How does an encephalitic tick affect the human body? - briefly
An encephalitic tick transmits viruses that invade the central nervous system, producing inflammation, fever, headache, and neurological deficits such as confusion or paralysis. Prompt diagnosis and antiviral or supportive treatment are required to limit morbidity and mortality.
How does an encephalitic tick affect the human body? - in detail
A tick infected with the tick‑borne encephalitis virus injects saliva containing the pathogen while feeding. The virus enters the bloodstream through the bite wound and spreads to regional lymph nodes, where it begins replication. Within 7–14 days, the pathogen crosses the blood‑brain barrier, initiating the neurological phase.
During the initial stage, patients experience systemic signs such as fever, headache, myalgia, and malaise. These manifestations reflect the host’s innate immune response, including the release of cytokines (IL‑6, TNF‑α) and activation of acute‑phase proteins.
The second stage is characterized by central nervous system involvement. Typical manifestations include:
- High‑grade fever persisting beyond 48 h
- Severe headache often localized to the occipital region
- Nuchal rigidity indicating meningitis
- Photophobia and phonophobia
- Altered mental status ranging from confusion to coma
- Focal neurological deficits (cranial nerve palsies, ataxia, tremor)
- Seizures in severe cases
Inflammation of the meninges and brain parenchyma leads to increased intracranial pressure, cerebral edema, and neuronal injury. Cytotoxic T‑cells and microglial activation contribute to demyelination and axonal loss, which may become permanent.
Laboratory evaluation reveals lymphocytic pleocytosis in cerebrospinal fluid, elevated protein, and normal glucose. Serological testing detects specific IgM antibodies; polymerase chain reaction can confirm viral RNA in blood or CSF during early infection.
Management is supportive. Intravenous fluid therapy maintains perfusion, antipyretics control fever, and anticonvulsants treat seizures. In severe edema, corticosteroids may be considered to reduce inflammation, although evidence of benefit is limited. No antiviral agents are approved for this infection; recovery relies on the host’s adaptive immunity, which typically produces neutralizing IgG antibodies within weeks.
Long‑term sequelae affect up to 30 % of survivors and include chronic fatigue, cognitive impairment, persistent gait disturbances, and hearing loss. Rehabilitation focuses on physical therapy, neuropsychological support, and occupational therapy to mitigate functional deficits.
Prevention relies on tick avoidance (protective clothing, repellents), prompt removal of attached ticks, and vaccination in endemic regions. The vaccine induces robust humoral immunity, reducing the risk of infection and severe neurological disease.