After how long do encephalitis symptoms appear in a person after a tick bite?

Understanding Tick-Borne Encephalitis

What is Tick-Borne Encephalitis (TBE)?

Pathogen and Transmission

The agents most frequently linked to encephalitic disease after a tick bite are viruses transmitted through the tick’s salivary secretions. The principal culprits include:

Tick‑borne encephalitis virus (TBEV) – a flavivirus endemic to Europe and Asia.
Powassan virus (POWV) – a flavivirus found in North America, transmitted by Ixodes species.
Louping‑ill virus – a less common flavivirus affecting sheep and occasionally humans in the United Kingdom.

Transmission occurs when an infected nymph or adult tick attaches to the host and injects saliva containing viral particles. Co‑feeding, where uninfected ticks acquire the virus from nearby infected ticks without systemic infection of the host, also contributes to spread. The virus replicates locally at the bite site, then disseminates via the bloodstream to the central nervous system, where it induces inflammation of the brain.

Incubation periods differ among these pathogens, influencing the timing of neurological signs:

TBEV: symptoms typically emerge 7–14 days after exposure; occasional cases appear up to 28 days later.
POWV: onset ranges from 1 to 5 weeks, with a median of about 2 weeks.
Louping‑ill virus: clinical signs usually develop within 5–10 days.

These intervals reflect the time required for viral replication, hematogenous spread, and breach of the blood‑brain barrier. Early recognition of the tick bite and awareness of regional pathogen prevalence improve diagnostic accuracy and enable timely antiviral or supportive therapy.

Geographic Distribution and Risk Areas

Tick‑borne encephalitis (TBE) is confined to temperate zones where the vector ticks, primarily Ixodes ricinus in western Europe and Ixodes persulcatus in eastern Eurasia, thrive. The virus circulates in wildlife reservoirs—rodents and small mammals—and reaches humans through tick bites, making the distribution of the disease inseparable from the habitats of these tick species.

Key risk regions include:

Central and Eastern Europe: Austria, Czech Republic, Germany, Hungary, Poland, Slovakia, Slovenia, Switzerland.
Scandinavia and the Baltic states: Denmark, Estonia, Finland, Latvia, Lithuania, Norway, Sweden.
Russia: European part, Siberian forest belt, Far East.
Asia: Northern China, Mongolia, Japan (Hokkaido), South Korea.

High‑risk areas are typically mixed forests, meadows, and shrublands at elevations up to 1,500 m where tick density peaks during spring, early summer, and autumn. Occupational exposure (forestry, agriculture) and recreational activities (hiking, camping) increase the probability of a bite, and consequently, the chance of developing encephalitic symptoms after the incubation period.

The Tick Bite and Initial Infection

How Ticks Transmit TBE Virus

Ticks acquire the tick‑borne encephalitis (TBE) virus while feeding on infected small mammals, primarily rodents. The virus persists in the tick’s midgut and migrates to the salivary glands during subsequent molts or feeding cycles.

During a blood meal, the tick inserts its hypostome into the host’s skin and secretes saliva that contains anticoagulants and immunomodulatory proteins. The TBE virus is released with the saliva, entering the host’s dermal capillaries and lymphatic vessels. This direct inoculation bypasses the skin barrier and delivers infectious particles to the bloodstream.

Key steps in transmission:

Tick attaches to host and begins feeding.
Saliva containing TBE virus is secreted into the bite site.
Virus enters host circulation and disseminates to peripheral tissues.
Primary replication occurs in lymph nodes and spleen.
Secondary spread reaches the central nervous system, leading to encephalitic disease.

The interval between the bite and the appearance of encephalitic manifestations typically ranges from 7 to 14 days, with a median of about 10 days. Early symptoms may include fever, headache, and malaise; neurological signs such as confusion, ataxia, or seizures develop as the virus invades the brain. Prompt recognition of this latency window is essential for clinical monitoring and early intervention.

Factors Influencing Viral Load

Viral load determines the speed at which encephalitic manifestations become clinically apparent after a tick attachment. Several variables shape the quantity of virus introduced and its replication dynamics.

Tick species and feeding duration: larger vectors and prolonged engorgement deliver higher inocula.
Pathogen strain virulence: more aggressive strains replicate faster, increasing early viral concentrations.
Inoculum size: the number of virions transferred at the bite sets the initial burden.
Host immune competence: immunosuppression, advanced age, or pre‑existing conditions reduce early viral clearance.
Genetic susceptibility: polymorphisms in innate immune receptors affect replication thresholds.
Co‑infection with other tick‑borne agents: synergistic interactions can amplify viral replication.
Environmental temperature: higher ambient temperatures accelerate viral replication within the host.

