats for ticks and the TBE virus. People living or recreating in these areas are at greater risk.
Climate changes, including milder winters and longer warm seasons, may extend tick activity periods and increase TBE cases in some regions.
Occupational Exposure
Certain professions face higher TBE risk due to regular tick exposure. Forestry workers, farmers, and agricultural laborers frequently work in environments where ticks are prevalent.
Military personnel conducting field exercises in endemic regions are also vulnerable. Their prolonged outdoor activities increase the chance of tick bites.
Park rangers and outdoor guides who spend extended time in forested areas encounter similar risks. Protective clothing and tick checks are critical preventive measures.
Occupations connected to animal husbandry or wildlife surveillance further elevate exposure, as animals can carry ticks closer to human environments.