Tick-Borne Encephalitis (TBE): Symptoms, Causes & Prevention

What Is Tick-Borne Encephalitis?

Tick-borne encephalitis (TBE) is a viral infection caused by the TBE virus, a member of the flavivirus family. The virus primarily attacks the central nervous system, causing inflammation of the brain (encephalitis) and/or the protective membranes surrounding the brain and spinal cord (meningitis). TBE is transmitted mainly through the bite of infected Ixodes ticks.

Tick-borne encephalitis represents one of the most significant tick-borne viral infections affecting humans in Europe and Asia. The TBE virus belongs to the same viral family as the viruses causing dengue fever, yellow fever, and Zika virus. Unlike many other infections, TBE cannot be treated with antibiotics because it is caused by a virus rather than bacteria, making prevention through vaccination critically important.

The disease was first clinically described in Austria in 1931 and the virus was isolated in Russia in 1937. Since then, our understanding of TBE has expanded significantly, leading to the development of highly effective vaccines that have dramatically reduced disease incidence in countries with high vaccination coverage, such as Austria where vaccination rates exceed 80%.

TBE exists in three main subtypes, each associated with different geographic regions and varying degrees of disease severity. The European subtype, transmitted primarily by Ixodes ricinus ticks, causes a milder form of the disease with mortality rates of 1-2%. The Siberian and Far Eastern subtypes, transmitted by Ixodes persulcatus ticks, tend to cause more severe disease with mortality rates reaching 20-40% for the Far Eastern subtype.

How TBE Virus Affects the Body

After a tick bite, the TBE virus enters the bloodstream and initially replicates in dendritic cells at the site of the bite. From there, the virus spreads through the lymphatic system and bloodstream, potentially reaching the central nervous system. The virus has a particular affinity for neurons, the cells that form the nervous system, which explains why neurological symptoms predominate in severe cases.

The immune response to TBE virus infection is complex. While the immune system eventually clears the virus in most cases, the inflammatory response itself can contribute to tissue damage in the brain and spinal cord. This is why some patients experience long-lasting neurological symptoms even after the acute infection has resolved.

Epidemiology and Geographic Distribution

TBE is endemic across a vast geographic belt stretching from Western Europe through Russia to the Pacific coast, and into parts of China, Mongolia, Japan, and South Korea. The highest incidence rates occur in the Baltic states (Lithuania, Latvia, Estonia), Czech Republic, Slovenia, and parts of Russia. However, the geographic range of TBE is expanding, likely due to climate change affecting tick populations and human behavior patterns.

Each year, approximately 10,000 to 15,000 clinical cases of TBE are reported globally, though the actual number is likely higher due to underreporting and cases with mild symptoms that go undiagnosed. The incidence varies dramatically between regions, ranging from less than 0.1 cases per 100,000 population in some Western European countries to over 20 cases per 100,000 in highly endemic areas of the Baltic states and Russia.

What Are the Symptoms of Tick-Borne Encephalitis?

TBE typically follows a biphasic (two-phase) pattern. The first phase presents with flu-like symptoms including fever, fatigue, headache, and muscle pain lasting about one week. After a symptom-free interval of 1-20 days, approximately one-third of patients develop the second phase with neurological symptoms such as severe headache, high fever, neck stiffness, confusion, and in severe cases, paralysis or seizures.

Understanding the symptom progression of TBE is crucial for early recognition and appropriate medical care. Not all infected individuals develop symptoms – studies suggest that 70-98% of infections may be asymptomatic or cause such mild symptoms that medical attention is never sought. However, for those who do develop clinical disease, the presentation can range from mild meningitis to severe encephalomyelitis with permanent neurological damage.

First Phase: Viremic (Flu-like) Phase

The initial phase of TBE typically begins 7-14 days after the tick bite, though the incubation period can range from 4 to 28 days. During this phase, the virus is circulating in the bloodstream (viremia), and symptoms resemble those of many other viral infections:

• Fever: Usually moderate (38-39°C/100-102°F), lasting 2-7 days
• Fatigue and malaise: General feeling of being unwell, often pronounced
• Headache: Often diffuse and persistent
• Muscle pain (myalgia): Particularly in the limbs and back
• Joint pain (arthralgia): Less common than muscle pain
• Nausea and loss of appetite: May be accompanied by abdominal discomfort

This first phase resolves spontaneously in about 70% of patients, who recover fully without progressing to the neurological phase. The symptoms during this phase are often attributed to common viral infections like influenza, and the connection to a tick bite may not be recognized, especially if the tick went unnoticed.

Asymptomatic Interval

Following the resolution of the first phase, patients typically experience a period of apparent recovery lasting 1-20 days (average 7 days). During this interval, patients may feel completely well, leading them to believe they have recovered from what seemed like a routine viral illness. This asymptomatic period can make the subsequent onset of neurological symptoms particularly alarming and may delay the connection to the earlier illness or tick bite.