Elevated viral load shortens the latent interval before neurological symptoms appear, while lower loads extend the asymptomatic period. Monitoring these factors helps predict disease progression and informs timely therapeutic intervention.

Incubation Period and Symptom Onset

Typical Incubation Period

Biphasic Course of TBE

Tick‑borne encephalitis (TBE) typically follows a biphasic pattern. After a tick bite, the virus incubates for about 7 – 14 days before the first clinical manifestation appears. The initial phase presents with nonspecific, flu‑like symptoms such as fever, headache, myalgia and malaise. This stage lasts 3 – 7 days and is often mistaken for a mild viral infection.

A brief asymptomatic interval follows the first phase; it may last 1 – 3 days but can extend up to a week. During this pause, viral replication continues, and the pathogen spreads to the central nervous system. The second phase emerges when neurological involvement becomes evident. Symptoms include meningitis, encephalitis, or meningo‑encephalitis, characterized by stiff neck, photophobia, altered mental status, seizures, or focal deficits. The onset of these signs typically occurs 5 – 10 days after the resolution of the initial flu‑like illness, which translates to roughly 10 – 21 days after the tick bite.

Key temporal markers of the biphasic course:

Incubation: 7 – 14 days post‑exposure.
First (systemic) phase: 3 – 7 days of flu‑like illness.
Asymptomatic interval: 1 – 7 days.
Second (neurological) phase: 5 – 10 days after the first phase, i.e., 10 – 21 days after the bite.

Early recognition of the transition from the first to the second phase is critical for timely antiviral or supportive therapy and for preventing severe neurological sequelae.

Stage One: Prodromal Phase

The prodromal phase marks the earliest manifestation of encephalitic infection following a tick attachment. On average, nonspecific systemic signs appear within 3 – 10 days after the bite, although incubation can be shorter or extend to two weeks depending on pathogen load and host immunity.

Typical prodromal manifestations include:

Low‑grade fever
Headache of mild to moderate intensity
Generalized fatigue
Myalgia or arthralgia
Nausea or loss of appetite

These symptoms are often indistinguishable from other viral illnesses, which can delay clinical suspicion. The prodromal period usually lasts 2 – 5 days before neurological signs such as altered mental status, seizures, or focal deficits emerge, indicating progression to the encephalitic stage. Early recognition of this window is critical for prompt diagnostic testing and initiation of antimicrobial or antiviral therapy.

Symptoms of the Prodromal Phase

The prodromal phase follows the tick bite by a period of several days to two weeks, during which nonspecific systemic signs emerge before overt encephalitic manifestations. Early indicators reflect the body’s response to the pathogen and include:

Fever ranging from mild to moderate, often fluctuating.
Headache of varying intensity, not localized to a specific region.
Malaise and generalized fatigue.
Muscle aches, particularly in the neck, shoulders, and back.
Nausea or loss of appetite.
Irritability or subtle changes in behavior, sometimes perceived as increased restlessness.

These symptoms may be mistaken for a common viral infection, yet their concurrence after exposure to a tick warrants close monitoring. Prompt recognition of the prodromal pattern enables earlier diagnostic testing and initiation of therapy, potentially mitigating progression to full‑blown encephalitis.

Duration of the Prodromal Phase

Tick‑borne encephalitis usually follows a three‑stage course. After the bite, the virus replicates at the inoculation site and then spreads systemically, leading to a short prodromal period before central‑nervous‑system involvement.

The prodromal phase typically lasts between one and five days. During this interval patients present with nonspecific signs such as fever, fatigue, headache, myalgia, and occasional gastrointestinal upset. The onset of these symptoms occurs roughly one to two weeks after exposure, marking the transition from incubation to prodrome.

Key factors influencing the length of the prodrome include:

Viral subtype (European, Siberian, or Far‑Eastern strains) – Far‑Eastern variants often produce a shorter, more abrupt prodrome.
Age and immune competence – Older or immunocompromised individuals may experience a prolonged prodromal stage.
Tick attachment duration – Longer feeding times can accelerate viral entry, slightly reducing the prodrome length.

When the prodromal signs resolve, the second phase begins, characterized by neurological manifestations such as meningitis, encephalitis, or meningoencephalitis. Prompt recognition of the early nonspecific symptoms is essential for timely diagnosis and supportive care.

