Russian spring-summer encephalitis. Tick-borne encephalitis

Diseases of tick-borne encephalitis on the territory of the Soviet Union have already occurred in the distant past, mainly among the population of the remote taiga regions of Siberia and the Far East, which in pre-revolutionary Russia were deprived of medical care.

Starting in 1934, scientific expeditions were sent to the Far East, which in a short time studied the etiology, distribution routes, clinical picture, treatment and prevention of a previously unknown disease. A special merit in this belongs to A. G. Panov, who described this disease and called it spring-summer encephalitis.

Pathomorphology. A picture of inflammation of predominantly soft meninges, anterior horns of the cervical spinal cord and nuclei of the medulla oblongata is found: edema and hyperemia against the background of stasis and fibrinoid necrosis of the vessel wall, perivascular infiltration by lymphoid and monocytic elements, degeneration and death of neurons. Less pronounced changes are noted in the cerebral cortex and basal ganglia.

Clinic. The incubation period lasts 7-31 days, and the longer the incubation period, the more severe the disease. The beginning is sharp. A few hours before the development of a pronounced picture of encephalitis, prodromal phenomena are noted in the form of general malaise, chills, headache, and nausea. Then there is an acute increase in body temperature up to 39-40 ° C, the appearance of cerebral and focal symptoms. Depending on the predominance of certain pathological symptoms in the clinical picture of the disease, 5 main clinical forms of tick-borne encephalitis are distinguished: 1) bulbopontine, 2) meningoencephalitic, 3) meningeal, 4) polyradiculoneuritis, 5) erased, or abortive.

In the bulbopontine form, on the 2-3rd day of the disease, flaccid paralysis of the face, neck and limbs (usually the upper ones) develops with hypotension and areflexia: the head falls on the chest, the patient cannot hold it, the arms hang like whips. After 3-4 weeks, atrophy of the paralyzed muscles develops. In severe cases, the motor nuclei of the medulla oblongata are involved in the process, resulting in paralysis of the constrictors of the pharynx, soft palate, vocal cords, and tongue; the act of swallowing, speech, voice are disturbed, atrophy of the tongue and fibrillar twitches are noted, respiratory and cardiac activity disorders are possible.

The meningoencephalitic form of tick-borne encephalitis proceeds as a diffuse or focal inflammation of the brain and is characterized by the presence in the clinical picture of signs of impaired consciousness, delirium, convulsions, severe meningeal symptoms.

The meningeal form proceeds according to the type of serous meningitis with unsharply expressed cerebral phenomena.

In the polyradiculoneuritis form, the clinical picture is dominated by signs of damage to the peripheral nervous system in the form of pain, sensory disturbances in the distal extremities, a decrease or disappearance of reflexes, etc.

The erased form proceeds with mild signs of irritation of the meninges.

As a general infectious process, tick-borne encephalitis is accompanied by leukocytosis (up to 10-15-109 in 1 l), an increase in ESR up to 15-20 mm/h. In the cerebrospinal fluid lymphocytic pleocytosis.

Flow. The disease is severe. Lethal outcome in previous years was observed in the Far East up to 20%.

The recovery period lasts up to several months. As residual effects, persistent atrophic paralysis of the muscles of the neck and shoulder girdle, as well as a picture of Kozhevnikov epilepsy, characterized by the presence of constant clonic convulsions in a certain muscle group and periodically developing general convulsive epileptic seizures, are observed. Kozhevnikovskaya epilepsy usually manifests itself 2-3 months after the acute period of the meningoencephalitic form of tick-borne encephalitis.

In some cases, the disease takes on a progressive course, when more and more atrophic paralysis gradually appears, i.e., the disease takes on the character of chronic poliomyelitis.

Treatment. In the first hours from the onset of the disease, it is recommended to inject intramuscularly the serum of those who have recovered from this disease (50-75 ml daily) or the immune serum of horses, goats, sheep (10-20 ml each) for 4-6 days, ribonuclease 30 mg every other day. 4 hours for 10-12 days; intravenously 40% glucose solution - 20 ml; intramuscularly, 10 ml of a 25% solution of magnesium sulfate (to reduce swelling of the brain and membranes), repeated lumbar punctures to reduce intracranial hypertension, thiamine, pyridoxine, ascorbic acid.

