What are the symptoms of encephalitis transmitted by a tick bite?

Introduction to Tick-Borne Encephalitis

What is Tick-Borne Encephalitis?

Tick‑borne encephalitis (TBE) is a viral infection of the central nervous system transmitted primarily by the bite of infected Ixodes ticks. The etiologic agent belongs to the Flaviviridae family and circulates in wildlife reservoirs, especially small mammals, which maintain the virus in endemic regions.

The disease occurs across large parts of Europe and northern Asia, with peak incidence in forested areas where tick activity is high during the warmer months. Occupational exposure, outdoor recreation, and lack of personal protection increase the likelihood of infection.

After a bite, the incubation period ranges from 7 to 14 days. The clinical course often follows a biphasic pattern. The first phase presents with nonspecific, flu‑like symptoms; after a brief asymptomatic interval, the second phase involves neurological involvement.

Common neurological manifestations include:

Severe headache
Neck stiffness
Fever persisting beyond the first phase
Photophobia
Confusion or altered consciousness
Focal neurological deficits (e.g., weakness, ataxia)
Seizures
Nausea and vomiting

In some cases, meningeal irritation predominates, while in others encephalitic features such as seizures and profound mental status changes are evident. Cerebellar ataxia may develop during recovery, leaving lasting motor impairment in a minority of patients.

The disease can be fatal or result in permanent neurological sequelae, especially in older individuals or those with compromised immune systems. Early recognition and supportive care improve outcomes, while vaccination remains the most effective preventive measure.

Transmission Mechanism

Ticks act as vectors by injecting infected saliva directly into the dermal tissue during feeding. The process begins when a tick attaches to the host’s skin and creates a feeding cavity. Salivary glands release anticoagulants and immunomodulatory proteins that facilitate prolonged blood intake and suppress local immune responses. If the tick harbors a neurotropic virus—such as tick‑borne encephalitis virus, Powassan virus, or other flaviviruses—viral particles are introduced with the saliva.

After inoculation, the virus replicates locally in skin cells and migrates to regional lymph nodes. Within 24–72 hours, viral replication expands, leading to viremia. The circulating virus crosses the blood‑brain barrier either by infecting endothelial cells, exploiting immune‑cell trafficking, or through direct disruption of the barrier’s integrity. Once inside the central nervous system, the pathogen infects neurons and glial cells, initiating the inflammatory cascade that manifests as encephalitis.

Key steps in the transmission pathway include:

Tick attachment and formation of a feeding lesion.
Salivary injection containing viral particles and immunosuppressive compounds.
Local replication in skin and lymphatic tissue.
Systemic spread via bloodstream (viremia).
Breach of the blood‑brain barrier and infection of central nervous system cells.

Early Stage Symptoms («Prodromal Phase»)

General Non-Specific Symptoms

Fever and Malaise

Fever is the most common early indicator of tick‑borne encephalitis. Body temperature typically rises above 38 °C (100.4 °F) within 3–10 days after the bite. The rise may be sudden or gradual, often reaching 39–40 °C (102.2–104 °F) during the acute phase. Fever may fluctuate, presenting with chills, sweating, and an elevated heart rate. Persistent high temperature distinguishes the infection from mild, self‑limited tick reactions.

Malaise accompanies the febrile response and reflects systemic involvement. Patients describe a generalized sense of weakness, fatigue, and lack of energy that interferes with daily activities. Malaise often appears concurrently with fever and may worsen as the illness progresses. It can be accompanied by:

Headache of moderate intensity
Muscle aches, especially in the neck and back
Reduced appetite and dehydration risk

Together, fever and malaise signal the onset of neurological involvement and warrant prompt medical evaluation.

Headache and Muscle Aches

Headache is a frequent early manifestation of tick‑borne encephalitis. It typically presents as a persistent, throbbing pain that may worsen with movement or light exposure. The intensity can range from mild discomfort to severe pressure, often unresponsive to standard analgesics until the infection progresses. In some cases, the headache precedes neurological signs such as confusion or photophobia, serving as a clinical clue to the underlying viral inflammation of the central nervous system.

Muscle aches accompany the headache in many patients. The myalgia is usually diffuse, affecting the neck, shoulders, and lower back, and may be described as aching or stiffening. It often appears simultaneously with fever and can persist for several days, diminishing only after antiviral therapy or supportive care reduces systemic inflammation. Both symptoms together signal the need for prompt diagnostic testing and early treatment to prevent complications.

