Taiga encephalitis how infection occurs. Taiga encephalitis

Tick-borne encephalitis (spring-summer type encephalitis, taiga encephalitis) is a viral infection that affects the central and peripheral nervous system. Severe complications of acute infection can result in paralysis and death.

The main carriers of the encephalitis virus in nature are ixodid ticks, whose habitat is located throughout the forest and forest-steppe temperate climatic zone of the Eurasian continent. Despite a significant number of species of ixodid ticks, only two species are of real epidemiological significance: Ixodes persulcatus ( taiga tick) in the Asian and in some areas of the European part, Ixodes Ricinus ( European wood tick) - in the European part.

Tick-borne encephalitis is characterized by a strict spring-summer seasonality of the onset of the disease, associated with the seasonal activity of carriers. In the range of I. persulcatus, the disease occurs in spring and the first half of summer (May-June), when the biological activity of this tick species is highest. For ticks of the species I. Ricinus, there is an increase in biological activity twice per season, and in the range of this tick, 2 peaks of the seasonal incidence of tick-borne encephalitis are characteristic: in spring (May-June) and at the end of summer (August-September).

infection human tick-borne encephalitis virus occurs during the blood-sucking of virusophoric ticks. The blood-sucking of the female tick continues for many days, and when fully saturated, it increases in weight 80-120 times. Bloodsucking of males usually lasts several hours and may go unnoticed. Transmission of the tick-borne encephalitis virus can occur in the first minutes of a tick sticking to a person. Infection through the digestive and gastrointestinal tracts is also possible when ingesting raw milk from goats and cows infected with tick-borne encephalitis.

Signs of tick-borne encephalitis. The incubation period of tick-borne encephalitis lasts an average of 7-14 days with fluctuations from one day to 30 days. Transient weakness in the limbs, neck muscles, numbness of the skin of the face and neck are noted. The disease often begins acutely, with chills and fever up to 38-40°C. The fever lasts from 2 to 10 days. There are general malaise, severe headache, nausea and vomiting, weakness, fatigue, sleep disturbances. In the acute period, hyperemia (overflow of the blood vessels of the circulatory system of any organ or area of ​​the body) of the skin of the face, neck and chest, the mucous membrane of the oropharynx, injection of the sclera and conjunctiva is noted.

Pain all over the body and limbs. Muscle pains are characteristic, especially significant in muscle groups, in which paresis (partial loss of muscle strength) and paralysis usually occur in the future. From the moment of the onset of the disease, there may be clouding of consciousness, stupor, the intensification of which can reach the degree of coma. Often, erythema of various sizes (reddening of the skin caused by capillary expansion) appears at the site of tick suction.

If symptoms of tick-borne encephalitis are detected, the patient should be urgently placed in an infectious diseases hospital for intensive treatment.

Treatment patients with tick-borne encephalitis is carried out according to general principles, regardless of previous preventive vaccinations or the use of specific gamma globulin (a drug containing antibacterial and antiviral antibodies) for prophylactic purposes.

In the acute period of the disease, even in mild forms, patients should be prescribed bed rest until the symptoms of intoxication disappear. Almost complete restriction of movement, gentle transportation, minimization of pain irritations improve the prognosis of the disease. No less important role in the treatment is the rational nutrition of patients. The diet is prescribed taking into account functional disorders of the stomach, intestines, liver.

Taking into account the violations of vitamin balance observed in a number of patients with tick-borne encephalitis, it is necessary to prescribe vitamins of groups B and C. Ascorbic acid, which stimulates the function of the adrenal glands, as well as improves the antitoxic and pigmentary functions of the liver, should be administered in an amount of 300 to 1000 mg per day.

Prevention of tick-borne encephalitis

The most effective defense against tick-borne encephalitis is vaccination. Clinically healthy people are allowed to be vaccinated after examination by a therapist. You can only get vaccinated in institutions licensed for this type of activity.

Modern vaccines contain an inactivated (killed) tick-borne encephalitis virus. After the vaccine is administered, the immune system recognizes the viral antigens and learns to fight the virus. Trained cells of the immune system begin to produce antibodies (immunoglobulins) that block the development of the virus that has entered the body. To maintain a protective concentration of immunoglobulin for a long time, it is necessary to administer several doses of the vaccine.

The effectiveness of vaccination can be assessed by the concentration of protective antibodies in the blood (IgG to tick-borne encephalitis virus).

Tick-borne encephalitis vaccines registered in Russia:
- Tick-borne encephalitis vaccine cultured purified concentrated inactivated dry - for children over 4 years of age and adults.
- EnceVir - for children over 3 years old and adults.
- FSME-IMMUNE Injection - from 16 years old.
- FSME-IMMUNE Junior - for children from 1 to 16 years old. (Children should be vaccinated during their first year of life if they are at risk of contracting tick-borne encephalitis.)
- Encepur adult - from 12 years old.
- Enzepur for children - for children from 1 to 11 years old.

The above vaccines differ in virus strains, antigen dose, degree of purification, and additional components. According to the principle of action, these vaccines are the same. Imported vaccines are able to develop immunity to Russian strains of tick-borne encephalitis virus.