Second Phase: Neurological Phase

Approximately 20-30% of patients who experience the first phase go on to develop neurological manifestations. This second phase represents the invasion of the central nervous system by the virus and can present in several forms:

Meningitis (inflammation of the meninges):

• Severe headache, often described as the worst headache of their life
• High fever (often 39-40°C/102-104°F)
• Neck stiffness (nuchal rigidity)
• Sensitivity to light (photophobia)
• Nausea and vomiting

Meningoencephalitis (inflammation of brain and meninges):

• All symptoms of meningitis plus:
• Altered consciousness, confusion, drowsiness
• Cognitive difficulties (problems with concentration, memory)
• Behavioral changes
• Tremors, particularly of the hands and face
• Speech difficulties
• Seizures (in approximately 10% of cases)

Myelitis (spinal cord inflammation) or Meningoencephalomyelitis:

• Weakness or paralysis, particularly affecting the shoulders and arms
• Sensory disturbances
• Bladder and bowel dysfunction
• Respiratory failure in severe cases (requiring mechanical ventilation)

Symptoms in Different Age Groups

The presentation and severity of TBE vary significantly with age. Children typically experience milder disease with better outcomes – severe neurological complications are relatively rare in those under 14 years. In contrast, adults over 50 years of age face significantly higher risks of severe disease, longer hospitalization, and long-term neurological sequelae. The mortality rate also increases with age, being negligible in children but reaching 2-4% in elderly patients with the European subtype.

What Causes Tick-Borne Encephalitis?

TBE is caused by the tick-borne encephalitis virus (TBEV), a flavivirus transmitted primarily through the bite of infected Ixodes ticks. The virus is maintained in nature through a cycle involving ticks and small mammals. Humans are incidental hosts who can become infected when bitten by infected ticks during outdoor activities in endemic areas.

The TBE virus is a small, enveloped RNA virus measuring approximately 50 nanometers in diameter. It belongs to the Flaviviridae family, genus Flavivirus, which includes other important human pathogens such as dengue, yellow fever, Japanese encephalitis, West Nile, and Zika viruses. The virus genome encodes for structural proteins that form the viral particle and non-structural proteins essential for viral replication.

The Tick Vector

Two main tick species transmit TBE virus to humans. In Europe, Ixodes ricinus (the castor bean tick or sheep tick) is the primary vector, while in Asia, Ixodes persulcatus (the taiga tick) serves this role. These hard-bodied ticks have a three-stage life cycle (larva, nymph, adult), and each stage requires a blood meal to progress to the next. All three stages can carry and transmit TBE virus, though nymphs are responsible for most human infections due to their small size making them less likely to be noticed and removed.

Ticks become infected with TBE virus by feeding on infected reservoir animals, primarily small rodents such as mice and voles, as well as larger mammals like deer and other wildlife. Once infected, a tick remains infected for life and can transmit the virus to humans during subsequent blood meals. Importantly, viral transmission can occur within minutes of tick attachment, unlike Lyme disease where transmission typically requires 24-48 hours of attachment.

Risk Factors for Infection

Several factors increase the risk of acquiring TBE:

• Geographic location: Living in or traveling to TBE-endemic areas significantly increases risk
• Outdoor activities: Hiking, camping, forestry work, farming, hunting, and other activities in tick habitats
• Seasonal exposure: Peak transmission occurs in spring (April-June) and autumn (September-November) when tick activity is highest
• Lack of vaccination: Unvaccinated individuals in endemic areas face the highest risk
• Occupational exposure: Forest workers, farmers, hunters, and military personnel have elevated risk
• Consumption of unpasteurized dairy: Raw milk from infected goats, sheep, or cows can transmit TBE (approximately 1% of cases)

Non-Tick Transmission Routes

While tick bites account for the vast majority of TBE cases, the virus can rarely be transmitted through other routes. Consumption of unpasteurized dairy products from infected animals has caused outbreaks, particularly in Eastern Europe. This alimentary (food-borne) transmission route accounts for approximately 1% of cases. Pasteurization effectively eliminates the virus, making commercially pasteurized dairy products safe.

Laboratory-acquired infections have been documented in research settings, and theoretical risk exists for transmission through blood transfusion or organ transplantation, though documented cases are extremely rare. Mother-to-child transmission during pregnancy is possible but very uncommon.

How Is Tick-Borne Encephalitis Diagnosed?

TBE diagnosis relies primarily on detecting TBE-specific antibodies (IgM and IgG) in blood or cerebrospinal fluid, combined with clinical presentation and history of potential tick exposure. Lumbar puncture typically reveals characteristic findings of viral meningitis. MRI imaging may show inflammatory changes in severe cases but is often normal in milder disease.