In the recovery period, anticholinesterase agents (prozerin, galantamine, nivalin in the form of subcutaneous injections), strychnine, biostimulants (aloe, plasmol, FiBS, vitreous body), exercise therapy, and massage should be prescribed.

Prevention should be carried out in the direction of the fight against ticks in the developed forest areas, personal protection measures against tick attacks, active and passive immunization.

Preventive measures that help reduce the number of ticks in forest areas consist in the destruction of the hosts of ticks - wild animals - reservoirs of "encephalitis viruses", in the use of "trapping herds", i.e. grazing on working sites in the forest, followed by treatment of animals with various acaricides, personal protective measures: inspection of linen and body every 2 hours of stay in the forest, soaking clothing with a water-soap emulsion containing 5% of preparation K, or an emulsion with turpentine and lysol, lubricating the skin of the neck and hands with camphor, thymol or mint ointment.

In connection with the isolation of the tick-borne encephalitis virus, it was possible to carry out prophylactic vaccinations using specific vaccines. Vaccination of teams working in the taiga forest areas is mandatory. For the first time, 3 ml of a specific vaccine is injected intramuscularly. After 10 days, the vaccine is re-introduced in an amount of 6 ml.

At bulbopontine form on the 2-3rd day of the disease, flaccid paralysis of the face, neck and limbs (usually the upper ones) develops with hypotension and areflexia: the head falls on the chest, the patient cannot hold it, the arms hang like whips. After 3-4 weeks, atrophy of the paralyzed muscles develops. In severe cases, the motor nuclei of the medulla oblongata are involved in the process, resulting in paralysis of the constrictors of the pharynx, soft palate, vocal cords, and tongue; the act of swallowing, speech, voice are disturbed, atrophy of the tongue and fibrillar twitches are noted, respiratory and cardiac activity disorders are possible.

Meningoencephalitic form tick-borne encephalitis proceeds as a diffuse or focal inflammation of the brain and is characterized by the presence in the clinical picture of signs of impaired consciousness, delirium, convulsions, severe meningeal symptoms.

meningeal form proceeds according to the type of serous meningitis with unsharply expressed cerebral phenomena.

At polyradiculoneuritic form the clinical picture is dominated by signs of damage to the peripheral nervous system in the form of pain syndrome, impaired sensitivity in the distal extremities, reduction or disappearance of reflexes, etc.

Erased form proceeds with mild signs of irritation of the meninges.

As a general infectious process, tick-borne encephalitis is accompanied by leukocytosis (up to 10-15-10 9 in 1 l), an increase in ESR up to 15-20 mm / h. In the cerebrospinal fluid lymphocytic pleocytosis.

Flow. The disease is severe. Lethal outcome in previous years was observed in the Far East up to 20%.

The recovery period lasts up to several months. As residual effects, persistent atrophic paralysis of the muscles of the neck and shoulder girdle is observed, as well as a picture Kozhevnikovskaya epilepsy, characterized by the presence of constant clonic convulsions in a certain muscle group and periodically developing general convulsive epileptic seizures. Kozhevnikovskaya epilepsy usually manifests itself 2-3 months after the acute period of the meningoencephalitic form of tick-borne encephalitis.

In some cases, the disease takes on a progressive course, when more and more atrophic paralysis gradually appears, i.e., the disease takes on the character of chronic poliomyelitis.

In the recovery period, anticholinester agents should be prescribed (prozerin, galantamine, nivalin in the form of subcutaneous injections), strychnine, biostimulants (aloe, plasmol, FiBS, vitreous body), exercise therapy, massage.

Prevention should be carried out in the direction of the fight against ticks in the developed forest areas, personal protection measures against tick attacks, active and passive immunization.

Preventive measures that help reduce the number of ticks in forest areas consist in the destruction of the hosts of ticks - wild animals - reservoirs of "encephalitis viruses", in the use of "trapping herds", i.e. grazing on working sites in the forest, followed by treatment of animals with various acaricides, personal protective measures: examination of linen and body every 2 hours of stay in the forest, soaking clothing with a water-soap emulsion containing 5% of preparation K, or an emulsion with turpentine and lysol, lubricating the skin of the neck and hands with camphor, thymol or mint ointment.