Vaccination is carried out after the end of the tick season. In most regions of Russia, it is possible to be vaccinated from November. However, in case of urgent need (for example, if you have to travel to a natural focus of tick-borne encephalitis), you can get vaccinated in the summer. In this case, the protective level of antibodies appears after 21-28 days (depending on the vaccine and the vaccination schedule).

Immunity appears two weeks after the second dose, regardless of the type of vaccine and the chosen regimen. The third dose is administered to consolidate the result. Emergency schemes are not designed to protect after a tick bite, but to develop immunity as quickly as possible if the standard vaccination deadlines were missed.

Local side reactions include: redness, induration, soreness, swelling at the injection site, urticaria (an allergic rash resembling that of a nettle burn), an increase in lymph nodes nearby the injection site. Usual local reactions are observed in 5% of those vaccinated. The duration of these reactions can be up to 5 days.

Common post-vaccination reactions include a rash covering large areas of the body, fever, anxiety, sleep and appetite disturbances, headache, dizziness, short-term loss of consciousness, cyanosis, cold extremities. The frequency of temperature reactions to Russian vaccines does not exceed 7%.

If a tick is bitten, it should be removed immediately. It should be borne in mind that the probability of contracting tick-borne encephalitis depends on the amount of virus that enters during the “bite” of the tick, that is, on the time during which the tick was in a sucking state. If you do not have the opportunity to seek help from a medical institution, then the tick will have to be removed on your own.

When removing a tick yourself, the following recommendations should be observed:

A strong thread as close as possible to the proboscis of the tick is tied into a knot, the tick is removed by pulling it up. Sharp movements are not allowed.

If, when removing the tick, its head came off, which looks like a black dot, the suction site is wiped with cotton wool or a bandage moistened with alcohol, and then the head is removed with a sterile needle (previously calcined on fire). Just like a normal splinter is removed.

Removal of the tick must be done with caution, without squeezing it, since this may squeeze out the contents of the tick, along with pathogens, into the wound. It is important not to break the tick when removed - the remaining part in the skin can cause inflammation and suppuration. At the same time, it should be taken into account that when the tick head is torn off, the infection process can continue, since a significant concentration of the TBE virus is present in the salivary glands and ducts.

There are no grounds for some recommendations that, for better removal, it is recommended to apply ointment dressings to the sucking tick or use oil solutions.

After removing the tick, the skin at the site of its suction is treated with tincture of iodine or alcohol. Bandaging is usually not required.

After removing the tick, save it for testing for infection - usually such a test can be done in an infectious diseases hospital. After removing the tick, place it in a small glass bottle with a tight lid and put a piece of cotton wool slightly moistened with water. Close the bottle with a cap and store it in the refrigerator. For microscopic diagnosis, the tick must be delivered to the laboratory alive.

The material was prepared on the basis of information from open sources

Encephalitis is an inflammatory disease of the central nervous system, or rather a group of diseases that are characterized by virus damage to the substance of the brain or spinal cord, fever, intoxication, paralysis. Perhaps the most famous is tick-borne encephalitis - a disease that, despite the rapid progress of medicine, requires complex and lengthy treatment and still poses a great danger to the life of an infected person.

It is much easier to prevent infection - therefore it is worth knowing who is the carrier of encephalitis and how exactly the virus is transmitted. We will consider these questions.

How is tick-borne encephalitis transmitted?

The encephalitis virus is carried by a tick, which in turn is infected from infected animals, on whose blood it feeds. The tick carries the virus throughout its life, becoming its carrier to people.

Interestingly, a wild animal that carries the encephalitis pathogen does not suffer from the virus. In the taiga, where tick-borne encephalitis is widespread, animals in the course of a long evolution have fully adapted to the virus, as, for example, African species to diseases transmitted by the tsetse fly.

Who can get encephalitis from?

Ticks are a very widely represented subclass of animals, there are tens of thousands of species, but only a few of them are dangerous to humans. To avoid danger, you need to remember well which tick carries encephalitis and what it looks like.

Different subtypes of tick-borne encephalitis virus carry ixodid ticks:

• taiga tick(Far Eastern, Siberian subtype)

• Dog Tick(European EC subtype)

The Far Eastern subtype is the most dangerous, it is characterized by the highest mortality rate.

By the way, not everyone knows that you can get encephalitis not only through a tick bite, but also from the previous carrier of the encephalitis pathogen - through raw goat and cow milk. Such cases are very rare, but do not ignore this information! Especially considering that, unlike a tick bite, you can completely control and easily prevent the risk of infection through milk. Outside the body of the carrier, the virus is no longer so tenacious, and is completely destroyed if the milk is boiled.

Be vigilant and attentive, study the epidemiological situation in your area, and your outdoor recreation will not be spoiled by the fear of encountering ticks.

Update: December 2018

Tick-borne encephalitis is a viral disease, the causative agent of which is transmitted to a person with ticks, characterized by natural foci of infection and a certain seasonality associated with the activity of ticks.

The causative agent of pathology is an RNA virus from the genus Flaviviruses. The disease has many names: taiga encephalitis, spring-summer encephalitis, Russian Far Eastern encephalitis.