Diagnosing TBE can be challenging, particularly during the first phase when symptoms are non-specific and may be attributed to other viral infections. A high index of suspicion is necessary in patients with compatible symptoms who have been in endemic areas during tick season. The diagnosis becomes more straightforward when the characteristic biphasic illness pattern is recognized and neurological symptoms develop.

Laboratory Diagnosis

Serological testing is the cornerstone of TBE diagnosis. Detection of TBE-specific IgM antibodies in serum indicates recent infection and typically becomes positive within the first week of neurological symptoms (second phase). IgG antibodies appear shortly after and persist for years, providing long-term immunity. When testing cerebrospinal fluid (CSF), the presence of intrathecally produced TBE-specific IgM strongly supports the diagnosis.

Important considerations: IgM antibodies may persist for months after acute infection, so positive IgM alone does not necessarily indicate current infection. Cross-reactivity with other flaviviruses (such as dengue or yellow fever vaccines) can occur, requiring careful interpretation in travelers. A fourfold rise in IgG antibody titers between acute and convalescent samples confirms recent infection.

PCR testing (polymerase chain reaction) can detect TBE viral RNA in blood during the first phase of illness but has limited utility because viremia has typically resolved by the time patients present with neurological symptoms. PCR testing of CSF has low sensitivity.

Cerebrospinal Fluid Analysis

Lumbar puncture is typically performed in patients presenting with meningitis or encephalitis symptoms. Characteristic CSF findings in TBE include:

• Pleocytosis: Elevated white blood cell count, typically 10-500 cells/μL
• Cell type: Initially may show neutrophil predominance, shifting to lymphocyte predominance
• Protein: Mildly to moderately elevated (typically 0.5-1.0 g/L)
• Glucose: Normal (distinguishing viral from bacterial meningitis)
• Opening pressure: May be elevated

Neuroimaging

Brain MRI may be performed in patients with encephalitis to assess the extent of inflammation and exclude other diagnoses. Findings in TBE may include:

• Signal changes in the thalamus, basal ganglia, or brainstem
• Spinal cord involvement in myelitis cases
• However, MRI is often normal, particularly in milder cases

CT scanning is less sensitive than MRI and is typically normal in TBE. Its main role is to exclude other conditions such as hemorrhage or mass lesions before lumbar puncture.

How Is Tick-Borne Encephalitis Treated?

There is no specific antiviral treatment for TBE. Management is supportive, focusing on symptom relief, maintaining hydration, and treating complications. Patients with severe neurological symptoms require hospitalization, with intensive care for those with encephalitis, myelitis, or respiratory complications. Recovery can take weeks to months, and rehabilitation may be necessary for patients with lasting neurological deficits.

The absence of specific antiviral therapy for TBE underscores the critical importance of prevention through vaccination. While several antiviral agents have been investigated in laboratory studies, none have demonstrated clinical efficacy in humans. Treatment therefore focuses on supporting the patient through the acute illness and managing complications as they arise.

Supportive Care Measures

Most patients with TBE require hospitalization for monitoring and supportive care. Key elements of management include:

• Rest and monitoring: Close neurological observation for signs of deterioration
• Hydration: Intravenous fluids if oral intake is compromised
• Pain management: Analgesics for headache; NSAIDs may be used with caution
• Fever control: Antipyretics (paracetamol/acetaminophen) as needed
• Nausea treatment: Antiemetics if vomiting is problematic
• Sedation: May be necessary for severely agitated patients

Management of Severe Cases

Patients with severe encephalitis or myelitis may require intensive care unit admission. Critical care interventions may include:

• Airway management: Intubation and mechanical ventilation for patients with respiratory failure or severely impaired consciousness
• Seizure management: Anticonvulsant medications for patients experiencing seizures
• Intracranial pressure management: Monitoring and treatment if cerebral edema develops
• Prevention of complications: DVT prophylaxis, pressure ulcer prevention, nutritional support

Prognosis and Long-term Outcomes

The prognosis for TBE varies depending on disease severity, viral subtype, and patient age. For the European subtype, mortality is approximately 1-2%, but long-term neurological sequelae affect 30-40% of patients with neurological involvement. Common persistent symptoms include:

• Cognitive difficulties (concentration, memory, executive function)
• Fatigue and reduced stamina
• Headaches
• Balance and coordination problems
• Weakness, particularly in shoulder and arm muscles
• Mood changes, depression, irritability

Recovery can continue for months to years, with most improvement occurring in the first year. Some patients, however, experience permanent disability. The Far Eastern subtype carries a much worse prognosis, with mortality rates of 20-40% and higher rates of permanent neurological damage.

How Can You Prevent Tick-Borne Encephalitis?

