What symptoms develop after a bite from an encephalitis‑causing tick?

Understanding Tick-borne Encephalitis (TBE)

The TBE Virus and Transmission

Incubation Period of TBE

Tick‑borne encephalitis (TBE) develops after a bite from an infected Ixodes tick. The interval between the bite and the first clinical signs, known as the incubation period, typically lasts 7–14 days. Some cases present as early as 4 days, while others may not manifest until 28 days post‑exposure.

Factors that modify this interval include the specific TBE virus subtype (European, Siberian, or Far‑Eastern), the amount of virus transmitted, the duration of tick attachment, and the immune status of the host. Younger individuals and those with compromised immunity often experience a shorter incubation span.

The disease often follows a biphasic pattern. After the incubation period, the initial phase appears with nonspecific, flu‑like symptoms such as fever, headache, and malaise. This phase lasts 1–5 days and may resolve spontaneously. A symptom‑free interval of 1–7 days can precede the second phase, during which neurological manifestations emerge (meningitis, encephalitis, or meningoencephalitis).

Typical incubation: 7–14 days
Early onset: ≥4 days
Late onset: ≤28 days
First phase duration: 1–5 days
Asymptomatic interval: 1–7 days

Understanding the incubation timeline aids clinicians in recognizing early signs and differentiating TBE from other tick‑borne illnesses.

Initial Symptoms of Tick-borne Encephalitis

Prodromal Phase: Flu-like Symptoms

Fever and Chills

Fever and chills are common early manifestations after a bite from a tick capable of transmitting encephalitis. The febrile response typically emerges within 3–7 days of exposure, with body temperature rising to 38–40 °C (100.4–104 °F). The increase may be sustained or intermittent, often accompanied by rigors that generate intense cold sensations despite elevated core temperature.

Chills appear as involuntary muscle tremors or shivering episodes that coincide with the onset of fever. They frequently precede the peak temperature and can recur each time the temperature spikes. The sensation is described as a sudden wave of cold, prompting patients to seek warmth and cover themselves with blankets.

Both signs serve as clinical alerts for possible viral neuroinvasion. Their presence warrants prompt medical evaluation, laboratory testing for tick‑borne pathogens, and initiation of supportive care. Early detection improves outcomes by allowing timely antiviral therapy when indicated.

Key characteristics:

Onset: 3–7 days post‑bite
Temperature range: 38–40 °C (100.4–104 °F)
Pattern: continuous or intermittent spikes
Chills: shivering episodes aligned with temperature rises
Clinical action: immediate assessment, laboratory confirmation, supportive management

Headache and Muscle Aches

A bite from a tick that transmits an encephalitic virus frequently triggers early systemic complaints before neurological involvement becomes apparent. Headache and muscle aches constitute the most common initial manifestations.

Headache typically appears within 24–72 hours after exposure. It is often described as a constant, dull pressure that may intensify with movement or light exposure. The pain usually localizes to the frontal or occipital region but can become generalized as the infection progresses. Accompanying symptoms may include photophobia and mild nausea, but these are secondary to the primary cranial discomfort.

Muscle aches (myalgia) develop concurrently or shortly after the headache. They present as diffuse, aching sensations affecting the neck, shoulders, back, and proximal limb muscles. The intensity ranges from mild soreness to severe, limiting daily activities. Myalgia often worsens with exertion and may be accompanied by low‑grade fever and fatigue, reflecting the body’s inflammatory response to viral replication.

Key points:

Onset: 1–3 days post‑bite
Headache: constant, dull, frontal/occipital, may worsen with movement or light
Myalgia: diffuse, proximal muscles, exacerbated by activity, may coexist with fever
Progression: symptoms can intensify, signaling possible advancement to central nervous system involvement

Prompt recognition of these early signs facilitates timely medical evaluation and reduces the risk of severe encephalitic complications.