In what countries and localities does the pathology occur?

You can get sick with tick-borne encephalitis in some regions of Russia (Urals, Siberia, the European part), Kazakhstan, Mongolia, China, Japan, Korea, the Baltic countries, Sweden, Germany, Norway, Denmark, Poland, Ukraine, France, Romania, Belarus and others.

How does infection occur?

The main source of infection in nature are ixodid ticks (see also). It is in their body that the virus multiplies and matures.

• And the ticks themselves receive the pathogen from wild animals (hares, squirrels, chipmunks, hedgehogs), domestic animals (goats, sheep) and some birds (woodpecker, black grouse, capercaillie, hazel grouse).
• The peak incidence occurs in May-June, when ticks become especially aggressive and attack people. Persons of such professions as hunters, huntsmen, geologists, lumberjacks and others, as well as tourists, fall into the risk group.
• You can also pick up a tick while relaxing in the forest.
• The virus is in the body of the tick for life, can be transmitted to offspring.
• The virus enters the human body when a tick bites with its saliva or when ticks are rubbed into the skin (for example, when a person combs and damages the skin).
• Another important route of invasion is food. The causative agent of the disease can enter the body when drinking contaminated unboiled milk or its products (cheese, cottage cheese).
• There are also known cases of infection of laboratory assistants who examined the infected material, pathologists, biologists, virologists, epidemiologists.
• The pathology is not transmitted from person to person.

Why is nerve tissue affected?

The virus that causes this disease has a tropism (traction, desire) for the nervous tissue. It multiplies in the cells of the gray matter and vessels of the brain and spinal cord, spinal ganglia and cerebrospinal fluid. Then, after a couple of days, the viruses enter the blood en masse and spread to all organs and tissues.

Classification

Currently, there are 5 main variants of the virus:

• Western (Central European)
• Far Eastern
• Greek-Turkish
• East Siberian
• Ural-Siberian

This separation is associated with a mutation of the RNA of the pathogen. The clinical picture of these types is also different. It is believed that the western and Greek-Turkish variants proceed with a milder course, less often lead to lethality. Oriental, on the contrary, more often lead to paralysis and death.

How is the disease progressing?

The incubation period (the time from the moment of infection to the appearance of the first symptoms) is approximately 10-14 days. This period can be lengthened in people who received it in childhood.

The first signs of the disease (what you should pay attention to): usually a week after outdoor recreation, a person suddenly has a headache, nausea, vomiting that does not bring relief, severe weakness.

Then cerebral symptoms join: paralysis of the extremities, strabismus, pain along the nerve endings, convulsions, (see).

Tick-borne encephalitis has several clinical forms:

• erased;
• polyradiculoneuritic;
• meningeal;
• two-wave;
• feverish;
• meningoencephalitic.

How to recognize the form of tick-borne encephalitis by symptoms:

	feverish (15-40% of all cases)	Meningeal (30-70% of cases)	Meningoencephalitic (in 10-30%)
Tick ​​bite site	Absent, pain at the site of the bite.
Start	Sharp, sudden. Body temperature rises to 38-39C vomiting, nausea, chills headache increased weakness.	Acute sudden onset. Intense headache, vomiting that does not bring relief. Awesome chills. Severe general weakness, anorexia.
Muscle damage	Pain in the muscles of the neck, back, waist. Fibrillar twitching of muscles. Numbness of limbs.	None.	None.
Symptoms of CNS damage	None.	From the 2-3rd day of the illness, the symptom of Kernig, Brudzinsky, "tripod" appears. The consciousness is confused, the patient is agitated, then inhibited.	From the first hours of the disease, meningeal signs (rigidity of the neck muscles), hallucinations, delirium, and convulsive seizures occur. Consciousness is impaired up to a deep coma. Speech disorders. Swallowing disorder, tongue atrophy.
Duration	The fever usually lasts for a week.		The fever persists for up to two weeks.
	None.		Pain along the nerve trunks. Cerebellar disorders (staggering gait). Pathological reflexes. Signs of damage to the cranial nerves. Paralysis of the limbs. The development of strabismus.
Appearance of the patient		The face and upper half of the body are purple-red. The sclera are injected.
Outcome of the disease	This form of encephalitis is characterized by a favorable outcome, a fairly quick recovery.	The outcome is favorable, but residual symptoms may persist for several months.	The most severe form, the outcome is doubtful. In most cases, life-threatening complications (cerebral edema, epilepsy) occur.

