How can one know if a person has tick‑borne encephalitis and what symptoms appear? - briefly
Diagnosis is based on the presence of acute neurological signs together with serologic detection of specific antibodies or PCR analysis of cerebrospinal fluid. Typical manifestations include abrupt fever, intense headache, neck stiffness, vomiting, followed by confusion, seizures, and focal deficits such as facial palsy or limb weakness.
How can one know if a person has tick‑borne encephalitis and what symptoms appear? - in detail
Tick‑borne encephalitis (TBE) is diagnosed through a combination of clinical assessment, laboratory testing, and epidemiological information. Initial suspicion arises when a patient presents with a febrile illness following exposure to tick habitats, especially in endemic regions. A thorough history should include recent outdoor activities, travel to known risk zones, and any documented tick bites.
Diagnostic procedures consist of:
- Serological analysis detecting specific IgM and IgG antibodies against TBE virus; a rise in antibody titer between acute and convalescent samples confirms infection.
- Polymerase chain reaction (PCR) of cerebrospinal fluid (CSF) or blood during the early viremic phase; PCR sensitivity declines after the first week.
- Lumbar puncture revealing CSF pleocytosis, elevated protein, and normal glucose, which supports central nervous system involvement.
Typical symptom progression occurs in two phases. The first phase presents with nonspecific flu‑like manifestations such as high fever, headache, myalgia, and malaise. After a brief asymptomatic interval, the second phase involves neurological signs, which may include:
- Severe headache and neck stiffness
- Photophobia
- Nausea and vomiting
- Altered mental status ranging from confusion to coma
- Focal neurological deficits (e.g., cranial nerve palsy, ataxia, paresis)
- Seizures in severe cases
In children, seizures and encephalitic signs predominate, while adults more frequently develop meningitis or meningo‑encephalitis. Persistent post‑infectious sequelae—cognitive impairment, gait disturbances, and chronic fatigue—may appear months after acute illness.
Prompt recognition relies on correlating exposure risk, early systemic symptoms, and subsequent neuro‑psychiatric signs, followed by targeted serological and molecular testing to confirm TBE infection. Early supportive care and monitoring reduce the likelihood of severe complications.