Fatigue and Malaise

Fatigue frequently appears within the first few days after a tick bite that transmits encephalitic viruses. Patients report a persistent lack of energy that does not improve with rest and may progress to profound exhaustion. The symptom reflects systemic viral replication and the host’s inflammatory response, which disrupt neuronal metabolism and disrupt sleep‑wake regulation.

Malaise accompanies fatigue and manifests as a generalized sense of discomfort or unease. It often precedes more specific neurological signs such as headache, photophobia, or altered mental status. The feeling of being unwell can be diffuse, affecting appetite, motivation, and physical performance.

Key clinical observations:

Onset: 24 – 72 hours post‑exposure, sometimes earlier if co‑infection occurs.
Duration: persists for several days to weeks, may fluctuate with fever spikes.
Severity: ranges from mild weariness to incapacitating exhaustion, influencing daily activities.
Correlation: intensity usually aligns with fever and other systemic manifestations.
Management: supportive care, adequate hydration, and monitoring for progression to encephalitic involvement.

Recognition of these early, nonspecific signs enables prompt medical evaluation, reduces diagnostic delay, and improves outcomes when antiviral or immunomodulatory therapy becomes necessary.

Nausea and Vomiting

Nausea and vomiting frequently appear early in the clinical course following a bite from a tick capable of transmitting encephalitic viruses. The gastrointestinal upset often precedes neurologic signs such as headache, fever, or altered mental status, providing an early clue to infection.

The pathophysiology involves viral invasion of the gastrointestinal tract and central nervous system. Cytokine release and direct irritation of the vomiting center in the medulla trigger the emetic response. In many cases, vomiting occurs within 24–72 hours after exposure, although delayed onset up to a week has been reported.

Key clinical considerations:

Timing: Onset typically ranges from a few hours to several days post‑bite.
Severity: Episodes can be mild and self‑limiting or severe enough to cause dehydration and electrolyte imbalance.
Associated findings: Often accompanied by fever, malaise, and headache; persistent vomiting may signal progression toward encephalitis.
Differential diagnosis: Gastroenteritis, medication side effects, and other tick‑borne illnesses (e.g., Lyme disease) must be excluded.

Management focuses on supportive care and early antiviral therapy when indicated. Intravenous fluids restore volume and correct electrolyte disturbances; antiemetic agents such as ondansetron reduce nausea and prevent aspiration. Monitoring for evolving neurologic deficits is essential, as rapid escalation can occur in encephalitic infections. Prompt recognition of gastrointestinal symptoms therefore contributes to timely intervention and improves prognosis.

Second Phase: Neurological Involvement

Meningitis Manifestations

Severe Headache

Severe headache often appears within days of a bite from a tick that transmits encephalitic viruses. The pain is typically throbbing, unrelenting, and may intensify with movement or changes in posture. It frequently co‑occurs with photophobia, phonophobia, and nausea, indicating involvement of the central nervous system.

Key clinical features of the headache include:

Sudden onset or rapid escalation in intensity
Diffuse or frontal localization, sometimes radiating to the temples
Resistance to standard analgesics, requiring stronger medication for relief
Accompanying signs such as fever, neck stiffness, or altered mental status, which suggest progression toward meningitis or encephalitis

Prompt recognition of this symptom is critical, as it signals possible viral invasion of the brain and warrants immediate medical evaluation, laboratory testing, and, when indicated, antiviral therapy. Ignoring the headache can delay diagnosis and increase the risk of neurological complications.

Neck Stiffness

Neck stiffness frequently appears in the early neurological phase of tick‑borne encephalitis. The toxin‑induced inflammation of the meninges irritates cervical spinal roots, producing a rigid, painful neck that limits flexion. Patients often describe a sensation of tightness or resistance when attempting to touch the chin to the chest. The symptom may emerge 3–7 days after the tick bite, coinciding with fever, headache, and photophobia.