	Polio or typical	Polyradiculoneuritis	Two-wave, "milky"
Tick ​​bite site	The area is reddened, swollen. Nearby lymph nodes are enlarged. There is no itching, pain at the site of the bite.
Start	Gradual (appears weakness, numbness in the limbs). Then the temperature rises, vomiting, headache, nausea join.		The first wave resembles a feverish form. Then comes the interfebrile period (up to two weeks). The second wave is heavier and longer than the first.
Muscle damage	Intense muscle pain in the neck, neck, upper and lower extremities, buttocks. Due to the resulting weakness of the neck muscles, a symptom of a “hanging head”, “pterygoid shoulder blades” occurs.		The disease proceeds according to the meningoencephalitic or poliomyelitis type. This form occurs more often when drinking raw milk, therefore it is accompanied by diarrhea, flatulence, enlargement of the liver and spleen, and abdominal pain.
Duration	The fever persists for up to two weeks.
Symptoms of CNS damage	The cells of the spinal cord are predominantly affected, so the patient develops atony and muscle atrophy, prolapse of tendon reflexes. Damage to the diaphragm and intercostal muscles can lead to respiratory arrest.	None.
Appearance of the patient	Red face, sclera and mucous membranes are injected
Symptoms of peripheral nerve damage	Flaccid paresis and paralysis of the limbs. Symptom of "torticollis". Lack of temperature, pain and other types of sensitivity in the limbs.	Numbness, crawling, or hypersensitivity. Burning, pain along the nerve fibers. The appearance of symptoms of sciatica.
Outcome of the disease	It usually ends well. Up to six months, flaccid paralysis can persist.

The disease usually ends in recovery. The death of the patient occurs in 5-10% of cases.

During the recovery period after an illness, the following may persist for a long time (3-4 months):

• general weakness,
• sleep and memory disturbances,
• reduced intelligence,
• paresis of the extremities with muscle atrophy.
• Sometimes paralysis can be persistent, and even progress over time.
• In some cases, cosmetic defects also persist (facial asymmetry, torticollis, strabismus).

What complications should be feared?

• edema-swelling of the brain, followed by respiratory arrest and death. It can develop on about 4-6 days of illness;
• hemorrhage in the brain against the background of complete well-being;
• gastrointestinal bleeding in the "milk" form;
• the development of Kozhevnikov epilepsy, which persists for life;
• infectious-toxic;
• malignant paralysis of the Landry type.

How to identify pathology?

Diagnosis can be made based on a confirmed tick bite. Confirm the disease using special diagnostic methods:

Research method	What reveals?
General blood analysis	From the first days of the disease, an increase in leukocytes (more precisely, neutrophils), a decrease or absence of lymphocytes are revealed. ESR is moderately increased. During the period of fever, a decrease in the number of platelets and red blood cells is possible.
General urine analysis	Moderate proteinuria (the appearance of protein in the urine), cylindruria (cylinders in the urine).
Spinal puncture	The cerebrospinal fluid is clear or opalescent, fibrin film falls out. Increase in the number of lymphocytes (up to 500 cells), protein. The concentration of glucose and chlorides remains normal. Weakly positive Pandey and Nonne-Apelt reactions. Changes in the cerebrospinal fluid can persist for quite a long time (up to six months) after recovery.
Electroencephalogram	It is prescribed to clarify the depth of damage to higher nervous activity, with the development of convulsive syndrome, Kozhevnikov epilepsy.
CT or MRI of the brain	These methods are recommended for the development of complications (cerebral edema, cerebral hemorrhage).
ECHO-KG	It is prescribed to confirm infectious-toxic myocarditis, heart rhythm disturbances of central origin.
Virological method	Based on the isolation of viruses from the blood, cerebrospinal fluid. The information content of the study is low, about 40%.
Express diagnostics (ELISA, RNGA, RSK, RTGA)	A fairly quick method that allows you to make a preliminary diagnosis. It is based on the detection of specific antiviral antibodies.
PCR	The examination is based on the detection of viral RNA in the blood, cerebrospinal fluid, dairy products, ticks themselves, and infected animals.

What should I do if bitten by a tick?

If a tick has invaded human skin, it should be removed in a medical facility. It is not recommended to do this on your own, as you can damage his body and not completely extract it. In the case when there are no hospitals nearby, but you need to urgently remove the tick, you need to do the following:

• the skin is abundantly lubricated with petroleum jelly or oil (to stop the flow of oxygen to the tick)
• then it is grasped with tweezers and carefully rotated counterclockwise is removed from the human skin
• after extraction, it is necessary to go to the hospital on the first day after the bite for vaccination - a specific donor immunoglobulin is injected intramuscularly in 3 ml.

Treatment

All sick people are necessarily hospitalized in a hospital (infectious or neurological department)! They are shown strict bed rest. Patients should be in intensive care units or under the constant supervision of medical personnel due to the unpredictability of the pathology. With the development of complications, patients are transferred to the intensive care unit.

Medical treatment

• etiotropic therapy (aimed directly at the destruction of the pathogen) - specific donor immunoglobulin, homologous donor polyglobulin, leukocyte donor interferon, reaferon, laferon, intron-A, neovir, etc .;
• infusion therapy - with solutions of glucose, Ringer, trisol, Sterofundin;
• antipyretic drugs - infulgan. It is forbidden to use acetylsalicylic acid because of possible complications on the liver;
• glucocorticosteroids (methylprednisolone, prednisolone) - drugs of this group prevent damage to the brain and spinal cord, reduce their swelling;
• anticonvulsant therapy - sodium oxybutyrate, magnesium sulfate, sibazon;
• decongestants - mannitol, furosemide, l-lysine aescinate;
• neurotrophics - complex vitamins of group B (neurorubin,);
• substances that improve microcirculation in the brain - thiotriazoline, trental, dipyridamole,;
• hyperbaric oxygenation.