The most effective prevention against TBE is vaccination, which provides over 95% protection after completing the 3-dose primary series. Additional measures include wearing protective clothing, using tick repellents, avoiding tick habitats, performing thorough tick checks after outdoor activities, and promptly removing any attached ticks. Avoiding unpasteurized dairy products in endemic areas eliminates the rare food-borne transmission route.

Prevention of TBE operates on multiple levels: population-level protection through vaccination programs, individual protective behaviors during outdoor activities, and environmental measures to reduce tick exposure. The combination of these approaches has proven highly effective in reducing TBE incidence in countries with comprehensive prevention programs.

TBE Vaccination

TBE vaccines are among the most effective vaccines available, providing protection exceeding 95% after completion of the primary series. Several licensed vaccines are available globally, all based on inactivated (killed) virus and considered safe and well-tolerated.

Primary vaccination schedule:

• First dose: Day 0 (chosen date)
• Second dose: 1-3 months after first dose
• Third dose: 5-12 months after second dose (completes primary series)

Booster doses: After the primary series, booster doses are recommended every 3-5 years for continued protection. More frequent boosters may be needed for immunocompromised individuals or those over 60 years of age.

Who should be vaccinated?

• Residents of TBE-endemic areas
• Travelers to endemic areas who will have outdoor exposure
• Occupational risk groups (forestry workers, farmers, military personnel)
• Laboratory workers handling TBE virus

Personal Protective Measures

In addition to vaccination, several behavioral measures reduce tick bite risk:

Protective clothing:

• Wear long pants tucked into socks or boots
• Wear long-sleeved shirts tucked into pants
• Choose light-colored clothing (makes ticks easier to spot)
• Consider treating clothing with permethrin (an insecticide)

Tick repellents:

• Apply DEET-based repellents (20-30% concentration) to exposed skin
• Reapply according to product instructions
• Picaridin and IR3535 are alternative active ingredients

Tick Checks and Removal

Performing thorough tick checks after spending time outdoors is essential. Check your entire body, paying special attention to:

• Hairline and scalp
• Behind and inside ears
• Armpits
• Groin area
• Behind knees
• Between toes

If you find an attached tick:

1. Use fine-tipped tweezers to grasp the tick as close to the skin as possible
2. Pull upward with steady, even pressure – do not twist or jerk
3. After removal, clean the bite area with antiseptic
4. Monitor the site for signs of infection
5. Note the date of the bite in case symptoms develop later

When Should You See a Doctor After a Tick Bite?

Seek medical attention if you develop fever, headache, fatigue, or muscle aches within 4 weeks of a tick bite in a TBE-endemic area. Seek emergency care immediately if you experience severe headache with neck stiffness, confusion, seizures, weakness or paralysis, or difficulty staying awake. Early medical evaluation is important even with mild symptoms if you are unvaccinated and were exposed in an endemic area.

Not every tick bite requires medical attention – the vast majority of tick bites, even in endemic areas, do not result in TBE infection. However, knowing when to seek care can ensure prompt diagnosis and appropriate management if infection does occur.

Situations Requiring Medical Consultation

Contact your healthcare provider in the following circumstances:

• You develop flu-like symptoms (fever, headache, fatigue, muscle aches) within 4 weeks of a tick bite
• You have been in a TBE-endemic area and develop unexplained fever and headache
• You are unvaccinated and had significant tick exposure in an endemic area
• You want to discuss TBE vaccination before or after travel to endemic areas

Emergency Situations

Call emergency services or go to an emergency department immediately if you experience:

• Severe headache combined with high fever and neck stiffness
• Confusion, disorientation, or difficulty staying awake
• Seizures
• Sudden weakness or paralysis in any part of the body
• Difficulty speaking or understanding speech
• Difficulty breathing

Where Is Tick-Borne Encephalitis Found?

TBE is endemic in a geographic belt spanning from Western Europe through Russia to the Pacific coast of Asia. The highest risk areas include Austria, Czech Republic, Germany, Switzerland, Baltic states, Poland, and parts of Russia and Asia. The geographic range is expanding, with new endemic foci being identified in previously unaffected areas.

Europe

Highest risk countries:

• Baltic states (Lithuania, Latvia, Estonia): Among the highest incidence rates globally
• Czech Republic: Well-established endemic area
• Slovenia: High incidence in forested regions
• Austria: Historically high risk; reduced through vaccination

Moderate risk countries:

• Germany: Endemic in southern states (Bavaria, Baden-Württemberg)
• Switzerland: Northern and eastern regions
• Poland: Northeastern regions particularly affected
• Sweden: Endemic areas around Stockholm and along Baltic coast
• Finland: Åland Islands and southwestern coastal areas

Russia and Asia

• Russia: TBE is endemic across much of Russia, from the western border to the Pacific coast
• China: Northeastern provinces, particularly Heilongjiang and Jilin
• Mongolia: Northern regions
• Japan: Hokkaido island
• South Korea: Sporadic cases reported