Typical characteristics of the cervical rigidity include:

Limited range of motion in all directions, especially forward flexion.
Tenderness over the paraspinal muscles and posterior neck.
Absence of focal weakness or sensory loss in the upper limbs.
Association with other meningeal signs such as positive Kernig or Brudzinski reflexes.

Neck stiffness signals meningeal involvement and warrants immediate medical evaluation. Lumbar puncture usually reveals pleocytosis with a predominance of lymphocytes, elevated protein, and normal glucose, confirming viral meningitis. Antiviral therapy is not indicated; supportive care, analgesics, and antipyretics are standard. Hospital admission is recommended for monitoring of progression to encephalitic manifestations, including altered consciousness, seizures, or focal neurological deficits.

Early recognition of cervical rigidity enables prompt diagnosis, reduces the risk of complications, and guides appropriate supportive management.

Sensitivity to Light (Photophobia)

Photophobia frequently appears early in the clinical course of tick‑borne encephalitis. The symptom manifests as discomfort or pain when exposed to bright light, often prompting patients to keep eyes partially closed or seek dim environments. The underlying mechanism involves inflammation of the meninges and cortical irritation, which heightens sensitivity of the optic pathways and disrupts normal pupillary responses.

Typical characteristics of light sensitivity in this context include:

Onset within days of the tick bite, coinciding with the prodromal phase of infection.
Accompanying headache, fever, and malaise, suggesting meningeal involvement.
Worsening of visual discomfort during activities that generate glare, such as outdoor exposure or screen use.
Relief when ambient light is reduced, often leading to the use of sunglasses or darkened rooms.

Assessment should document the intensity and duration of photophobia, correlate it with other neurologic signs (e.g., neck stiffness, altered mental status), and consider lumbar puncture to confirm encephalitic inflammation. Management focuses on supportive care—analgesics, antipyretics, and environmental light control—while antiviral or immunomodulatory therapy addresses the underlying viral cause. Persistent or severe photophobia may signal progression to encephalitic complications and warrants close monitoring.

Encephalitis Manifestations

Altered Mental Status

Altered mental status is a hallmark manifestation of central nervous system infection transmitted by an encephalitis‑bearing tick. The condition may appear within days to weeks after the bite, often following an initial febrile phase.

Typical presentations include:

Confusion: disorientation to time, place, or person, with difficulty concentrating.
Lethargy: reduced responsiveness, excessive sleepiness, or inability to sustain wakefulness.
Agitation or irritability: restlessness, aggression, or inappropriate emotional responses.
Hallucinations: visual or auditory distortions without external stimuli.
Seizure activity: focal or generalized convulsions, sometimes preceded by altered awareness.
Progressive loss of consciousness: transition from stupor to coma as inflammation spreads.

Neurological examination frequently reveals impaired cognition combined with other signs of encephalitis, such as neck stiffness, focal deficits, or abnormal reflexes. Laboratory analysis may show elevated cerebrospinal fluid protein, lymphocytic pleocytosis, and detection of viral RNA or antibodies. Early recognition of mental status changes prompts antiviral therapy, supportive care, and monitoring for complications like respiratory failure or increased intracranial pressure.

Disorientation and Confusion

Disorientation and confusion often emerge within a few days after a tick bite that transmits encephalitic viruses. Patients may experience difficulty recognizing familiar environments, inability to follow simple commands, and a marked decline in short‑term memory. These cognitive disturbances can fluctuate, becoming more pronounced during periods of fever or when the infection spreads to the central nervous system.

Key clinical observations include:

Inability to maintain coherent conversation
Misidentification of people, objects, or locations
Disrupted sense of time and place
Impaired judgment and decision‑making
Episodes of agitation alternating with lethargy

Prompt neurological assessment and laboratory testing for viral encephalitis are essential. Early antiviral therapy, supportive care, and monitoring for worsening mental status improve outcomes and reduce the risk of permanent cognitive deficits.