During the recovery period, physical therapy procedures, therapeutic massage, and sessions with a rehabilitator are shown.

How to protect yourself from tick bites?

The virus can remain active in the external environment in the cold for a long time (at -60 C it can persist for decades), but high temperatures are its weak point. It dies after a couple of minutes when boiled. Therefore, it is very important to boil milk, not to consume untested dairy products.

If, by virtue of your profession, you must stay in the forest or are on vacation, to protect yourself from ticks, you should:

• wear close-fitting clothing
• apply special repellents
• carefully inspect the skin when leaving the forest

In the end, I would like to add that tick-borne encephalitis is a fairly serious disease. If during your stay in the forest (especially in an epidemiologically disadvantaged area) you were attacked by a tick, and then after some time you developed a fever for no reason, you should immediately consult a doctor. The earlier treatment is started, the greater the likelihood of a favorable outcome and full recovery.

- (encephalitis acarinarum orientalis; synonym: Far Eastern encephalitis, Russian spring-summer encephalitis, taiga encephalitis, endemic spring encephalitis) acute viral natural focal infectious disease with transmissible (through ixodic ... ... Big Medical Dictionary

Tick-borne encephalitis- (syn.: taiga encephalitis, spring-summer encephalitis) - an acute viral disease characterized by damage to the gray matter of the brain and spinal cord with the development of paresis and paralysis. The causative agent is arbovirus. It is thermolabile, sensitive to ... ...

See Tick-borne encephalitis spring-summer ... Big Medical Dictionary

Tick-borne encephalitis, spring-summer, taiga- Caused by neurotropic viruses from the group of arboviruses. The carriers and keepers of the infection are ixodid ticks. The incubation period after a bite by an infected tick is from 2 to 20 days, more often from 7 to 14 days, with alimentary infection - from ... ... Encyclopedic Dictionary of Psychology and Pedagogy

FAR EAST ENCEPHALITIS- (taiga, spring-summer, tick-borne, Russian encephalitis) - naturally focal neuroinfection. The disease began to be registered since 1932 in connection with the development of the taiga zone of the Far East. In 1935, A. G. Panov established her nosological independence and ... ... Encyclopedic Dictionary of Psychology and Pedagogy

Same as tick-borne encephalitis. * * * TAIGA ENCEPHALITIS TAIGA ENCEPHALITIS, the same as tick-borne encephalitis (see Tick-borne encephalitis) ... encyclopedic Dictionary

Tick-borne encephalitis: infection, signs and methods of protection- Tick-borne encephalitis (spring-summer-type encephalitis, taiga encephalitis) is a viral infection that affects the central and peripheral nervous system. Severe complications of acute infection can result in paralysis and death. ... ... Encyclopedia of newsmakers

- (taiga, spring-summer encephalitis), an acute viral disease with pronounced natural foci. Characterized by brain damage with the development of paralysis. The source of the virus is various animals, the carrier is a tick. Serotherapy is used. * * * … encyclopedic Dictionary

- (taiga spring-summer encephalitis), an acute viral disease with pronounced natural foci. Characterized by brain damage with the development of paralysis. The source of the virus is various animals, the carrier is a tick. Serotherapy is used... Big Encyclopedic Dictionary

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Disease code A84.0 (ICD-10)

Syn. : tick-borne encephalitis, taiga encephalitis, Russian Far Eastern encephalitis, spring-summer meningoencephalitis, tick-borne encephalomyelitis, etc.

Tick-borne encephalitis (encephalitis acarina) is a viral natural focal transmissible disease with a primary lesion of the central nervous system.

Three nosogeographic variants of the disease are known - eastern, western and two-wave (two-wave milk fever), which differ in a number of clinical and epidemiological parameters.

Historical information

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Severe diseases accompanied by damage to the central nervous system and leading to high mortality began to be noted, starting from 1932, in a number of regions of the taiga zone of the Far East. In 1935 A.G. Panov established the clinical independence of the disease, attributed it to encephalitis B. Complex expeditions of the People's Commissariat of Health of the USSR, led by L.A. Zilber, E.N. Pavlovsky, A.A. Smorodintsev, I.I. strains of encephalitis pathogens, established the role of ixodid ticks as carriers of viruses, studied in general terms the epidemiological features of the infection, its clinical manifestations, pathomorphology, developed methods for specific prevention and treatment of the disease. In 1951–1954 A.A. Smorodintsev, M.P. Chumakov and others in the western regions of the USSR described a peculiar nosogeographic form of tick-borne encephalitis - two-wave milk fever (Independence of two-wave milk fever, established by A.A. Smorodintsev in 1951–1955, is currently time is questioned by many researchers).

Etiology

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The causative agent of tick-borne encephalitis belongs to the complex of tick-borne encephalitis viruses of the genus Flavivirus, family Togaviridae, ecological group Arboviruses. Viruses have the form of round particles 25–40 nm in size, contain RNA surrounded by a protein coat. The introduction of viral RNA into animals in an experiment causes them a disease similar to that caused by a complete virus. There are eastern ("persulcate") and western ("ricinus") antigenic variants of viruses that cause various nosogeographic forms of tick-borne encephalitis.

