How does encephalitis develop after a tick bite? - briefly
A tick bite introduces neurotropic pathogens, such as Borrelia burgdorferi, into the bloodstream. These agents spread, cross the blood‑brain barrier, and incite inflammation of brain tissue, producing encephalitis.
How does encephalitis develop after a tick bite? - in detail
A tick that has fed on an infected reservoir host can transmit the tick‑borne encephalitis (TBE) virus during its subsequent attachment to a human. The virus is deposited in the dermal tissue together with tick saliva, which contains immunomodulatory compounds that facilitate viral entry.
Within minutes to hours, the virus infects keratinocytes, fibroblasts, and resident dendritic cells at the bite site. These cells produce viral progeny that spread to regional lymph nodes, where replication amplifies the viral load. The resulting viremia allows the pathogen to reach distant organs, including the central nervous system (CNS).
Crossing the blood‑brain barrier occurs through several mechanisms:
- Direct infection of endothelial cells lining cerebral vessels, compromising barrier integrity.
- Transmigration of infected leukocytes (the “Trojan horse” model) that carry virus across the barrier.
- Disruption of tight junction proteins by viral proteases and inflammatory cytokines.
Once inside the CNS, the virus preferentially infects neurons and glial cells. Replication within neurons triggers cell‑autonomous apoptosis and necrosis. Activated microglia and infiltrating immune cells release pro‑inflammatory cytokines (IL‑6, TNF‑α, IFN‑γ) and chemokines, amplifying neuronal injury and causing cerebral edema.
The clinical course typically follows three phases:
- Early systemic phase – fever, malaise, and flu‑like symptoms appear 3–14 days after the bite, reflecting peripheral replication.
- Neurological phase – after a brief asymptomatic interval, meningitis, encephalitis, or meningo‑encephalitis develop, marked by headache, neck stiffness, altered consciousness, and focal neurological deficits.
- Recovery or sequelae – most patients improve within weeks, but a proportion retain persistent cognitive, motor, or psychiatric deficits due to irreversible neuronal loss.
Key determinants of disease severity include viral strain virulence, inoculum size, host age, and preexisting immunity. Prompt antiviral supportive care and, where available, vaccination against TBE can reduce the likelihood of CNS involvement.