How does encephalitis present after a tick bite in a dog?

How does encephalitis present after a tick bite in a dog? - briefly

After a tick bite, canine encephalitis usually appears as sudden neurological disturbances such as seizures, ataxia, altered mentation, and fever. Additional signs may include facial paralysis, cranial nerve deficits, and progressive weakness.

How does encephalitis present after a tick bite in a dog? - in detail

Encephalitis that develops after a tick attachment in dogs typically appears within a few days to two weeks following the bite. The virus transmitted by the tick, most often a member of the Flaviviridae or Rickettsiales families, induces inflammation of the brain parenchyma, leading to a characteristic cluster of neurologic abnormalities.

Common clinical manifestations include:

  • Fever ranging from 39.5 °C to 41 °C.
  • Lethargy and reduced appetite.
  • Disorientation or altered mental status, such as staring or unresponsiveness.
  • Ataxia affecting one or all limbs, often accompanied by a wide-based gait.
  • Head tilt, circling, or abnormal eye movements (nystagmus).
  • Muscle tremors or generalized shaking.
  • Seizure activity, which may be focal or generalized.
  • Cranial nerve deficits, including facial paralysis or loss of pupillary reflexes.
  • Painful neck rigidity or resistance to head movement.

Laboratory evaluation frequently reveals a mild to moderate leukocytosis, elevated inflammatory markers (e.g., C‑reactive protein), and, in severe cases, electrolyte disturbances. Cerebrospinal fluid analysis shows a pleocytosis with a predominance of lymphocytes, increased protein concentration, and normal to slightly decreased glucose. Polymerase chain reaction (PCR) testing of CSF or blood can identify the specific tick‑borne pathogen, confirming the etiologic agent.

Magnetic resonance imaging (MRI) of the brain commonly demonstrates hyperintense lesions in the gray matter, especially in the thalamus, hippocampus, and brainstem, consistent with inflammatory edema. Contrast enhancement may be present around affected regions.

Therapeutic management focuses on supportive care and targeted antimicrobial or antiviral agents when a specific organism is identified. Standard measures include:

  • Intravenous fluid therapy to maintain hydration and correct electrolyte imbalances.
  • Antipyretics to control fever.
  • Anticonvulsants (e.g., phenobarbital or levetiracetam) for seizure control.
  • Broad‑spectrum antibiotics (e.g., doxycycline) for suspected bacterial co‑infection.
  • Antiviral drugs (e.g., ribavirin) when indicated by pathogen identification.

Prognosis varies with the rapidity of diagnosis, severity of neurologic signs, and the specific pathogen involved. Early intervention often results in full recovery, whereas delayed treatment can lead to persistent deficits or fatal outcomes. Continuous monitoring of neurologic status and repeat imaging are essential to assess treatment response and detect complications such as intracranial hypertension or secondary infections.