Nausea and Vomiting

Nausea and vomiting frequently appear early in the clinical course of tick‑borne encephalitis, often preceding neurological manifestations. The gastrointestinal upset results from viral invasion of the central nervous system, which disrupts the brainstem vomiting center and triggers autonomic dysregulation. Patients may report sudden onset of queasiness, followed by one or more episodes of emesis, sometimes accompanied by loss of appetite.

Onset typically occurs 3–7 days after the tick bite, coinciding with the prodromal phase of infection.
Frequency ranges from mild, occasional vomiting to persistent, severe emesis that can lead to dehydration.
Presence of nausea or vomiting increases the likelihood of subsequent meningo‑encephalitic signs such as headache, photophobia, and altered mental status.
Laboratory evaluation should include complete blood count, electrolytes, and serum glucose to detect dehydration or metabolic disturbances caused by repeated vomiting.
Management focuses on anti‑emetic therapy (e.g., ondansetron), fluid replacement, and monitoring for progression to neurological impairment.

Recognition of these gastrointestinal symptoms facilitates early diagnosis and timely initiation of supportive care, reducing the risk of complications associated with tick‑transmitted encephalitic infection.

Neurological Stage Symptoms («Meningeal and Encephalitic Phase»)

Signs of Meningitis

Stiff Neck

Stiff neck frequently appears in patients with tick‑borne encephalitis and signals irritation of the meninges or cervical muscles. The rigidity restricts forward flexion, often accompanied by pain that worsens with neck movement. Examination typically reveals resistance to passive extension and a palpable tension in the trapezius and sternocleidomastoid muscles. In some cases, the stiffness extends to the upper thoracic spine, limiting rotation and lateral bending. The symptom arises from inflammatory cytokines released during viral invasion of the central nervous system, which increase muscle tone and provoke pain receptors. Presence of a stiff neck alongside fever, headache, or altered mental status warrants immediate medical evaluation, as it may indicate progressing meningitis or encephalitis. Prompt lumbar puncture and antiviral therapy improve outcomes, making early recognition of cervical rigidity essential for effective treatment.

Photophobia

Photophobia, or heightened sensitivity to light, frequently appears in patients with encephalitis acquired through tick exposure. The symptom reflects irritation of the ocular and cortical pathways that process visual stimuli, often accompanying meningeal inflammation.

Discomfort or pain when looking at bright sources, including sunlight, fluorescent lighting, or computer screens.
Reflexive closing of eyes or avoidance of well‑lit environments.
Worsening of headache intensity in bright settings.
May coexist with other visual disturbances such as blurred vision or diplopia.

Clinical assessment should include direct questioning about light‑induced pain, observation of eye‑closing behavior, and evaluation of accompanying signs like neck stiffness, fever, and altered mental status. Ophthalmologic examination helps exclude primary eye disease. Management focuses on treating the underlying viral encephalitis, controlling intracranial pressure, and providing symptomatic relief with dim lighting, sunglasses, and analgesics when necessary. Prompt recognition of photophobia contributes to early diagnosis and improves monitoring of disease progression.

Altered Mental Status

Altered mental status (AMS) is a frequent early indicator of central nervous system infection following a tick bite that transmits encephalitic viruses. It reflects dysfunction of cerebral cortical and subcortical networks and often precedes more overt neurologic deficits.

Typical manifestations of AMS in this context include:

Disorientation to time, place, or person
Confusion with impaired concentration and memory
Lethargy ranging from mild drowsiness to profound somnolence
Agitation or inexplicable irritability
Seizure activity, both focal and generalized
Progression to stupor or coma in severe cases

Onset usually occurs within days to weeks after the bite, coinciding with the prodromal phase of infection. Rapid deterioration warrants immediate hospital admission, continuous neurologic monitoring, and exclusion of alternative causes such as metabolic disturbances or drug toxicity.

Diagnostic evaluation combines clinical observation of AMS with supportive findings: cerebrospinal fluid pleocytosis, elevated protein, and detection of viral RNA or antibodies specific to tick‑borne encephalitis agents. Neuroimaging may reveal edema or focal lesions, but normal scans do not exclude the diagnosis.

Management centers on stabilization of airway, breathing, and circulation, seizure control, and reduction of intracranial pressure. Antiviral agents, when indicated, should be administered promptly, and supportive care continued until mental status normalizes or a definitive outcome is established.

Signs of Encephalitis

Severe Headache

Severe headache is a primary manifestation of tick‑borne encephalitis and often appears early in the disease course. The pain typically presents as a constant, throbbing pressure that may involve the whole head or be localized to the frontal or occipital regions. Patients frequently describe the intensity as exceeding that of ordinary tension‑type headaches, sometimes resembling migraine without aura.