The virus is cultivated in chicken embryos and cell cultures of various origins.

Of the laboratory animals, white mice, suckling cotton rats, hamsters, monkeys are most susceptible to the virus, and of domestic animals, sheep, goats, piglets and horses.

Sustainability . The tick-borne encephalitis virus has varying degrees of resistance to environmental factors: when heated to 60 ° C, it dies after 10 minutes, and when boiled, after 2 minutes. The virus is rapidly destroyed by ultraviolet irradiation, exposure to Lysol and chlorine-containing drugs.

Antigenic properties tick-borne encephalitis viruses differ from the properties of other arboviruses, which is used for serological identification of tick-borne encephalitis.

Epidemiology

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Tick-borne encephalitis is a transmissible natural focal infection.

Main reservoirs and carriers pathogens are ixodid ticks Ixodes persulcatus, which prevail in the eastern regions of Russia, and Ixodes ricinus, which lives mainly in the western regions of Russia and a number of European countries, as well as some other types of ixodid and gamasid ticks. 5–6 days after bloodsucking on an infected animal, the virus penetrates into all organs of the tick, concentrating in the reproductive apparatus, intestines, salivary glands, persists throughout the life of the arthropod (2–4 years), which determines the mechanism of infection of animals and humans and transovarial and transphase transmission of the virus in ticks. In various foci of the disease, tick infection reaches 1-3%, and in some years - 15-20%. %.

Additional tanks tick-borne encephalitis viruses are about 130 species of rodents and other wild mammals - "hosts" of ticks: hedgehogs, moles, squirrels, chipmunks, voles, shrews, etc., as well as some birds: hazel grouse, nuthatch, finches, blackbirds, etc.

Mechanism of infection . Virus carriers are ixodid ticks. A person most often becomes infected with tick-borne encephalitis in a transmissible way through the bite of a virusophoric tick; the probability of infection increases with the duration of bloodsucking. Crushing mites during removal and introducing viruses to the mucous membranes of the eye or damaged areas can also lead to infection in vivo and laboratory conditions. There is an alimentary way of human infection with tick-borne encephalitis by eating raw goat or cow's milk.

The habitat of the main reservoirs of viruses determines the boundaries of the foci of infection.

There are three types of foci of the disease:

• Type I - natural foci in the wild;
• Type II - transitional foci with a modified composition of biocenosis components as a result of human economic activity;
• Type III - anthropourgical (secondary) foci in areas near settlements, where, in addition to rodents, domestic animals also become hosts for ticks. Depending on biotic and abiotic factors, 7 groups of focal regions are distinguished. Foci of tick-borne encephalitis are known in the taiga zone of the Far East, in the forest regions of Siberia, the Urals, East Kazakhstan, the European part of Russia, the Czech Republic, Slovakia, Bulgaria, Austria, Venfia, Poland, Sweden, and Finland.

seasonality. The incidence of tick-borne encephalitis is seasonal, reaching a maximum in May-June. The second, less pronounced increase in the incidence is observed in late summer - early autumn, due to the number and activity of ticks in nature.

Pathogenesis and pathological anatomical picture

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The entrance gate of infection in transmissible infection is the skin, and in alimentary - the mucous membrane of the digestive tract.

After replication in the area of ​​the entrance gate, the virus disseminates hematogenously and lymphogenously to the lymph nodes, internal organs and reaches the central nervous system, where it has a direct effect on nerve cells and induces a mesenchymal-inflammatory reaction that enhances the pathogenic effect of the virus. With alimentary infection, a visceral phase with viremia and virus replication in the internal organs is observed first, and then secondary viremia occurs with damage to the central nervous system (two-wave meningoencephalitis). In some cases, the process takes a chronic progressive course with the progression of morphological damage.

The pathological process involves the gray matter of the brain and spinal cord, especially the motor neurons of the spinal cord and brain stem. There is damage to the nervous tissue in the midbrain, thalamic and hypothalamic regions, in the cerebral cortex and cerebellum. In the roots of the peripheral nerves, a picture of interstitial neuritis develops. Naturally, the soft membranes of the brain are damaged.

At autopsy, swelling of the meninges and brain substance, expansion and plethora of blood vessels, hemorrhages, signs of impaired CSF and hemodynamics are often found. Already in the early, pre-paralytic phase of the disease, microglial proliferation, the phenomenon of neurophagy, are noted. The most pronounced necrobiotic processes develop in the anterior horns of the cervical spinal cord, in the nuclei of the cranial nerves, and in the reticular substance.

The plethora of internal organs is usually noted, hemorrhages in the serous membranes, the mucous membrane of the stomach, respiratory tract, and intestines are not uncommon.

In the acute course of the process, slow repair of damage is observed and stable immunity is formed. Violations of the immune status determine the steadily progressive course of the disease with persistent irreversible paresis and paralysis.

Clinical picture (Symptoms)

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The incubation period lasts 3–21 days, with an average of 10–14 days.