Tick-borne encephalitis causes a filterable neurotropic tick-borne encephalitis virus, the clinical picture was first described by A. G. Panov. Transmitters of the virus and its reservoir in nature are ticks (Ixodes persulcatus). The seasonality of the disease is due to the biology of ticks that appear in large numbers in the spring and summer. The disease is found in many regions: in the Far East, in Siberia, in the Urals, in Kazakhstan, Belarus, the Baltic states, Transcarpathian, Leningrad and Moscow regions.

The tick-borne encephalitis virus belongs to the Flaviviridae family, the Flavivirus genus, to the ecological group of arboviruses, that is, viruses transmitted by arthropods: ticks, mosquitoes and other insects. The virus enters the human body in 2 ways: through a tick bite and alimentary. Alimentary infection occurs when raw milk is consumed, as well as dairy products prepared from the milk of infected cows and goats. When bitten by a tick, the virus immediately enters the bloodstream. However, with both methods of infection, the virus enters the nervous system hematogenously and through the perineural spaces.

The incubation period for a tick bite lasts from 1 to 30, and in rare cases - up to 60 days, with an alimentary method of infection - 4-7 days. The duration of the incubation period and the severity of the course of the disease depend on the amount and virulence of the virus, as well as on the immunoreactivity of the human body. Numerous tick bites are more dangerous than single ones.

Pathomorphology of tick-borne encephalitis

Microscopic examination of the brain and membranes reveals their hyperemia and edema, infiltrates from mono- and polynuclear cells, mesothermal and gliosis reactions. Inflammatory-degenerative changes in neurons are localized
predominantly in the anterior horns of the cervical segments of the spinal cord, the nuclei of the medulla oblongata, the brain bridge, and the cerebral cortex. Destructive vasculitis with necrotic foci and punctate hemorrhages are characteristic. For the chronic stage of tick-borne encephalitis, fibrous changes in the membranes of the brain with the formation of adhesions and arachnoid cysts, and pronounced proliferation of glia are typical. The most severe, irreversible lesions occur in the cells of the anterior horns of the cervical segments of the spinal cord.

Clinical picture

In the classification of tick-borne encephalitis, depending on the prevalence of general infectious, sheath or focal symptoms of damage to the nervous system, various clinical forms are distinguished: non-focal and focal. Non-focal include febrile, meningeal and erased, focal - poliomyelitis (spinal), polioencephalitic (stem), polioencephalomyelitis (stem-spinal), encephalitic and meningoencephalitic forms. The frequency of clinical forms varies in different regions with a tendency to decrease in focal forms from the Far East to the western regions.

In all clinical forms, the disease begins acutely, with a rise in body temperature to 39-40 ° C and above, chills, severe headache, repeated vomiting. Characterized by bursting pain in the lower back, calves, muscle and radicular pain. It is rarely possible to identify the prodromal period, during which patients complain of malaise, general weakness, moderate headache.

In the first days of the disease, hyperemia of the skin, injection of the sclera are usually noted, gastrointestinal disorders (loose stools, abdominal pain) are possible, less often - sore throat. The highest body temperature occurs on the 2nd day of the disease, it can remain high for another 5-8 days. However, in most cases, the temperature curve has a "two-hump" character: with an interval of 2-5 days between the first and second rise, followed by a rapid decrease and prolonged subfebrile condition. The second rise in temperature corresponds to the penetration of viruses into the nervous system and the development of neurological symptoms.

From the first days of the disease, cerebral symptoms (headache, vomiting, epileptic seizures), disorders of consciousness of various depths up to coma, meningeal symptoms (general hyperesthesia, stiff neck muscles, symptoms of Kernig and Brudzinsky) are usually expressed. Many patients have pronounced mental disorders: delusions, visual and auditory hallucinations, agitation or depression.

Neurological symptoms of tick-borne encephalitis are diverse. In accordance with their prevalence and severity, the following clinical forms are distinguished: polioencephalomyelitis, poliomyelitis, meningeal, meningoencephalitic, encephalitic, febrile, polyradiculoneuritic.