Seizures

Seizures represent a serious neurologic manifestation that can emerge after infection with a tick‑borne encephalitis virus. The virus reaches the central nervous system, disrupts neuronal excitability, and may precipitate convulsive activity.

Incidence: Seizures occur in approximately 5–15 % of confirmed cases, with higher rates in severe encephalitic presentations.
Onset timing: Convulsions typically appear during the acute phase, 5–14 days after the initial bite, but may also develop during the convalescent period if inflammation persists.
Clinical patterns: Patients may experience focal seizures with motor or sensory symptoms, generalized tonic‑clonic seizures, or status epilepticus in the most critical cases.
Diagnostic clues: Electroencephalography often shows diffuse slowing, focal epileptiform discharges, or periodic sharp wave complexes. Magnetic resonance imaging may reveal hyperintensities in the basal ganglia, thalamus, or cortical regions correlating with seizure foci.
Management: Immediate control with benzodiazepines is recommended, followed by maintenance therapy using agents such as levetiracetam, valproic acid, or phenobarbital. Antiviral treatment (e.g., interferon‑α) does not directly affect seizures but may limit viral replication.
Prognosis: Early seizure control reduces the risk of long‑term epilepsy. Persistent seizures after recovery are reported in up to 3 % of patients, often associated with extensive cortical damage.

Recognizing seizures promptly after a tick‑borne encephalitic infection is essential for preventing secondary brain injury and improving overall outcomes.

Speech Difficulties (Dysphasia)

Speech difficulties, specifically dysphasia, frequently appear during the neurological phase of tick‑borne encephalitis. The virus infiltrates the cerebral cortex, basal ganglia, and brain stem, disrupting language networks. Patients may exhibit reduced verbal output, impaired word finding, or distorted articulation, often co‑occurring with other focal deficits such as facial weakness or impaired coordination.

Typical manifestations include:

Expressive dysphasia – limited ability to produce fluent speech, frequent pauses, and simplified sentence structure.
Receptive dysphasia – difficulty comprehending spoken language, misinterpretation of commands, and reduced comprehension of complex sentences.
Mixed dysphasia – combination of expressive and receptive impairments, leading to incoherent discourse.

Onset usually follows the initial febrile stage by several days, coinciding with the emergence of meningitic or encephalitic signs. Neurological examination often reveals:

Slowed speech tempo.
Paraphasic errors (substituting similar‑sounding words).
Gaping pauses before lexical retrieval.
Inconsistent comprehension of multi‑step instructions.

Diagnostic confirmation relies on cerebrospinal fluid analysis showing lymphocytic pleocytosis and elevated protein, alongside serologic detection of specific IgM antibodies. Neuroimaging may display hyperintensities in language‑related cortical regions, supporting the clinical picture.

Prognosis varies. Early antiviral therapy and supportive care improve outcomes, but residual dysphasia can persist for weeks to months. Rehabilitation strategies focus on:

Structured speech‑language therapy targeting word‑finding and sentence formation.
Cognitive‑linguistic exercises to reinforce auditory comprehension.
Gradual re‑introduction of complex verbal tasks under professional supervision.

Monitoring progress through standardized language assessments enables timely adjustment of therapeutic intensity and informs expectations for functional recovery.

Movement Disorders (Tremors, Ataxia)

After a bite from a tick that transmits encephalitis‑causing viruses, patients frequently exhibit disturbances of motor control. The central nervous system inflammation interferes with cerebellar and basal‑ganglia pathways, producing observable movement abnormalities.

Typical motor manifestations include:

Tremor – rhythmic oscillations of limbs or trunk, often appearing at rest and intensifying with intentional movement; may be unilateral or bilateral depending on lesion location.
Ataxia – loss of coordination manifested as gait instability, dysmetria on finger‑to‑nose testing, and difficulty performing rapid alternating movements; usually reflects cerebellar involvement.

