Etiology and transmission routes
The causative agent of the disease is an RNA-containing virus from the arbovirus group. There are three main subtypes: Central European, Siberian, and Far Eastern. The latter variant is characterized by the most severe clinical course. The pathogen is labile in the environment (rapidly inactivated by heat and ultraviolet radiation), yet resistant to acidic environments and retains virulence in unpasteurized milk for a long time.
Natural reservoirs and vectors are ixodid ticks (the castor bean tick in Europe and the taiga tick in Siberia and the Far East). An infected insect remains a carrier of the virus throughout its life.
Two main routes of transmission are distinguished:
- Transcutaneous. The virus penetrates through the skin during a bite. It is important to remember that even immediate removal of the attached tick does not rule out the risk of infection.
- Alimentary (food-borne). Associated with the consumption of raw milk from infected animals (most commonly goats and sheep). This route is characteristic of familial outbreaks of the disease.
Pathogenesis and development of infection
Primary viral replication begins directly at the site of entry. Then the pathogen enters the systemic circulation, triggering the viremia stage. The severity of the disease depends on whether the virus can cross the blood-brain barrier (BBB). The arbovirus exhibits pronounced neurotropism and targets the gray matter—neurons of the spinal cord and brain.
In the vast majority of cases (about 90–95%), the infection is subclinical (mild), establishing lasting immunity. In such situations, the fact of contact with the virus is established only serologically.
If a manifest form develops, it has an acute onset. The prodromal period lasts no more than 1–2 days or is entirely absent. The debut is marked by a sharp rise in temperature (up to 38–40 °C), chills, and body aches. An erythema often appears at the bite site. All further clinical manifestations are built on a combination of three syndromes: general intoxication, generalized cerebral symptoms, and focal signs.
Clinical Forms
The manifestations of the disease are divided into two groups depending on the presence of local nervous system involvement.
Non-focal forms:
- Febrile (about 20% of cases). The virus does not cross the BBB. Against the background of fever lasting up to 10 days, severe intoxication predominates (weakness, myalgia, headache, anorexia). Meningeal and focal symptoms are absent; cerebrospinal fluid (CSF) is intact. The prognosis is most favorable.
- Meningeal (30–50%). The virus affects the meninges. A pronounced meningeal syndrome occurs (intense headache, vomiting, photophobia, nuchal rigidity, positive Kernig's and Brudzinski's signs). Lymphocytic pleocytosis is detected in the CSF.
Focal forms (up to 10% of cases): The virus destroys neurons of the brain and/or spinal cord, causing polioencephalomyelitis. Meningoencephalitis, polioencephalitis, myelitis, and poliomeningoencephalitis are distinguished. Severity correlates with the extent of necrosis. Characterized by the development of flaccid paresis and paralysis of the neck and shoulder girdle musculature (pathognomonic "dropped head" sign), as well as involvement of the X, XI, and XII cranial nerve pairs. The prognosis is unfavorable: mortality reaches 20%, and in 10–15% of patients, the process transitions into a chronic progressive course (with relapses within 1–2 years).
Diagnostics and treatment principles
The diagnosis is based on clinical and epidemiological data (taking into account seasonality and presence in endemic areas) and obligatory laboratory confirmation—recording a rise in specific antibody titers in dynamics (CFTest, HAI test, IFA, neutralization reaction). Differential diagnosis is carried out with neuroborreliosis (Lyme disease) and von Economo epidemic encephalitis.
Specific etiotropic drugs for tick-borne encephalitis do not exist. The basis of treatment is pathogenetic therapy: dehydration to combat cerebral edema, management of intoxication, administration of donor immunoglobulins, vitamins, and anticholinesterase agents. In emergency conditions (bulbar syndrome, cerebral edema), emergency intravenous administration of glucocorticosteroids (prednisolone 2–5 mg/kg) is necessary. Anticonvulsants (diazepam, droperidol, sodium oxybutyrate) are used in strictly dosed amounts to stop seizures. During the convalescence period, physical rehabilitation (massage, exercise therapy, kinesitherapy) plays a key role.
Prevention can be specific (scheduled vaccination with preparations such as Encepur) and nonspecific (repellents, clothing). Emergency care includes the administration of a vaccine or immunoglobulin strictly within the first 72 hours after a bite. The alimentary transmission route is prevented by boiling goat and cow milk.
To understand the terminology of focal forms of neuroinfections, memorize the roots: "poli(o)-" — involvement of gray matter (neurons), "leuko-" — white matter (fibers), "pan-" — total involvement, "myelo-" — spinal cord, "encephalo-" — brain.
Class and exam questions
Does immediate removal of a tick rule out infection?
No. The virus penetrates transcutaneously directly at the moment of the bite, so the speed of removing the parasite does not guarantee the absence of infection.
Can you contract encephalitis without a bite?
Yes, the alimentary route exists. Infection often occurs when consuming raw (unpasteurized) milk from infected goats or sheep.
What is the difference in CSF between the febrile and meningeal forms?
In the febrile form, the virus does not cross the BBB, and the CSF remains intact (without pathological changes). In the meningeal form, the meninges are affected, leading to the appearance of lymphocytic pleocytosis in the CSF.
What else to study on this topic
- Pathophysiology and clinical presentation of bulbar syndrome in focal forms of encephalitis.
- Differential diagnosis of neuroborreliosis (Lyme disease) and tick-borne encephalitis.
- Chronic progressive course of the infection: mechanisms and long-term prognosis.
- Principles of titration and dosage of anticonvulsants in seizure syndrome.
- Interpretation of serological reaction results (CFTest, HAI test) in the dynamics of the disease.
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