Stage Two: Neurological Phase

Onset of Neurological Symptoms

Tick‑borne encephalitis (TBE) follows a biphasic clinical course. After the bite, the virus incubates for a period that typically ranges from 7 to 14 days. During this interval, most individuals remain asymptomatic, although some may experience a brief febrile phase lasting 2–5 days.

Neurological manifestations usually appear after the initial febrile stage resolves. The second phase often begins 5–10 days after the fever subsides, resulting in symptoms such as headache, neck stiffness, photophobia, and altered mental status. In severe cases, focal neurological deficits, seizures, or coma may develop.

Factors influencing the exact timing include:

Viral strain virulence
Tick attachment duration
Host age and immune status

Early recognition of the transition from systemic to neurological signs is essential for timely diagnosis and management. Prompt antiviral therapy and supportive care improve outcomes, especially when treatment begins within the first week of neurological symptom onset.

Manifestations of Encephalitis

Encephalitis transmitted by tick bites typically manifests after an incubation period of about one to two weeks, though cases have been reported up to four weeks post‑exposure. The latency reflects viral replication and spread from the bite site to the central nervous system.

Common clinical features include:

Sudden onset of high fever
Severe headache, often retro‑orbital
Neck rigidity and photophobia
Altered consciousness ranging from confusion to coma
Focal neurological deficits such as weakness, aphasia, or ataxia
Seizure activity, both generalized and focal
Movement abnormalities, including tremor or dystonia
Psychiatric disturbances, for example agitation or hallucinations

Rapid recognition of these signs is essential for initiating antiviral therapy and supportive care, which can reduce morbidity and improve outcomes.

Meningitis

Tick bites can transmit Borrelia burgdorferi, Babesia, and the virus that causes tick‑borne encephalitis (TBE). When the TBE virus reaches the central nervous system, it may present as meningitis, encephalitis, or a mixed picture. The meningitic form typically develops earlier than pure encephalitis.

The incubation period for TBE ranges from 4 to 28 days. Clinical data show that meningitis symptoms—headache, neck stiffness, photophobia, and mild fever—most often emerge within 7 to 14 days after the bite. In a minority of cases, neurological signs appear as early as 4 days or as late as 21 days.

Key points for clinicians:

Onset of meningitic symptoms: 7 – 14 days post‑exposure (average 10 days).
Early presentation (≤ 5 days) suggests a rapid viral spread or co‑infection.
Late presentation (≥ 15 days) may indicate a prolonged incubation or delayed immune response.
Progression to encephalitis can occur after meningitis, typically 3 – 5 days later, extending the overall symptom window to 10 – 20 days.

Recognizing the typical time frame for meningitis after a tick bite enables timely diagnostic testing, antiviral therapy where appropriate, and supportive care, reducing the risk of severe neurological sequelae.

Myelitis

Myelitis refers to inflammation of the spinal cord, often caused by infectious agents transmitted through tick bites. Tick‑borne viruses such as tick‑borne encephalitis virus (TBEV) and Borrelia burgdorferi can trigger both encephalitic and myelitic processes, producing a combined neuroinflammatory syndrome.

The latency between a tick attachment and the emergence of neurological signs varies by pathogen. For TBEV, the incubation period typically spans 7 – 14 days; encephalitic manifestations may appear within this window, while myelitis often develops concurrently or shortly thereafter. Reported patterns include:

5 – 10 days: early flu‑like symptoms, possible mild meningitis.
7 – 14 days: onset of encephalitic signs (headache, confusion, seizures).
10 – 21 days: emergence of myelitic symptoms (limb weakness, sensory deficits, urinary retention).

When myelitis accompanies encephalitis, clinicians observe a rapid progression from central nervous system involvement to spinal cord dysfunction, sometimes within a few days of the first encephalitic sign.

Diagnostic work‑up emphasizes cerebrospinal fluid analysis (elevated protein, lymphocytic pleocytosis), magnetic resonance imaging of the brain and spinal cord (hyperintense lesions on T2‑weighted sequences), and serological testing for specific tick‑borne pathogens. Early antiviral therapy for TBEV and appropriate antimicrobial treatment for Borrelia reduce the risk of permanent neurological impairment.

Timely recognition of the overlapping timeline for encephalitic and myelitic symptoms after a tick bite is essential for prompt intervention and optimal patient outcomes.