These signs often emerge during the acute encephalitic phase or within days of neurological deterioration. Their severity correlates with the extent of cerebral edema and can progress to persistent disability if the inflammatory process is not promptly controlled. Early recognition of tremor and ataxia guides diagnostic imaging, cerebrospinal‑fluid analysis, and antiviral therapy, thereby reducing the risk of long‑term motor impairment.

Weakness or Paralysis

Weakness and paralysis frequently appear after a tick bite that transmits an encephalitic virus. The deficit may develop within days to weeks of the initial exposure and often follows the early febrile phase. Typical patterns include:

Sudden loss of strength in one or more limbs, usually asymmetric.
Flaccid paralysis of facial muscles, commonly presenting as unilateral facial droop.
Progressive involvement of proximal muscles, leading to difficulty rising from a seated position or climbing stairs.
Respiratory muscle weakness that can compromise ventilation and require mechanical support.
Absence of reflexes in affected limbs, sometimes accompanied by sensory disturbances such as tingling or numbness.

Neurological examination often reveals reduced motor power (Medical Research Council grade ≤3) with preserved sensation, indicating a primarily motor neuropathy. Electrophysiological studies show decreased compound muscle action potentials, supporting a peripheral nerve or anterior horn cell pathology. Early recognition of these signs is essential for prompt antiviral therapy and supportive care, which can limit permanent deficits.

Myelitis Manifestations

Spinal Cord Inflammation

After a bite from a tick carrying an encephalitis‑causing virus, inflammation of the spinal cord (viral myelitis) may develop. The inflammatory process disrupts neural pathways, producing a distinct set of clinical signs.

Typical manifestations include:

Sharp or burning pain localized to the spine or radiating to the limbs.
Progressive muscle weakness, often beginning in the lower extremities and advancing upward.
Reduced or absent sensation to touch, temperature, and vibration in the affected dermatomes.
Loss of reflexes or, conversely, exaggerated reflexes depending on the lesion level.
Urinary retention or incontinence caused by impaired autonomic control.
Gait instability or difficulty maintaining balance, especially when standing or walking.

These symptoms may appear within days to weeks after exposure and can evolve rapidly. Prompt neurological assessment and imaging are essential for confirming spinal cord involvement and initiating antiviral or anti‑inflammatory therapy. Early intervention improves the likelihood of functional recovery and reduces the risk of permanent deficits.

Sensory Disturbances

After a bite from a tick capable of transmitting encephalitic viruses, patients frequently experience disturbances of sensation that may precede or accompany neurological involvement. These sensory changes arise from viral invasion of peripheral nerves, dorsal root ganglia, or central sensory pathways.

Common manifestations include:

Paresthesia: tingling or “pins‑and‑needles” sensations, often beginning in the extremities and spreading proximally.
Dysesthesia: abnormal, unpleasant sensations such as burning, itching, or electric‑shock–like pain.
Hypoesthesia or anesthesia: reduced or absent perception of light touch, temperature, or vibration.
Visual disturbances: photopsia, blurred vision, or transient loss of visual fields when optic pathways are affected.
Auditory anomalies: ringing in the ears (tinnitus) or diminished hearing acuity linked to involvement of the auditory nerve.
Facial numbness or altered taste sensation, indicating cranial nerve involvement.

The onset of sensory symptoms typically occurs within days to weeks after the bite, may fluctuate, and can progress rapidly if encephalitis develops. Early recognition of these signs is essential for prompt diagnostic evaluation, including serologic testing for tick‑borne encephalitis viruses and neuroimaging to assess central nervous system involvement. Timely antiviral or supportive therapy can mitigate progression to severe neurological deficits.

Motor Weakness

Motor weakness often appears as an early neurological sign after a bite from a tick that transmits encephalitic viruses. The weakness typically develops within days to a few weeks of the exposure, coinciding with the onset of central nervous system inflammation. It may affect one limb (focal paresis) or involve multiple muscle groups (generalized weakness), and can progress rapidly if untreated.

