Benign forms
These variants of the disease proceed without organic damage to the nervous system and, as a rule, end in complete recovery.
The febrile form occurs most frequently, but often goes unrecognized. The disease starts acutely: without a prodrome, the temperature spikes to 38–39°C, accompanied by chills, myalgia, weakness, and nausea. Objectively, tachycardia and arterial hypotension are recorded. Leukopenia is typical in the complete blood count. In some patients, severe intoxication leads to meningism — the presence of classic meningeal signs with an absolutely normal cerebrospinal fluid composition. Fever lasts from several hours to 7 days.
The biphasic course is a specific variant in which the first wave (3–7 days) is mild, followed by a period of apyrexia (up to 14 days) during which only asthenia persists. The second wave is always longer and more severe: neurological symptoms appear, and unlike the first wave, leukocytosis develops in the blood.
Meningeal and meningoencephalitic forms
These forms are associated with the involvement of the meninges and the brain parenchyma in the pathological process.
The meningeal form is most commonly diagnosed in clinical practice. The intoxication syndrome is pronounced: hectic fever up to 40°C, tachypnea, oliguria. The patient suffers from intense headache that worsens with movement and repetitive vomiting that brings no relief. Photophobia, hyperacusis, and objective signs of meningeal irritation (nuchal rigidity, Kernig's and Brudzinski's signs) are prominent. The CSF shows a picture of serous meningitis with lymphocytic pleocytosis, and CSF normalization significantly lags behind clinical recovery. The outcome is always favorable.
The meningoencephalitic form is distinguished by a severe clinical course and high mortality. Against the background of meningeal syndrome, general cerebral and focal neurological deficits rapidly progress within 1–2 days. Tremor, nystagmus, and epileptic seizures may occur. Asymmetrical cranial nerve palsies are characteristic (especially n. oculomotorius and n. facialis). Consciousness is depressed down to a coma or, conversely, transitions into a delirious state.
Involvement of the peripheral nervous system and spinal cord
These forms lead to persistent disabling consequences due to the development of paresis and paralysis.
- The poliomyelitic form (develops in almost 30% of patients). It debuts with fasciculations and sudden limb weakness accompanied by fever. Flaccid paresis develops, predominantly affecting the muscles of the neck and shoulder girdle. The outcome is marked by persistent atrophy and characteristic residual manifestations: "dropped head", "humped posture". An ominous complication is ascending Landry's spinal paralysis.
- The polyradiculoneuritic form (3–4%). Characterized by nerve root involvement. Patients complain of tingling sensations ("pins and needles") and pain along the nerve trunks. Polyneuropathic sensory disturbances and positive Lasegue's and Wassermann's signs are detected.
Chronic course and subclinical variants
Indigenous residents of endemic areas frequently exhibit the subclinical form: there are no clinical manifestations, but antibodies circulate in the blood. Under the influence of stress, physiotherapy, or trauma, it can transform into a primary progressive form of encephalitis.
In 3–11% of patients who have had the acute form, a chronic progressive course develops. It lasts for decades and manifests as hyperkinetic syndrome, Kozhevnikov's epilepsy, or clinical features of amyotrophic lateral sclerosis (ALS). PCR diagnostics is used to confirm viral persistence in such cases.
Fundamentals of laboratory diagnostics
A comprehensive approach is used to confirm the diagnosis:
- ELISA: used for verification starting from the 4th–5th day. A diagnostic IgM antibody titer is considered to be 1:1280 and higher. If IgM circulates for more than a year, it is a marker of chronicity.
- HI test (HAI): most commonly used for retrospective analysis or assessing vaccination efficacy. A 4-fold increase in the antibody titer is diagnostically significant.
- PCR: detection of viral RNA. Mandatory when examining CSF if the clinical picture does not rule out encephalitis and serological tests are negative.
Briefly: answers to topical questions
What are the exact regimens and dosages for administering specific immunoglobulin in the treatment of severe tick-borne encephalitis?
In the treatment of focal (severe) forms of tick-borne encephalitis, specific immunoglobulin is administered intramuscularly at a single dose of 0.1 mL/kg of body weight.
Dosing regimen for focal forms:
- Frequency of administration — every 8–10 hours.
- Duration of the course — at least 6 days (until body temperature drops and neurological symptoms regress).
In extremely severe cases of the disease, a single dose of the drug can be increased to 0.15 mL/kg of body weight.
What brain MRI findings are characteristic of the meningoencephalitic form of tick-borne encephalitis?
The provided sources do not specify MRI features characteristic precisely of the meningoencephalitic form of tick-borne encephalitis.
The following is indicated:
- Brain MRI with contrast enhancement is indicated for all patients with focal forms of TBE.
- In encephalitis, neuroimaging may reveal inflammatory foci.
- Brain CT and MRI allow the exclusion of other lesions: infarction, hemorrhage, tumor, abscess.
To memorize the permanent outcomes of the poliomyelitic form, use the visual image of the patient: flaccid paresis of the neck muscles leads to the "dropped head onto the chest" phenomenon, while compensatorily a "proud posture" or "humped stooped posture" with trunk-throwing of the arms develops.
Class and exam questions
What is the difference between meningism in the febrile form and true meningitis?
In meningism, objective meningeal signs are present (due to severe intoxication), yet the cerebrospinal fluid remains completely normal with no signs of inflammation.
How does the blood count change during the biphasic course of TBE?
During the first (mild) wave, leukopenia is frequently observed in the hemogram. During the second, more severe wave accompanied by neurological symptoms, leukocytosis appears in the blood.
What critical mistake can be made before taking a blood sample for analysis?
Drawing blood after the administration of tick-borne gamma globulin. The administered donor antibodies will make the patient's own serological diagnosis impossible.
What else to study on this topic
- Criteria for differential diagnosis of TBE and severe influenza
- Specific manifestations of ixodid tick-borne borreliosis (Lyme disease)
- Clinical picture of tick-borne spotted fevers and primary affect
- Laboratory features of monocytic and granulocytic ehrlichiosis
- Dynamics of CSF changes in serous meningitis
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