Key clinical features of the headache include:

Sudden onset following a recent tick exposure.
Persistence for several days, often worsening at night or with physical activity.
Limited response to over‑the‑counter analgesics.
Association with additional neurological signs such as fever, neck stiffness, or altered mental status.

Recognition of this symptom, especially when coupled with recent tick contact and systemic signs, should prompt immediate medical evaluation and appropriate laboratory testing for viral encephalitis. Early diagnosis facilitates timely antiviral therapy and supportive care, reducing the risk of long‑term neurological complications.

Dizziness and Vertigo

Dizziness and vertigo are frequent neurologic manifestations of tick‑borne encephalitis. The imbalance may appear suddenly or develop gradually as the infection progresses through the central nervous system. Patients often describe a sensation of the room spinning, loss of spatial orientation, or a feeling of light‑headedness that does not improve with rest.

Key characteristics include:

Sudden onset of unsteady gait or inability to stand without support.
Nausea and occasional vomiting associated with the spinning sensation.
Exacerbation when the head is moved, suggesting involvement of the vestibular pathways.
Absence of peripheral ear pathology; otoscopic examination typically normal.

These signs reflect inflammation of the brainstem and cerebellar structures that process vestibular information. Early recognition, coupled with prompt antiviral therapy and supportive care, reduces the risk of persistent balance deficits. Monitoring for accompanying symptoms—such as headache, fever, and altered consciousness—helps differentiate tick‑transmitted encephalitis from other causes of vertigo.

Tremors and Seizures

Tick‑borne encephalitis frequently presents with acute neurological disturbances, of which involuntary movements and convulsive episodes are among the most serious.

Tremors arise when the virus affects cerebellar pathways or basal‑ganglia circuits. Patients may exhibit:

Low‑frequency rhythmic shaking of the limbs or head
Postural tremor that worsens when maintaining a position
Action tremor that intensifies during purposeful movement

These motor signs often develop within days of the febrile phase and may persist despite resolution of systemic symptoms.

Seizures constitute another hallmark of central nervous system involvement. Typical features include:

Generalized tonic‑clonic seizures with loss of consciousness and bilateral motor activity
Focal seizures presenting as unilateral limb jerks, sensory disturbances, or automatisms
Myoclonic jerks that occur sporadically or in clusters

Electroencephalography frequently reveals diffuse slowing and intermittent epileptiform discharges. Prompt antiepileptic therapy, combined with antiviral treatment, reduces the risk of prolonged convulsive activity and subsequent neuronal damage.

Recognition of tremor patterns and seizure types facilitates early diagnosis, guides therapeutic decisions, and improves prognosis for individuals exposed to infected ticks.

Motor Weakness and Paralysis

Tick‑borne encephalitis frequently involves the motor system, producing weakness that may progress to complete paralysis. Weakness typically begins within days of the febrile phase, often affecting the lower limbs first, and may be asymmetric. Patients report difficulty initiating movements, reduced muscle strength on manual testing, and rapid fatigue during simple tasks.

Paralysis can develop when inflammation spreads to the anterior horn cells or peripheral nerves. It may present as focal deficits—such as facial droop or hand grip loss—or as generalized flaccid paralysis resembling poliomyelitis. Deep tendon reflexes are usually diminished or absent, and muscle tone may become flaccid. In severe cases, respiratory muscles become involved, requiring ventilatory support.

Key clinical points:

Sudden onset of limb weakness, often unilateral at first
Progression to bilateral involvement in 24‑48 hours if untreated
Loss of reflexes and muscle tone consistent with lower motor neuron injury
Potential facial, bulbar, or respiratory muscle involvement
Absence of sensory loss distinguishes motor‑dominant encephalitic presentations

Diagnosis relies on cerebrospinal fluid analysis showing pleocytosis, elevated protein, and serologic confirmation of tick‑borne viral antibodies. Imaging may reveal inflammation of the brainstem or spinal cord, supporting the motor findings.

Prompt antiviral therapy and supportive care—particularly respiratory monitoring—reduce the risk of permanent motor deficits. Rehabilitation programs focusing on strength training and functional recovery are essential for patients who retain residual weakness after the acute phase.

Speech and Swallowing Difficulties

Speech and swallowing impairments frequently appear in patients with tick‑borne encephalitis. Inflammation of the brainstem or cortical regions that control phonation and deglutition can disrupt the coordination of muscles required for articulate speech and safe swallowing. The deficits may develop suddenly or progress over several days as the infection advances.