Flow phases tick-borne encephalitis

• Initial phase occurring with a predominance of general toxic syndrome,
• Phase of neurological disorders, characterized by various variants of lesions of the central and peripheral nervous system,
• Outcomes phase(recovery with gradual recovery or preservation of residual neurological disorders, the formation of progressive chronic variants or the death of patients).

Forms tick-borne encephalitis

Depending on the depth and severity of neurological disorders, the following forms of the disease are distinguished:

• feverish,
• meningeal
• meningoencephalitic,
• meningoencephalopoliomyelitis,
• polyradiculoneuritis.

Feverish and meningeal forms are the main ones in western variants of tick-borne encephalitis, paralytic forms predominate in the eastern variant of the disease.

Types of tick-borne encephalitis

According to the severity of the clinical picture of the disease, the following types of tick-borne encephalitis are distinguished:

1) a disease with an abortive course(or mild illness), fever within 3–5 days, transient signs of serous meningitis, and recovery within 3–5 weeks;

2) diseases of moderate severity occurring with meningeal and cerebral symptoms that have benign dynamics with recovery within 1.5–2 months;

3) heavy molds with high mortality, protracted and incomplete recovery, persistent residual signs in the form of paresis, paralysis, muscle atrophy.

known lightning forms diseases ending fatally on the first day of the disease even before the development of a characteristic clinical picture, as well as chronic and recurrent forms of tick-borne encephalomyelitis.

In 8–15% of cases, a short prodrome is observed: headache, weakness, fatigue, sleep disturbance, radicular pain, numbness in the skin of the face or trunk, and mental disorders.

The disease usually develops acutely, suddenly . There is a high fever with a rise in temperature to 39-40.5 ° C lasting 3-12 days, fever, chills, excruciating headache, aching pain in the limbs, lumbar region, nausea, repeated vomiting, general hyperesthesia, photophobia, eye pain apples.

Usually, from the 3-4th day, and sometimes in the first hours of the disease, signs of focal CNS damage are observed: paresthesia, paresis of the extremities, diplopia, epileptiform convulsions. Consciousness in the first days of the disease is preserved, but the patients are inhibited, indifferent to the environment, drowsy. Stupefaction, delirium are occasionally observed, stupor and coma are possible.

In the acute period the face of the patients is hyperemic, the vessels of the sclera and conjunctiva are injected, there is hyperemia of the skin of the neck and chest. Characterized by bradycardia, muffled heart tones, arterial hypotension. Electrocardiographic signs of conduction disturbance, persistent but reversible signs of myocardial dystrophy are revealed. Severe myocardial dystrophy can cause the development of acute heart failure in patients, leading to a fatal outcome of the disease.

Hyperemia of the mucous membrane of the upper respiratory tract, shortness of breath, shortness of breath are often noted. Quite often early and late pneumonia come to light; the latter, occurring against the background of a violation of the central regulation of respiration and blood circulation, are unfavorable prognostically.

Characterized by changes in the digestive system in the form of tongue lining, while often there is a tremor of the tongue, bloating and stool retention. In cases of alimentary infection, hepatolienal syndrome is often noted.

In the acute period, neutrophilic leukocytosis (up to 10.0–20.0 * 10^9 / l), an increase in ESR, hypoglycemia, and transient proteinuria are observed.

• Febrile form of tick-borne encephalitis characterized by a benign course and is limited to the development of general toxic syndrome.
• meningeal form proceeds benignly with the development of general toxic syndrome and signs of serous meningitis.

Characterized by the occurrence of high fever, severe headache in the parieto-occipital region, aggravated by movement, repeated vomiting at the height of the headache, photophobia, hyperacusis and hyperesthesia of the skin, uneven tendon reflexes. From the first days of the disease, shell symptoms are revealed: stiff neck muscles, symptoms of Kernig, Brudzinsky, etc., which persist for 2–3 weeks. Some patients may experience transient encephalitic symptoms.

In the study of cerebrospinal fluid - an increase in its pressure to 200–400 mm of water column, moderate lymphocytic pleocytosis, a slight increase in the level of protein, glucose and chlorides.

• Meningoencephalitic form The disease is characterized by the development of diffuse or focal lesions of the brain.
• With diffuse tick-borne meningoencephalitis, in addition to general toxic and meningeal symptoms, a violation of the consciousness of patients from mild lethargy to deep stupor and coma is detected early.

With a favorable prognosis, consciousness clears up after 10–12 days, but drowsiness persists. In some patients in the acute febrile period, delirium, hallucinosis, psychomotor agitation with loss of orientation in time and environment are observed. In the first days of the disease, movement disorders are noted in the form of partial or generalized single or multiple epileptiform seizures, which usually worsens the prognosis. Fibrillar twitching of the muscles of the face and extremities, hand tremors, depression of deep reflexes, and a decrease in muscle tone are often observed.

• With focal meningoencephalitis clinical manifestations are determined by the zone of damage to the central nervous system.

The defeat of the white matter of one of the hemispheres of the brain entails the occurrence of spastic paresis of the right or left limbs and paresis of the facial and hypoglossal nerves on the same side. When the process is localized in the left hemisphere, a speech disorder also occurs.