The most typical polioencephalomyelitis (poliomyelitis) form of tick-borne encephalitis. In such patients, on the 3rd-4th day of illness, flaccid paresis or paralysis of the muscles of the neck, shoulder girdle, and proximal upper limbs develop. A typical "hanging head" pattern develops. Often flaccid paralysis is accompanied by bulbar disorders. Landry's ascending palsy sometimes occurs with weakness spreading from the lower limbs to the upper limbs, trunk muscles, respiratory muscles, muscles of the larynx and respiratory center.

Meningeal form of tick-borne encephalitis manifests itself in the form of acute serous meningitis with severe cerebral and meningeal symptoms. In the cerebrospinal fluid, a characteristic increase in pressure (up to 500 mm of water column), mixed lymphocytic-neutrophilic pleocytosis (up to 300 cells in 1 μl), proteinorachia up to 1 s / l are detected.

encephalitic form characterized by a combination of cerebral and focal symptoms. Depending on the predominant localization of the pathological process, bulbar, pontine, mesencephalic, subcortical, capsular, hemispheric syndromes occur. Disturbances of consciousness are possible, epileptic seizures are frequent.

Feverish (erased) form characterized by the development of general infectious symptoms without signs of organic damage to the nervous system. In some of these patients, meningeal symptoms may appear, but the cerebrospinal fluid is usually not changed. The febrile form of tick-borne encephalitis simulates a mild intercurrent disease with catarrhal symptoms and general malaise. Currently, most authors believe that the isolation of the erased form of tick-borne encephalitis is impractical due to the difficulties of clinical diagnosis, since this form occupies an intermediate position between febrile and meningeal. The polyradiculoneuritic form proceeds with signs of damage to the roots and nerves.

Dual wave viral meningoencephalitis in the middle of the last century, it was isolated as an independent disease by A. G. Panov, A. A. Smorodintsev and S. N. Davidenkov. Currently, it is considered as a two-wave course of tick-borne encephalitis. The disease begins acutely, without a prodromal period. Body temperature rises sharply to 38-39 ° C, chills, headache, dizziness, vomiting, pain in muscles and joints, sleep disorders appear. From the first days there are meningeal symptoms. After 5-7 days, the body temperature drops to normal or subnormal figures, however, after a temperature remission within 6-10 days, a second rise in body temperature (second temperature wave) occurs, lasting 10 days.

Focal symptoms may be absent or manifest as moderate central hemiparesis, cerebellar disorders, autonomic disorders with hyperhidrosis, hypoglycemia, anorexia. Sometimes mononeuritis, neuritis and radiculitis develop. In the cerebrospinal fluid, lymphocytic pleocytosis, an increase in protein content are found, in the blood - leukocytosis.

Tick-borne encephalitis is characterized by the presence of chronic, progressive forms of the disease. Among these variants of encephalitis, Kozhevnikov's epilepsy occurs in 4-18% of cases. The clinical picture is characterized by constant myoclonic twitches in certain muscle groups. Against this background, extended epileptic seizures periodically occur with clonic-tonic convulsions and loss of consciousness.

Kozhevnikovskaya epilepsy can be combined with other focal symptoms of tick-borne encephalitis (for example, flaccid paresis of the muscles of the upper limbs and neck). The course can be progressive (with the spread of myoclonus to other muscles and an increase in grand mal seizures), remitting (with remissions of various durations) and stable (without pronounced progression). In Kozhevnikov's epilepsy, the main pathomorphological changes of a destructive nature are found in the III-IV layers of the motor zone of the cerebral cortex.

A progressive course may be inherent in the poliomyelitis form of tick-borne encephalitis with an increase in flaccid paresis and muscle atrophy or the appearance of new paresis at different times after the acute phase of the disease. The clinical picture of this variant resembles amyotrophic lateral sclerosis.

Course and forecast

Symptoms of the disease increase within 7-10 days. Then focal symptoms begin to subside, cerebral and meningeal symptoms gradually disappear. With the meningeal form, recovery occurs in 2-3 weeks without consequences. Asthenic syndrome may remain for several months. With the poliomyelitis form, there is no complete recovery, without neurological disorders, atrophic paresis and paralysis, mainly of the cervical myotomes, persist.

