How does encephalitis manifest after a tick bite in a child? - briefly
A child who develops encephalitis after a tick attachment usually shows abrupt fever, intense headache, vomiting, confusion or decreased consciousness, and may experience seizures, neck rigidity, and focal neurological deficits. Symptoms often progress rapidly, requiring immediate medical evaluation and treatment.
How does encephalitis manifest after a tick bite in a child? - in detail
Encephalitis that follows a tick‑borne infection in a child typically presents within 5–14 days after the bite. The incubation period varies with the pathogen, most commonly Borrelia burgdorferi (Lyme disease) or Rickettsia spp., and may be shorter for viral agents such as Powassan virus.
Systemic signs often precede neurologic involvement and may include:
- Fever ≥ 38 °C, sometimes high‑grade
- Headache, often described as severe or “stabbing”
- Malaise, fatigue, and loss of appetite
- Myalgias or arthralgias, especially in the region of the bite
Neurological manifestations emerge rapidly and can be grouped as follows:
- Altered mental status – irritability, lethargy, confusion, or progressing to coma.
- Seizure activity – focal or generalized seizures; status epilepticus may develop.
- Motor dysfunction – weakness, paresis, or ataxia; gait instability is common.
- Cranial nerve involvement – facial palsy, diplopia, or dysphagia.
- Sensory disturbances – paresthesia, numbness, or visual field deficits.
- Autonomic instability – irregular heart rate, blood pressure fluctuations, or temperature dysregulation.
Physical examination may reveal a rash consistent with erythema migrans or a vesicular eruption, indicating the underlying tick‑borne disease. Meningeal signs (neck stiffness, Kernig’s or Brudzinski’s) can coexist, reflecting meningoencephalitis.
Diagnostic work‑up should include:
- Complete blood count with differential (leukocytosis or lymphopenia)
- Inflammatory markers (CRP, ESR) often elevated
- Serum serology for Lyme, Rocky Mountain spotted fever, or Powassan virus
- Cerebrospinal fluid analysis: pleocytosis (predominantly lymphocytic), elevated protein, normal or mildly reduced glucose
- PCR testing of CSF for viral agents when available
- MRI of the brain: hyperintense lesions in the basal ganglia, thalamus, or cortical regions; contrast enhancement may be present
- EEG: diffuse slowing or focal epileptiform discharges
Treatment protocols depend on the identified pathogen. Empiric antimicrobial therapy typically starts with intravenous ceftriaxone for suspected Lyme neuroborreliosis, combined with doxycycline when rickettsial disease is possible. Antiviral agents (e.g., ribavirin) are reserved for confirmed viral etiologies. Adjunctive measures include anticonvulsants for seizure control, corticosteroids for severe cerebral edema, and supportive care in an intensive‑care setting.
Prognosis varies. Early recognition and prompt antimicrobial therapy improve outcomes, reducing the risk of permanent neurologic deficits. Delayed treatment may result in persistent cognitive impairment, motor disability, or epilepsy. Regular follow‑up with neurodevelopmental assessment is essential to identify and address sequelae.