What is encephalitis from ticks? - briefly
Encephalitis acquired from tick bites is a viral brain inflammation, most often linked to pathogens like Powassan virus transmitted by infected Ixodes species. It manifests with fever, severe headache, altered mental status, and may advance to seizures or lasting neurological impairment.
What is encephalitis from ticks? - in detail
Tick‑borne encephalitis (TBE) is an acute viral infection of the central nervous system transmitted by the bite of infected ixodid ticks, primarily Ixodes ricinus and Ixodes persulcatus. The etiologic agent is a flavivirus that circulates in wildlife reservoirs—mainly small mammals—and is maintained through a tick‑rodent‑tick cycle. Humans become incidental hosts when a feeding tick introduces viral particles into the skin.
The disease follows a biphasic course in most patients. The first phase, lasting 3–8 days, presents with nonspecific febrile illness: high temperature, headache, myalgia, and malaise. After a brief asymptomatic interval, the second phase involves the nervous system, manifesting as:
- Meningitis (neck stiffness, photophobia, CSF pleocytosis)
- Encephalitis (confusion, seizures, focal neurological deficits)
- Myelitis or combined encephalomyelitis (paraparesis, bladder dysfunction)
Severe cases may progress to coma, respiratory failure, or long‑term sequelae such as cognitive impairment and gait disturbances. Mortality ranges from 1 % to 3 % in Europe, higher in the Far‑Eastern subtype.
Laboratory confirmation relies on detection of specific IgM antibodies in serum or cerebrospinal fluid, polymerase chain reaction (PCR) during the early viremic stage, and, when available, virus isolation. Imaging (MRI) often shows hyperintense lesions in the basal ganglia, thalamus, or brainstem, supporting the diagnosis but not replacing serology.
Management is primarily supportive: antipyretics, fluid balance, seizure control, and intensive care for respiratory compromise. No antiviral therapy has proven efficacy; experimental agents such as ribavirin have limited evidence. Rehabilitation addresses residual motor and cognitive deficits.
Prevention consists of personal protection against tick bites (protective clothing, repellents, prompt removal of attached ticks) and immunization. In endemic regions, inactivated vaccines administered in a three‑dose schedule confer high seroconversion rates and reduce disease incidence by up to 95 %. Post‑exposure prophylaxis is not effective; vaccination before exposure remains the cornerstone of control.
Epidemiologically, TBE is concentrated in temperate forest zones of Europe and northern Asia, with seasonal peaks in spring and early summer when nymphal ticks are most active. Climate change and expanding habitats have contributed to the northward spread of vector populations, increasing the risk for previously unaffected areas.