What are the symptoms of tick-borne encephalitis in humans? - briefly
Typical manifestations comprise abrupt fever, intense headache, neck stiffness, and vomiting, often accompanied by neurological signs such as confusion, tremor, or focal weakness. Severe progression may lead to meningitis, encephalitis, or myelitis, potentially resulting in lasting neurological impairment.
What are the symptoms of tick-borne encephalitis in humans? - in detail
Tick‑borne encephalitis (TBE) presents after an incubation period of 7‑14 days, occasionally extending to 21 days. The disease often follows a biphasic pattern.
The initial phase resembles a nonspecific viral infection. Common manifestations include fever, fatigue, headache, myalgia, arthralgia, and nausea. Some patients develop a mild meningitic picture with neck stiffness and photophobia. This stage typically lasts 2‑7 days and may resolve spontaneously, creating a brief asymptomatic interval before the second phase.
The second phase involves central‑nervous‑system involvement. Neurological symptoms may appear abruptly or evolve over several days. Frequent findings are:
- High‑grade fever persisting beyond the first phase
- Severe headache, often described as frontal or occipital
- Neck rigidity and positive meningeal signs
- Altered mental status ranging from confusion to stupor
- Photophobia and phonophobia
- Nausea and vomiting associated with increased intracranial pressure
- Cranial nerve dysfunction (e.g., facial palsy, diplopia)
- Motor deficits such as weakness, ataxia, or paralysis of limbs
- Tremor, myoclonus, or seizures in severe cases
- Long‑lasting cognitive impairment, including memory loss and reduced concentration
In a minority of patients, the disease progresses to encephalomyelitis, characterized by combined brain and spinal cord inflammation. This form may produce spastic paresis, urinary retention, and respiratory failure. Mortality rates vary from 1 % to 5 % in adults, with higher risk in older individuals and those with comorbidities. Survivors often retain neurological sequelae, especially persistent paresis, ataxia, or cognitive deficits.
Early recognition of the biphasic course and prompt supportive care, including antipyretics, hydration, and monitoring of intracranial pressure, improve outcomes. Antiviral therapy is not established; prevention relies on vaccination and tick‑avoidance measures.