How does a tick-borne encephalitis bite manifest in humans? - briefly
The bite initiates a flu‑like prodrome with fever, fatigue, headache and muscle aches. If the virus reaches the central nervous system, patients develop meningitis, encephalitis or meningoencephalitis, presenting with neck stiffness, confusion, seizures and, in severe cases, paralysis.
How does a tick-borne encephalitis bite manifest in humans? - in detail
Tick‑borne encephalitis (TBE) infection begins after a bite from an infected Ixodes tick. The virus is introduced into the skin and then spreads systemically, producing a biphasic illness in most patients.
Incubation
The interval between the bite and the first symptoms ranges from 4 to 28 days, most commonly 7–14 days. During this period the virus replicates in the dermal and lymphatic tissues without causing noticeable effects.
First (prodromal) phase
When viremia reaches the bloodstream, patients experience a sudden onset of nonspecific signs:
- fever (38–40 °C)
- headache
- malaise
- muscle aches
- nausea or vomiting
- sometimes a mild, transient rash at the bite site
These manifestations last 2–7 days and may resolve spontaneously, giving the impression of recovery.
Second (neurological) phase
After a brief asymptomatic interval (often 1–5 days), the virus penetrates the central nervous system. Neurological involvement presents as one of three patterns:
- Meningitis – neck stiffness, photophobia, mild mental confusion, elevated cerebrospinal fluid (CSF) white‑cell count with lymphocytic predominance.
- Meningoencephalitis – altered consciousness, disorientation, seizures, focal neurological deficits (e.g., weakness, ataxia), cranial nerve palsies.
- Myelitis – flaccid or spastic paralysis, sensory level, bladder dysfunction, often combined with encephalitic signs.
Symptoms may overlap; severe cases can progress to coma, respiratory failure, or long‑term sequelae such as persistent motor deficits, cognitive impairment, or epilepsy.
Laboratory findings
- CSF: pleocytosis (100–500 cells/µL), protein elevation, normal glucose.
- Serum and CSF: TBE‑specific IgM detectable within the first week of the neurological phase; IgG appears later.
- PCR for viral RNA is rarely positive after the prodromal stage.
Differential considerations
The clinical picture can resemble bacterial meningitis, other viral encephalitides (e.g., West Nile, herpes simplex), and Lyme neuroborreliosis. Distinguishing features include the biphasic course, absence of bacterial pathogens in CSF culture, and serologic confirmation of TBE virus.
Outcome
Mortality ranges from 1 % to 5 % in Europe, higher in eastern strains. Approximately 30 % of survivors retain some neurological impairment, most often related to motor function.
Prompt recognition of the two‑stage pattern and appropriate supportive care, including management of seizures, intracranial pressure, and respiratory support, improve prognosis. No specific antiviral therapy exists; prevention relies on tick avoidance and vaccination in endemic regions.