Typical manifestations include:

Slurred or nasal speech (dysarthria) caused by weakened facial or tongue muscles.
Inability to form distinct sounds, leading to reduced speech intelligibility.
Difficulty initiating or completing a swallow, often expressed as coughing, choking, or feeling of food sticking in the throat (dysphagia).
Frequent throat clearing or wet voice, indicating compromised airway protection.

Prompt neurological assessment, bedside swallow evaluation, and imaging of the central nervous system help differentiate these signs from peripheral neuropathies. Early intervention with speech‑language therapy and, when necessary, temporary enteral feeding reduces the risk of aspiration pneumonia and supports recovery of communication functions.

Cognitive Impairment

Cognitive impairment is a frequent manifestation of encephalitis acquired through tick exposure. Patients may experience reduced attention span, slowed information processing, and difficulty forming new memories. These deficits often appear within days of the initial febrile phase and can persist for weeks or months, depending on disease severity and timely treatment.

Typical presentations include:

Disorientation to time, place, or person
Impaired executive functions such as planning and problem solving
Short‑term memory loss, with preservation of long‑term recall in early stages
Language disturbances, ranging from slowed speech to difficulty finding words

Neuropsychological testing frequently reveals lower scores on tasks measuring working memory and verbal fluency. Imaging studies, particularly MRI, may show hyperintense lesions in the basal ganglia, thalamus, or hippocampus, regions critical for cognitive processing. Cerebrospinal fluid analysis often demonstrates lymphocytic pleocytosis and elevated protein, supporting the inflammatory nature of the condition.

Management focuses on antiviral therapy, supportive care, and early rehabilitation. Cognitive deficits improve in many cases after antiviral treatment, but persistent impairment may require occupational therapy, memory training, and pharmacologic adjuncts such as stimulants or cholinesterase inhibitors. Regular follow‑up assessments help track recovery and guide therapeutic adjustments.

Progression and Severity of Symptoms

Factors Influencing Severity

Age of Patient

Age significantly influences the clinical presentation of tick‑borne encephalitis. In infants and toddlers, fever and irritability often predominate, while seizures may occur without clear focal neurological signs. Young children (5‑12 years) typically exhibit headache, vomiting, and a sudden change in behavior; meningitic signs such as neck stiffness are common, but overt motor deficits are less frequent. Adolescents and most adults present with a classic triad: high fever, severe headache, and altered consciousness, frequently accompanied by photophobia and nausea. Motor weakness, ataxia, and cranial nerve palsies appear more often in this group, especially when the disease progresses to the encephalitic phase. Elderly patients display a higher propensity for confusion, delirium, and rapid deterioration, with a greater risk of respiratory complications and prolonged recovery.

Key age‑related symptom patterns:

Infants/toddlers: fever, irritability, seizures, minimal focal deficits.
Children (5‑12 y): headache, vomiting, behavioral change, meningismus.
Adolescents/Adults: high fever, severe headache, altered consciousness, photophobia, motor weakness, ataxia.
Elderly: confusion, delirium, rapid decline, respiratory distress, extended convalescence.

Viral Subtype

Tick-borne encephalitis (TBE) is caused by members of the Flaviviridae family that circulate in distinct geographic variants. The three recognized viral subtypes—European (Western), Siberian, and Far‑Eastern—exhibit differences in neuroinvasive potential and clinical course after a tick bite.

European (Western) subtype
• Biphasic illness: initial flu‑like phase (fever, malaise, headache) lasting 2–7 days, followed by a neurologic phase after a brief asymptomatic interval.
• Neurologic manifestations: meningeal signs, mild to moderate encephalitis, ataxia, occasional cranial nerve palsies.
• Mortality ≈ 1 %.
Siberian subtype
• Predominantly monophasic presentation with abrupt onset of high fever, severe headache, and profound lethargy.
• Neurologic involvement: extensive encephalitis, frequent seizures, prolonged altered consciousness, and higher rates of long‑term sequelae.
• Mortality ≈ 5–10 %.
Far‑Eastern subtype
• Rapid progression to severe encephalitis within days of symptom onset.
• Neurologic signs: intense confusion, seizures, coma, and frequent respiratory failure due to brain‑stem involvement.
• Mortality ≈ 20 %.

Other tick‑borne flaviviruses, such as Powassan virus and Louping‑ill virus, can produce encephalitic illness with overlapping symptoms—fever, headache, altered mental status, and focal neurologic deficits—but tend to be less common and lack the clear subtype stratification seen in TBE.

Recognition of the specific viral subtype guides prognosis and informs public‑health measures, as the Far‑Eastern variant carries the highest risk of fatal outcome, while the European subtype often resolves with supportive care. Accurate laboratory identification, typically by PCR or serology, remains essential for targeted clinical management.