Key clinical features include:

Reduced muscle strength measurable on manual testing, commonly graded 3/5 or lower.
Difficulty initiating voluntary movements, especially in the upper extremities.
Diminished reflexes or, conversely, hyperreflexia when upper motor neuron involvement predominates.
Accompanying symptoms such as headache, fever, and altered mental status, indicating concurrent encephalitic activity.

Diagnostic confirmation relies on serologic testing for tick‑borne encephalitis antibodies and neuroimaging that may show inflammatory changes in the brainstem or spinal cord. Electromyography can differentiate peripheral from central causes of weakness.

Management focuses on antiviral therapy when indicated, supportive care to maintain airway protection, and early physiotherapy to prevent muscle atrophy. Monitoring for progression is essential, as worsening weakness may signal expanding cerebral edema or secondary complications. Prompt intervention reduces the risk of permanent motor deficits.

Long-term Complications and Recovery

Post-Encephalitic Syndrome

Persistent Fatigue

Persistent fatigue commonly follows a bite from a tick that transmits encephalitic viruses. The exhaustion often appears within days to weeks after exposure, lasting from several weeks to months. Patients report difficulty sustaining physical activity, reduced endurance, and a sensation of mental weariness that does not improve with normal rest.

The fatigue is typically multifactorial. Viral replication in the central nervous system triggers inflammatory cytokines, which disrupt normal sleep‑wake regulation and mitochondrial energy production. Concurrent mild fever, headache, and muscle aches can amplify the perception of tiredness. In some cases, post‑infectious autonomic dysfunction contributes to orthostatic intolerance, further reducing stamina.

Clinical assessment should include:

Detailed timeline of symptom onset relative to the tick bite.
Evaluation of accompanying neurological signs such as headache, photophobia, or balance disturbances.
Laboratory tests for inflammatory markers, viral serology, and, when indicated, cerebrospinal fluid analysis.
Screening for secondary causes of fatigue, including anemia, thyroid dysfunction, and depressive disorders.

Management focuses on supportive care and gradual rehabilitation. Recommendations include:

Structured rest periods interspersed with low‑intensity activity to prevent deconditioning.
Hydration and balanced nutrition to support metabolic recovery.
Pharmacologic interventions such as short‑term corticosteroids or antiviral agents only when indicated by confirmed viral activity.
Referral to physical therapy for graded exercise programs tailored to the patient’s tolerance.

Persistent fatigue can impair daily functioning and delay return to work or school. Early recognition and systematic monitoring improve outcomes and reduce the risk of chronic post‑viral fatigue syndrome.

Cognitive Impairment

Cognitive impairment frequently follows infection with a tick‑borne encephalitis virus. Patients may experience reduced short‑term memory, difficulty retaining new information, and frequent lapses in recall. Attention span often narrows; tasks that require sustained focus become exhausting, and distractibility increases. Executive functions—planning, organizing, and decision‑making—are commonly compromised, leading to slowed problem‑solving and poor judgment. Processing speed declines, producing a noticeable lag between stimulus and response. Disorientation or confusion may arise, especially during the acute phase, and can persist for weeks or months.

Typical progression includes:

Onset of mild confusion within days of the bite, escalating to measurable deficits in memory and attention.
Peak impairment occurring during the encephalitic stage, usually 1–2 weeks after symptom emergence.
Gradual improvement over weeks, though residual deficits often remain, particularly in executive tasks and complex memory retrieval.

Neuropsychological testing quantifies deficits, while magnetic resonance imaging may reveal focal lesions in the hippocampus, frontal lobes, or thalamus that correlate with observed dysfunction. Early antiviral therapy and supportive care reduce inflammation, potentially limiting long‑term cognitive loss. Rehabilitation programs focused on memory strategies, attention training, and executive skill rebuilding improve functional outcomes. Continuous monitoring is essential to differentiate transient encephalitic effects from permanent neurological damage.