In the encephalitic form, impaired functions are restored slowly. The recovery period can take from several months to 2-3 years. The most severe course was noted in the meningoencephalitic form with a violent onset, rapidly onset coma, and death. High mortality (up to 25%) occurs in encephalitic and poliomyelitis forms with bulbar disorders.

In recent decades, due to extensive preventive measures, the course of tick-borne encephalitis has changed. Severe forms began to occur much less frequently. Meningeal and febrile forms predominate with a favorable outcome.

Diagnostics

In the diagnosis of tick-borne encephalitis, anamnestic data are of great importance: stay in an endemic focus, the profession of the patient, the spring-summer period, a tick bite, the use of goat milk or cheese. However, not every disease that occurs after such a bite is encephalitis. It is known that only 0.5-5.0% of all ticks are carriers of viruses. Accurate diagnosis of the disease is possible with the help of complement fixation reactions, neutralization and inhibition of hemagglutination. Of certain diagnostic value is the isolation of the virus from the blood and cerebrospinal fluid. In the blood, leukocytosis, an increase in ESR are noted, in the cerebrospinal fluid - an increase in protein up to 1 s / l, lymphocytic pleocytosis.

Differentiate tick-borne encephalitis follows from various forms of serous meningitis, typhus, Japanese mosquito encephalitis (in the Far East), acute poliomyelitis.

Immunity after tick-borne encephalitis persistent.

Prevention

They carry out measures to combat ticks, immunize the population, exterminate rodents in endemic foci, use special clothing to prevent tick bites. Prevention of tick-borne encephalitis includes specific and non-specific protection measures. The most effective way to prevent tick-borne encephalitis is vaccination.

The disease is caused by a filterable neurotropic tick-borne encephalitis virus, the clinical picture was first described by A.G. Panov. Transmitters of the virus and its reservoir in nature are ticks (Ixodes persulcatus).

The seasonality of the disease is due to the biology of ticks that appear in large numbers in the spring and summer. The disease is found in many regions: in the Far East, in Siberia, in the Urals, in Kazakhstan, Belarus, the Baltic states, Transcarpathian, Leningrad and Moscow regions.

Pathomorphology of tick-borne encephalitis

Microscopic examination of the brain and membranes reveals their hyperemia and edema, infiltrates from mono- and polynuclear cells, mesodermal and gliosis reactions. Inflammatory-degenerative changes in neurons are localized mainly in the anterior horns of the cervical segments of the spinal cord, the nuclei of the medulla oblongata, the brain bridge, and the cerebral cortex. Destructive vasculitis with necrotic foci and punctate hemorrhages are characteristic. For the chronic stage of tick-borne encephalitis, fibrous changes in the membranes of the brain with the formation of adhesions and arachnoid cysts, and pronounced proliferation of glia are typical. The most severe, irreversible lesions occur in the cells of the anterior horns of the cervical segments of the spinal cord.

Symptoms and clinical picture of tick-borne encephalitis

In the classification of tick-borne encephalitis, depending on the prevalence of highly infectious, sheath or focal symptoms of damage to the nervous system, various clinical forms are distinguished: non-focal and focal. Non-focal include febrile, meningeal and erased, focal - poliomyelitis (spinal), polioencephalitic (stem), polioencephalomyelitis (stem-spinal), encephalitic and meningoencephalitic forms. The frequency of clinical forms varies in different regions with a tendency to decrease in focal forms from the Far East to the western regions.

Classification of tick-borne encephalitis

Clinical form	Disease severity	The course of the disease	Disease outcomes
Nonfocal: erased; febrile; meningeal	Easy. Intermediate degree heavy	Acute	Recovery: - complete; - with neurological deficit
Focal: encephalitic; meningoencephalitic; polioencephalitic; poliomyelitis; polioencephalomyelitis; polyradiculoneuritis	Medium severity. heavy	Acute. Chronic: - primary chronic or secondary chronic; - stable; - progredient	Recovery: - complete; - with neurological deficit. Chronization. Death

However, in most cases, the temperature curve has a "two-hump" character: with an interval of 2-5 days between the first and second rise, followed by a rapid decrease and prolonged subfebrile condition. The second rise in temperature corresponds to the penetration of viruses into the nervous system and the development of neurological symptoms.