Encephalomyelitis

Encephalomyelitis transmitted by ticks, most commonly caused by the tick‑borne encephalitis virus (TBEV), follows a distinct incubation period. After a bite, the virus replicates in the skin before entering the bloodstream and crossing the blood‑brain barrier. Clinical manifestations typically emerge within a defined window.

Short incubation: 4–7 days, associated with rapid viral spread and early neurological signs.
Average incubation: 7–14 days, the most frequent range reported in epidemiological studies.
Extended incubation: up to 28 days, observed in cases with delayed immune response or low inoculum.

The initial phase often presents with nonspecific flu‑like symptoms—fever, headache, malaise. A symptom‑free interval may follow before the second phase, characterized by meningitis, encephalitis, or myelitis, appears. The transition between phases can occur within 1–3 days after the first neurological signs.

Risk factors influencing the timing include age, immune status, viral subtype, and the number of infected ticks. Prompt recognition of the incubation window enables early diagnostic testing and antiviral or supportive therapy, reducing the likelihood of severe neurological sequelae.

Severity and Prognosis

Tick‑borne encephalitis (TBE) typically manifests neurologically within a short incubation period, often 5–14 days after the bite, though a biphasic pattern may delay the second phase to 10–21 days. The clinical picture ranges from mild meningitis to severe encephalitis with paralysis or coma.

Severity is classified by neurological involvement:

Mild: headache, fever, neck stiffness; full recovery expected.
Moderate: focal neurological deficits, impaired consciousness; recovery common but may require rehabilitation.
Severe: extensive brain inflammation, respiratory failure, long‑term sequelae; mortality up to 2 % and permanent deficits in 10–30 % of survivors.

Prognosis depends on age, immune status, and promptness of supportive care. Children usually experience milder disease and recover without lasting impairment. Adults over 50 years face higher risk of severe outcomes. Early recognition and hospitalization improve survival and reduce neurological damage. Antiviral agents have limited efficacy; management focuses on intensive supportive measures and rehabilitation. Long‑term follow‑up is essential to monitor cognitive and motor deficits, which may persist despite apparent clinical resolution.

Factors Affecting Symptom Appearance

Viral Strain Differences

Tick‑borne encephalitis results from infection with several genetically distinct strains of the TBE virus, each influencing the latency between a bite and the onset of neurological signs.

The European subtype generally produces symptoms after 7–14 days, whereas the Siberian subtype shortens the interval to 5–10 days. The Far‑Eastern subtype accelerates the course further, with clinical manifestations appearing within 3–7 days. These differences reflect variations in viral replication speed, neuroinvasiveness, and host immune evasion mechanisms.

European subtype: 7–14 days
Siberian subtype: 5–10 days
Far‑Eastern subtype: 3–7 days

Shorter incubation periods correlate with higher mortality rates and more severe cerebral edema, demanding rapid diagnostic testing and early antiviral intervention. Recognizing the specific strain informs prognosis and guides public‑health response to tick exposure.

Host Immune Response

The interval between a tick attachment and the emergence of encephalitic manifestations is governed largely by the host’s immune dynamics. After the tick introduces a neurotropic virus, such as Powassan or tick‑borne encephalitis virus, the pathogen must overcome innate barriers before adaptive mechanisms become operative. Initial viral replication occurs locally at the bite site, typically within 24–48 hours, while innate cells—macrophages, dendritic cells, and natural killer cells—release interferon‑α/β and tumor‑necrosis factor‑α to restrict spread. If these early defenses fail, the virus disseminates via the bloodstream, reaching the central nervous system after an additional 3–7 days.

Adaptive immunity activates once antigen‑presenting cells migrate to regional lymph nodes. Naïve CD4⁺ and CD8⁺ T lymphocytes differentiate into virus‑specific effectors, producing interferon‑γ and perforin that target infected neurons. B‑cell activation yields IgM antibodies detectable around day 5–7, followed by class‑switching to IgG by day 10–14. The timing of symptom onset correlates with the point at which viral load in the brain exceeds the capacity of these adaptive responses, usually manifesting between 5 and 14 days post‑exposure.

Key immune events influencing the latency period include:

Early interferon response limiting systemic viremia.
Recruitment of dendritic cells that present viral antigens to T cells.
Expansion of virus‑specific CD8⁺ cytotoxic T lymphocytes.
Production of neutralizing antibodies (IgM → IgG transition).
Cytokine‑mediated disruption of the blood‑brain barrier, facilitating viral entry.

Understanding these sequential processes clarifies why encephalitis symptoms appear after a variable but measurable delay following a tick bite.