Mood Disorders

Tick‑borne encephalitis can trigger a spectrum of affective disturbances that emerge during the acute phase or persist into the convalescent period. The most frequently reported mood alterations include:

Persistent low mood or depressive symptoms, often accompanied by anhedonia and fatigue.
Heightened anxiety, manifested as restlessness, excessive worry, or panic‑like episodes.
Irritability and sudden emotional lability, leading to abrupt shifts from calm to agitation.
Apathy or reduced motivation, which may interfere with daily activities and rehabilitation efforts.

These affective manifestations result from neuroinflammatory processes that disrupt limbic circuitry, particularly the amygdala, hippocampus, and prefrontal cortex. Cytokine release (e.g., IL‑6, TNF‑α) and blood‑brain barrier permeability contribute to neurotransmitter imbalances, notably reduced serotonin and dopamine transmission.

Clinical evaluation should incorporate standardized mood scales (e.g., PHQ‑9, GAD‑7) alongside neurological assessment. Early identification enables timely intervention: selective serotonin reuptake inhibitors, short‑term anxiolytics, and cognitive‑behavioral strategies have demonstrated efficacy in mitigating symptom severity. Monitoring continues throughout recovery, as mood disturbances may persist for weeks to months after the infectious episode resolves.

Chronic Headaches

Chronic headaches frequently appear after a bite from a tick that transmits encephalitis‑causing viruses. The pain often begins weeks to months after the initial exposure, persisting beyond the acute phase of infection and may coexist with other neurological deficits.

These headaches are typically tension‑type or migraine‑like, presenting as bilateral pressure, throbbing sensations, or pulsatile pain. Intensity ranges from moderate to severe, and episodes can last from several hours to days. Patients often report aggravation by physical activity, stress, or changes in posture, while rest and analgesics provide limited relief.

Key clinical features include:

Daily or near‑daily occurrence lasting more than three months
Lack of clear peripheral cause (e.g., sinusitis, dental pathology)
Associated photophobia, phonophobia, or nausea in migraine‑like presentations
Possible coexistence with cognitive impairment, dizziness, or fatigue

Diagnostic evaluation should incorporate a detailed exposure history, neurological examination, and imaging to exclude intracranial complications. Laboratory testing for tick‑borne encephalitis antibodies confirms the underlying infection. Management combines antiviral or supportive therapy for the primary disease with targeted headache treatment: NSAIDs, triptans for migraine patterns, and preventive agents such as beta‑blockers, anticonvulsants, or antidepressants. Multidisciplinary follow‑up improves long‑term outcomes.

Prognosis and Risk Factors

Tick‑borne encephalitic infections typically follow a biphasic course: an initial febrile phase lasting 3–7 days, then a neurologic phase with meningitis, encephalitis, or meningo‑encephalitis. Most patients recover without permanent deficits; however, mortality ranges from 1 % to 20 % depending on the viral agent, and up to 30 % of survivors experience persistent cognitive, motor, or psychiatric impairment.

Prognostic outcomes correlate with several clinical and demographic variables. Early recognition and antiviral or supportive therapy improve survival and reduce sequelae. Advanced age, pre‑existing immunosuppression, and delayed hospital admission are consistently linked to poorer recovery. High viral load in cerebrospinal fluid and extensive brain edema on imaging also predict unfavorable courses.

Key risk factors for severe neurologic disease include:

Age ≥ 60 years
Chronic illnesses such as diabetes, cardiovascular disease, or renal failure
Immunocompromised status (e.g., HIV infection, chemotherapy, corticosteroid use)
Co‑infection with other tick‑borne pathogens (e.g., Borrelia burgdorferi)
Bite from tick species known to transmit highly neurovirulent strains
Lack of post‑exposure prophylaxis or vaccination where available

Patients presenting with rapid progression to coma, seizures, or focal neurological deficits require intensive monitoring; these signs markedly increase the likelihood of long‑term disability or death. Prompt, aggressive supportive care remains the primary determinant of outcome.