Immune Status

Immune competence determines the clinical picture of tick‑borne encephalitis. In individuals with normal immune function, the disease usually follows a biphasic course: an initial febrile phase lasting 3–7 days, then a neurologic phase with abrupt onset of headache, neck stiffness, photophobia, confusion, or seizures. In contrast, patients with weakened immunity—such as those receiving chemotherapy, organ‑transplant recipients, or persons with advanced HIV infection—often display an attenuated febrile stage and a prolonged, less specific neurologic phase. Their symptoms may include persistent low‑grade fever, gradual cognitive decline, focal neurological deficits, and delayed seizures. Immunosuppressed hosts are also prone to secondary bacterial meningitis and prolonged viral replication, which can extend the duration of encephalitic signs beyond two weeks.

Key differences linked to immune status:

Fever pattern: sharp, high‑grade in immunocompetent; low‑grade or absent in immunocompromised.
Onset speed: rapid neurologic deterioration in healthy individuals; slower, insidious progression in those with compromised immunity.
Severity of mental status changes: marked confusion or coma common in robust immune responses; milder, fluctuating cognition in weakened hosts.
Complications: higher incidence of secondary infections and persistent viral shedding in immunosuppressed patients.

Assessment of immune status should guide diagnostic urgency, antiviral therapy intensity, and monitoring for complications. Early recognition of atypical presentations in vulnerable patients reduces morbidity and improves outcomes.

Potential Long-Term Complications

Survivors of tick‑borne encephalitis frequently experience persistent health problems that extend beyond the acute infection. These sequelae reflect damage to the central nervous system and may impair daily functioning.

Persistent motor deficits such as weakness, ataxia, or tremor
Cognitive impairment, including reduced attention, memory loss, and slower information processing
Chronic headaches and persistent neck stiffness
Seizure disorders, often focal but occasionally generalized
Psychiatric manifestations, for example anxiety, depression, or mood swings
Sensorineural hearing loss or vestibular dysfunction leading to balance issues
Peripheral neuropathy with tingling, numbness, or burning sensations
Post‑infectious autoimmune conditions, notably Guillain‑Barré syndrome or chronic inflammatory demyelinating polyneuropathy
Prolonged fatigue that interferes with work or school performance

The likelihood of each complication varies with age, severity of the initial illness, and timeliness of treatment. Early neurological assessment and rehabilitation can mitigate long‑term disability. Ongoing monitoring is essential to identify emerging deficits and to adjust therapeutic strategies accordingly.

When to Seek Medical Attention

Red Flag Symptoms

Tick‑borne encephalitis can progress rapidly; certain clinical signs demand urgent evaluation. These red‑flag manifestations indicate severe central nervous system involvement and possible life‑threatening complications.

Sudden onset of high fever (≥ 38.5 °C) persisting beyond 48 hours
Intense, throbbing headache resistant to analgesics
Neck rigidity or pain with passive flexion of the neck
Marked confusion, disorientation, or inability to maintain alertness
New‑onset seizures, focal or generalized
Focal neurological deficits such as weakness, speech impairment, or visual field loss
Photophobia accompanied by vomiting or nausea
Rapid deterioration leading to coma or loss of protective reflexes

Presence of any of these symptoms requires immediate hospitalization, neuroimaging, and initiation of antiviral or supportive therapy as indicated. Early recognition improves prognosis and reduces the risk of permanent neurological damage.

Importance of Early Diagnosis

Early identification of tick‑borne encephalitis dramatically reduces the risk of permanent neurological damage. Prompt laboratory testing—typically polymerase chain reaction or serology—confirms viral presence before the inflammatory process progresses. Immediate treatment with antiviral agents and supportive care can halt neuronal injury, shorten hospital stay, and improve long‑term functional outcomes.

Benefits of rapid diagnosis include:

Prevention of severe complications such as seizures, focal deficits, and cognitive impairment.
Reduction of intensive‑care requirements by limiting cerebral edema and intracranial pressure spikes.
Faster initiation of corticosteroid therapy when indicated, which moderates inflammatory response.
Lower probability of chronic fatigue, mood disorders, or motor dysfunction that often follow delayed treatment.

Delays in recognition allow the virus to replicate unchecked, leading to widespread brain inflammation. Each 24‑hour interval without appropriate therapy correlates with measurable declines in neuro‑cognitive scores. Therefore, clinicians must maintain a high index of suspicion in patients presenting with fever, headache, neck stiffness, or altered mental status after recent tick exposure, and order diagnostic assays without hesitation.