Age and Co-morbidities

Tick‑borne encephalitis (TBE) does not develop uniformly; the interval between a tick attachment and the onset of neurological signs varies with the host’s physiological characteristics. Age influences the incubation period because immune competence declines with advancing years. Children often experience a shorter latency, sometimes as brief as five to seven days, whereas adults over 60 years frequently exhibit a prolonged interval, reaching 14–21 days before encephalitic manifestations appear. This pattern reflects age‑related alterations in innate and adaptive immune responses that affect viral replication and spread.

Co‑existing medical conditions modify the timeline as well. Chronic illnesses that impair immunity—such as diabetes mellitus, chronic kidney disease, or malignancies treated with chemotherapy—tend to extend the asymptomatic phase, allowing the virus to reach the central nervous system later. Cardiovascular disease and chronic obstructive pulmonary disease, while not directly immunosuppressive, can exacerbate systemic inflammation and delay symptom recognition, effectively lengthening the apparent incubation period. Conversely, individuals with robust immune function and no significant co‑morbidities may present with neurological symptoms at the lower end of the typical range.

Key points summarizing the influence of age and co‑morbidities:

Children (≤ 15 years): incubation 5–10 days, rapid progression to encephalitic signs.
Adults (30–50 years) without chronic disease: incubation 7–14 days, standard clinical course.
Elderly (> 60 years): incubation 10–21 days, higher probability of delayed onset.
Immunocompromised patients: incubation may exceed three weeks, with atypical presentations.
Patients with chronic systemic illnesses: incubation often extended beyond the average range, symptom severity may increase.

Understanding these demographic and health‑status factors enables clinicians to anticipate the window for symptom emergence after a tick bite, to monitor at‑risk patients more closely, and to initiate diagnostic testing promptly when neurological signs develop.

Diagnostic Methods and Challenges

Encephalitis following a tick bite presents a diagnostic window that depends on the incubation period, which can range from several days to weeks. Early identification relies on a combination of clinical evaluation and laboratory investigations.

Clinical assessment focuses on neurological deficits such as altered consciousness, focal weakness, or seizures. Because initial symptoms may mimic viral flu or meningitis, clinicians must maintain a high index of suspicion when a recent tick exposure is reported.

Laboratory confirmation includes:

Cerebrospinal fluid (CSF) analysis: elevated protein, lymphocytic pleocytosis, and normal or mildly reduced glucose suggest viral inflammation.
Serologic testing: detection of specific IgM and IgG antibodies against tick‑borne flaviviruses provides evidence of recent infection; paired sera collected 2–3 weeks apart improve accuracy.
Polymerase chain reaction (PCR): direct detection of viral RNA in CSF or blood offers rapid confirmation, though sensitivity declines after the first week of illness.
Magnetic resonance imaging (MRI): hyperintense lesions in the basal ganglia, thalamus, or cerebellum support the diagnosis but are not pathognomonic.

Challenges arise from several factors. The latency period varies widely, making it difficult to correlate symptom onset with exposure. Early CSF and serologic results may be negative, requiring repeat testing. Cross‑reactivity among flaviviruses can produce false‑positive serology, especially in regions where multiple tick‑borne pathogens coexist. Limited access to PCR and advanced imaging in rural settings delays definitive diagnosis. Finally, the non‑specific nature of initial systemic symptoms often leads to misclassification as a mild viral illness, postponing appropriate antiviral or supportive therapy.

Prevention and Management

Personal Protective Measures

Ticks can transmit pathogens that cause encephalitis, with clinical signs typically appearing 7‑14 days after the bite, though cases have been reported up to 30 days later. Prompt removal of attached ticks reduces the probability of infection, but prevention remains the most reliable strategy.

Wear long‑sleeved shirts and long trousers; tuck shirts into pants and pants into socks to create a barrier.
Apply EPA‑registered repellents containing DEET, picaridin, IR3535, or oil of lemon eucalyptus to exposed skin and clothing.
Treat footwear, leggings, and outer garments with permethrin; reapply according to label instructions.
Conduct full‑body tick inspections at least every two hours while in endemic areas; remove attached ticks with fine‑point tweezers, grasping close to the skin and pulling steadily.
Shower within 30 minutes of returning from outdoor activity; showering increases the likelihood of detecting and removing ticks.
Maintain yard by mowing grass short, removing leaf litter, and creating a mulch barrier between wooded areas and recreational zones.
Use rodent‑targeted acaricides or bait stations to lower the local tick population; follow local public‑health guidelines for application.