Damage to the white matter in the brainstem leads to the development of paresis of the cranial nerves on the side of the focus of inflammation and paresis of the extremities on the opposite side of the body (alternating syndrome). In the period of convalescence, motor disorders are restored within 2-3 months.

Along with symptoms of loss of motor functions, hyperkinesias can be observed in the form of clonic convulsions of the limbs or parts of the body. In some cases, persistent myoclonic hyperkinesis in combination with epileptiform seizures are included in the Kozhevnikov epilepsy syndrome. Possible attacks of Jacksonian epilepsy. Cortical and stem localization of the lesion leads to tic-like and choreiform muscle twitches.

A characteristic sign of tick-borne encephalitis is the combined movement of the cranial nerves, due to damage to the gray matter of the brain. Cranial nerves are involved in the pathological process with different frequency.

There is damage to the oculomotor nerves and sympathetic innervation of the eye, leading to ptosis, strabismus and diplopia. Often there is paresis of the facial nerve, less often the visual, auditory and vestibular nerves suffer.

The spread of the process to the region of the nuclei of the IX, X, XII pairs of cranial nerves, which is so characteristic of tick-borne encephalitis, leads to the onset of early bulbar symptoms: paresis of the soft palate, nasal voice, blurred speech, aphonia, impaired swallowing, increased salivation with filling of the respiratory tract with mucus, tachycardia, dyspnea. The frequency of bulbar disorders reaches 25%.

• Meningoencephalopoliomyelitis form of the disease characterized along with general toxic and meningeal syndromes by the appearance of signs of diffuse encephalitis, focal encephalitis and damage to the gray matter of the spinal cord. The latter are typical clinical signs of the disease, appear already in the first days of the disease and after 3-4 days become the most pronounced.

Patients develop early flaccid paresis of the muscles of the neck, trunk, limbs, symmetrically affecting the muscles of the neck, shoulder girdle, upper limbs, and sometimes the intercostal muscles and diaphragm. Motor disorders of the lower extremities are rarely detected and are slightly expressed, but ascending paralysis is also known, starting from the lower extremities and then spreading to the trunk and upper extremities. During the period of the outcome of the disease, along with paresis, there is a pronounced atrophy of the muscles, especially the deltoid, trapezius, biceps, triceps and pectorals. In this case, the head is not held in a vertical position, it hangs passively, the movements of the upper limbs are almost completely lost. Muscular atrophy is also observed in cases of convalescence with the disappearance of paresis.

• Polyradiculoneuritic form tick-borne encephalitis, observed in 2–4% of patients, manifests itself along with general toxic and meningeal symptoms, signs of damage to the roots and peripheral nerves. Characterized by paresthesia in the form of "crawling", tingling in the skin of various areas, pain along the nerve trunks, positive symptoms of "tension" (Lassega, etc.), sensitivity disorder in the distal extremities by the type of "gloves" and "socks".
• Dual wave meningoencephalitis(two-wave milk fever), recorded in European foci of tick-borne encephalitis, is characterized by the development of a two-phase temperature reaction, each lasting 2–15 days with an interval of 1–2 weeks, the predominance of a general toxic syndrome during the first temperature wave and the development of meningeal and cerebral signs with a repeated increase in temperature bodies with rapid positive dynamics and recovery without residual effects.

Diagnostics

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Clinical diagnosis of tick-borne encephalitis is based on a set of epidemiological and clinical and laboratory data that reveal the characteristic syndromes of the disease.

Specific diagnosis of the disease is carried out using virological and serological methods. The virological method involves the isolation of the virus from the blood and cerebrospinal fluid of the patient (in the first 5-7 days of illness) or the brain of dead people - by intracerebral infection of newborn white mice with the test material, as well as using cell culture and subsequent identification of the virus using the fluorescent antibody method (MFA).

Along with virological methods, serological methods are widely used to verify the diagnosis using RSK, RDPA, RPHA, ELISA, RN in paired blood sera of patients taken at intervals of 2-3 weeks.

At the same time, detoxification, dehydration therapy is carried out, in case of a severe course of the disease - anti-shock therapy, corticosteroids are prescribed, and respiratory failure is combated. With convulsive syndrome, a 25% solution of magnesium sulfate, Relanium, sodium hydroxybutyrate, barbiturates and other sedatives are used. In the period of subsiding of acute manifestations of the disease, vitamins of group B, prozerin, dibazol, antihistamines are prescribed. Patients are discharged after 2–3 weeks: after the temperature normalizes, in the absence of neurological disorders. Convalescents are subject to clinical examination.

Prevention

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In foci of tick-borne encephalitis, a set of measures is used to protect the population from tick attacks (anti-tick overalls, repellents - dimethyl and dibutyl phthalates), mutual examinations are carried out with the removal and destruction of detected ticks. After removing the attached ticks, a specific donor immunoglobulin is used (for adults, 3 ml intramuscularly). It is not recommended to use unboiled milk for food.

Specific prophylaxis is carried out according to epidemic indications 1–1.5 months before the season of tick activity. Tissue inactivated or live attenuated vaccines are injected 1 ml under the skin three times at intervals of 3 months to 1 year, followed by an annual revaccination of 1 ml of the vaccine.