Etiology of tick-borne encephalitis
The causative agent of tick-borne encephalitis is an arbovirus. According to the taxonomic classification, it belongs to the Flaviviridae family, genus Flavivirus. Depending on geographical distribution, two main nosogeographical variants of the virus are traditionally distinguished: the eastern and western subtypes.
In medical literature and historical context, the disease has many synonyms reflecting its seasonality and geography:
- Spring-summer type encephalitis;
- Taiga encephalitis;
- Russian epidemic encephalitis;
- Russian spring/summer encephalitis (refers to the eastern subtype);
- Early summer encephalitis;
- Fruhsommermeningoenzephalitis;
- Kumlinge’s disease (refers to the western subtype).
Epidemiological features
Tick-borne encephalitis is strictly a natural focal infection. This means that the pathogen constantly circulates in certain territories between vectors and reservoir hosts.
Reservoirs and vectors Ixodid ticks, as well as wild and domestic animals, act as the main reservoir of the virus in nature. The infection is characterized by pronounced spring-summer seasonality, coinciding with the period of maximum tick activity (for example, starting in May, when people massively travel to country houses and forest areas).
Mechanisms and routes of transmission:
- Transmissible route: implemented directly when an infected tick attaches to a human.
- Alimentary route: infection occurs when consuming unboiled goat's or cow's milk from infected animals.
An interesting epidemiological feature is the phenomenon of natural immunization of the population permanently residing in natural foci. This occurs due to repeated contacts with small doses of the virus that do not cause a full-blown clinical picture.
Statistics and medico-social significance
Annually, from 4,000 to 10,000 cases of tick-borne encephalitis are officially registered on the territory of the Russian Federation. However, the actual number of infected individuals significantly exceeds these figures. Hidden morbidity is formed due to mild and aborted forms of the infection, which often remain undiagnosed because patients do not seek medical help or the disease proceeds under the guise of a common ARVI.
Particular attention of the healthcare system to the problem of TBE is due to high mortality rates in severe courses, the risk of developing dangerous complications, and the formation of persistent neurological disorders (sequelae), such as paresis and paralysis, after recovering from the disease. Patients with suspected TBE require careful transportation strictly on a stretcher at the pre-hospital stage and mandatory hospitalization in an infectious diseases or neurological department.
Taking an epidemiological history (Anamnesis epidemica)
To make a correct diagnosis, the doctor needs to take a thorough epidemiological history, taking into account the endemicity of the region (for example, the forest areas of the Yaroslavl Oblast).
Key questions when taking an epidemiological history:
- Were there cases of tick attachment and subsequent removal (including self-removal)?
- Did the patient consume unboiled cow's or goat's milk?
- What is the health status of other family members who were with the patient in the endemic zone?
- Has the patient previously had tick-borne encephalitis?
- Is there a vaccination against TBE (vaccination status)?
- Was emergency prophylaxis (administration of specific immunoglobulin) performed after the bite?
- Does the patient have pets that could have brought a tick into the house?
Briefly: answers to topical questions
Which species of ixodid ticks are the main vectors of tick-borne encephalitis?
The main vectors of tick-borne encephalitis are two species of ixodid ticks:
- Taiga tick (Ixodes persulcatus).
- European castor bean tick (Ixodes ricinus).
Despite the fact that the virus has been detected in 14 species of ticks, human infection is almost always associated with these two species.
What clinical forms of tick-borne encephalitis are distinguished in the classification?
The clinical classification of acute tick-borne encephalitis distinguishes the following forms:
- Febrile
- Meningeal
- Meningoencephalitic
- Poliomyelitic
- Polyradiculoneuritic
Acute TBE is also classified by the number of temperature waves (single-wave and two-wave). Chronic tick-borne encephalitis is divided into:
- Primary progressive form
- Secondary progressive form
- Subacute form
In addition, forms of the course of the infectious process (acute, chronic, subclinical/latent) and severity (mild, moderate, severe) are distinguished.
Within what timeframe and in what doses is emergency prophylaxis with specific immunoglobulin carried out?
Emergency prophylaxis is carried out with tick-borne encephalitis immunoglobulin.
Timing of administration:
- sources indicate: strictly in the first 72 hours after tick attachment;
- it is also indicated: up to 4 days inclusive after the bite of a presumably infected tick.
Modern standard: test the removed tick for TBE virus antigens as quickly as possible using ELISA or PCR methods; administer the immunoglobulin injection only after the virus is detected in the tick.
Dosage and administration:
- 0.1 ml/kg;
- intramuscularly;
- once.
For quick memorization of transmission routes, remember the rule of the "Two C's": Blood-sucking (tick bite) and Cow's/Goat's milk (unboiled).
Class and exam questions
Why is the official TBE morbidity statistics in the Russian Federation underestimated compared to the real numbers?
The actual number of cases is significantly higher than the official 4,000–10,000 due to mild and abortive forms of infection that go unnoticed and undiagnosed.
Can you contract tick-borne encephalitis without a tick bite?
Yes, transmission is possible via the alimentary route through the consumption of raw (unboiled) goat's or cow's milk from an infected animal.
Which departments admit patients with suspected tick-borne encephalitis?
The patient must be hospitalized in a specialized infectious disease or neurological department.
What else to study on this topic
- Pathogenesis: entry portal, pathways of viral dissemination, and morphological changes in brain tissue.
- Clinical manifestations: encephalitic, meningeal, and intoxication syndromes, chronic forms.
- Differential diagnosis with Ixodes borreliosis (Lyme disease), ehrlichiosis, and leptospirosis.
- Specific treatment: administration of homologous immunoglobulin.
- Laboratory diagnosis: ELISA of serum and CSF for IgM antibodies and viral antigens, PCR.
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