What will happen after a bite from an encephalitic tick? - briefly
The bite introduces the virus, leading to an incubation period of several days to weeks, after which flu‑like symptoms may progress to meningitis or encephalitis with headache, stiff neck, and altered consciousness. Prompt medical evaluation and antiviral therapy are essential to reduce severe neurological damage.
What will happen after a bite from an encephalitic tick? - in detail
A bite from a tick infected with a neurotropic virus initiates a cascade of physiological events. Immediately after attachment, the tick injects saliva containing anticoagulants and immunomodulatory proteins that facilitate feeding and suppress local immune responses. This creates a small erythematous lesion, often painless, which may develop into a macule or papule within 24–48 hours.
Within days to weeks, the virus may disseminate from the skin to peripheral nerves. The incubation period varies from 5 days to several weeks, depending on viral load and host factors. Early systemic symptoms can include fever, headache, fatigue, and myalgia. These nonspecific signs often precede neurological involvement.
Neurological manifestation typically follows a biphasic pattern. The first phase, termed the “viral phase,” presents with meningitis‑like symptoms: stiff neck, photophobia, and mild confusion. Cerebrospinal fluid analysis usually reveals lymphocytic pleocytosis, elevated protein, and normal glucose.
If the infection progresses, the second phase, the “encephalitic phase,” emerges. Clinical features may encompass:
- Altered consciousness ranging from lethargy to coma
- Focal neurological deficits such as cranial nerve palsies
- Seizures, both focal and generalized
- Ataxia and tremor
- Behavioral changes and psychiatric symptoms
Magnetic resonance imaging often shows hyperintense lesions in the basal ganglia, thalamus, or brainstem. Electroencephalography may reveal diffuse slowing or epileptiform discharges.
Complications can include long‑term cognitive impairment, motor dysfunction, and persistent seizures. Mortality rates differ by viral strain but can reach 20 % in severe cases without prompt antiviral therapy.
Management focuses on supportive care, antiviral agents when indicated, and monitoring for neurological deterioration. Early recognition of the initial skin lesion and rapid laboratory confirmation improve prognosis. Rehabilitation may be required for residual deficits.