Consistent use of these measures shortens exposure time, lowers the chance of a tick bite, and consequently delays or prevents the onset of encephalitic disease.

Vaccination Against TBE

Tick‑borne encephalitis (TBE) is a viral infection transmitted by Ixodes ticks. The incubation period ranges from about one week to four weeks, with most cases showing neurological symptoms within two weeks after a bite. Vaccination provides the most reliable protection against infection and subsequent encephalitic disease.

The standard TBE vaccine regimen consists of three intramuscular injections. The first two doses are administered one to three months apart; the third dose follows 5–12 months after the second. Protective antibody levels appear two to four weeks after the third injection. Booster doses are recommended every three to five years, depending on age, exposure risk, and vaccine type. Maintaining up‑to‑date boosters ensures continued immunity during the period when tick bites are most likely.

Efficacy studies report seroconversion in more than 95 % of healthy adults after the complete primary series. Vaccinated individuals who are bitten by infected ticks experience a markedly lower probability of developing clinical TBE, and, if infection occurs, the disease course is usually milder and neurological complications are rare.

Key points for clinicians and travelers:

Primary series: three doses (0 – 1–3 months, third dose 5–12 months later).
Immunity onset: detectable antibodies 2–4 weeks after the final dose.
Booster interval: 3–5 years; shorter interval for older adults or high‑risk groups.
Protection level: >95 % seroconversion, substantial reduction in encephalitis risk.

Ensuring timely vaccination and adherence to booster schedules minimizes the window during which tick bites could lead to encephalitic symptoms.

Post-Exposure Prophylaxis

The interval between a tick attachment and the emergence of encephalitic manifestations typically ranges from 7 to 21 days, depending on the pathogen involved and the bite’s duration. Early neurologic signs—headache, fever, and malaise—often precede more specific symptoms such as confusion, seizures, or focal deficits. Prompt identification of the exposure window is essential for effective intervention.

Post‑exposure prophylaxis (PEP) aims to prevent infection after a confirmed or highly suspected tick bite. The strategy varies according to the regional prevalence of tick‑borne diseases and the identified species.

Single‑dose doxycycline (200 mg) administered within 72 hours reduces the risk of Lyme disease transmission; it does not prevent tick‑borne encephalitis (TBE) but may limit co‑infection.
In areas where TBE is endemic, an accelerated vaccination schedule (two doses 1 week apart) can be offered immediately after exposure for individuals lacking prior immunization.
For babesiosis or anaplasmosis risk, a 7‑day course of appropriate antibiotics (e.g., atovaquone‑azithromycin for babesiosis) should be considered when laboratory testing confirms infection.
Supportive care, including antipyretics and hydration, should accompany any pharmacologic regimen.

Monitoring the patient for fever, neurological changes, or rash during the first three weeks after the bite allows early detection of disease progression. If symptoms develop, laboratory confirmation (serology, PCR) and initiation of targeted antiviral or antimicrobial therapy are required to reduce morbidity and mortality.

Treatment Options for TBE

Tick‑borne encephalitis (TBE) requires prompt medical management once infection is suspected. The primary therapeutic goal is to reduce viral replication, control inflammation, and prevent neurological complications.

Antiviral agents are not routinely effective against TBE; therefore, treatment focuses on supportive care. Intravenous fluids, electrolyte balance, and temperature regulation are administered to maintain physiological stability. Respiratory support, including mechanical ventilation, is provided when encephalitic involvement compromises breathing.

Corticosteroids may be considered to attenuate cerebral edema, though evidence of benefit remains limited. Administration of dexamethasone or methylprednisolone follows standard dosing protocols for acute viral encephalitis, with careful monitoring for side‑effects.

Immunoglobulin therapy is not indicated for TBE, but passive immunization can be employed prophylactically in high‑risk individuals following exposure. Human TBE‑specific immunoglobulin, when available, is given as a single intramuscular dose.

Vaccination remains the most effective preventive measure. The inactivated TBE vaccine is administered in a three‑dose schedule, with booster doses every 3–5 years depending on regional risk assessment.

In summary, treatment of TBE consists of:

Intensive supportive care (fluid therapy, respiratory support, temperature control)
Consideration of corticosteroids for severe cerebral edema
Prophylactic immunoglobulin in selected exposure cases
Routine vaccination for high‑risk populations

Outcome improves when care is initiated early, before extensive neurological damage develops.