From the first days of the disease, general cerebral symptoms (headache, vomiting, epileptic seizures), disorders of consciousness of various depths up to coma, meningeal symptoms (general hyperesthesia, stiffness of the neck muscles, symptoms of Kernig and Brudzinsky) are usually expressed. Many patients have pronounced mental disorders: delusions, visual and auditory hallucinations, agitation or depression.

Neurological symptoms of tick-borne encephalitis are diverse. in accordance with their prevalence and severity, the following clinical forms are distinguished: polioencephalomyelitis, poliomyelitis, meningeal, meningoencephalitic, encephalitic, febrile, polyradiculoneuritic.

The most typical polioencephalomyelitic (poliomyelitis) form tick-borne encephalitis. In such patients, on the 3rd-4th day of illness, flaccid paresis or paralysis of the muscles of the neck, shoulder girdle, and proximal upper limbs develop. A typical "hanging head" pattern develops. Often flaccid paralysis is accompanied by bulbar disorders. Landry's ascending palsy sometimes occurs with weakness spreading from the lower limbs to the upper limbs, trunk muscles, respiratory muscles, muscles of the larynx and respiratory center.

meningeal form tick-borne encephalitis manifests itself in the form of acute serous meningitis with severe cerebral and meningeal symptoms. In the cerebrospinal fluid, a characteristic increase in pressure (up to 500 mm of water column), mixed lymphocytic-neutrophilic pleocytosis (up to 300 cells in 1 μl), proteinorachia up to 1 g / l are detected.

encephalitic form characterized by a combination of cerebral and focal symptoms. Depending on the predominant localization of the pathological process, bulbar, pontine, mesencephalic, subcortical, capsular, hemispheric Syndromes occur. Disturbances of consciousness are possible, epileptic seizures are frequent.

Feverish (erased) form characterized by the development of general infectious symptoms without signs of organic damage to the nervous system. in some of these patients, meningeal symptoms may appear, but the cerebrospinal fluid is usually not changed. The febrile form of tick-borne encephalitis simulates a mild intercurrent disease with catarrhal symptoms and general malaise. Currently, most authors believe that the isolation of an erased form of tick-borne encephalitis is impractical due to the difficulties of clinical diagnosis, since this form occupies an intermediate position between febrile and meningeal.

Polyradiculoneuritic form proceeds with signs of damage to the roots and nerves.

The disease begins acutely, without a prodromal period. The body temperature rises sharply to 38-39 ° C, chills, headache, dizziness, vomiting, pain in muscles and joints, sleep disorders appear. From the first days there are meningeal symptoms. After 5-7 days, the body temperature drops to normal or subnormal figures, however, after a temperature remission within 6-10 days, a second rise in body temperature (second temperature wave) occurs, lasting 10 days. Focal symptoms may be absent or present

In the form of moderate central hemiparesis, cerebellar disorders, autonomic disorders with hyperhidrosis, hypoglycemia, anorexia. Sometimes mononeuritis, neuritis and radiculitis develop. In the cerebrospinal fluid, lymphocytic pleocytosis, an increase in protein content are found, in the blood - leukocytosis.

Tick-borne encephalitis is characterized by the presence of chronic, progressive forms of the disease. Among these variants of encephalitis, in 4-18% of cases, Kozhevnikov's epilepsy is encountered. The clinical picture is characterized by constant myoclonic twitches in certain muscle groups. Against this background, extended epileptic seizures periodically occur with clonic-tonic convulsions and loss of consciousness. Kozhevnikovskaya epilepsy can be combined with other focal symptoms of tick-borne encephalitis (for example, flaccid paresis of the muscles of the upper limbs and neck). The course can be progressive (with the spread of myoclonus to other muscles and an increase in grand mal seizures), remitting (with remissions of various durations) and stable (without pronounced progression). In Kozhevnikov epilepsy, the main pathomorphological changes of a destructive nature are found in the III-IV layers of the motor zone of the cerebral cortex.

The course and prognosis of tick-borne encephalitis

Rice. Consequences of the postponed poliomyelitis form of tick-borne encephalitis.

In the encephalitic form, impaired functions are restored slowly.

The recovery period can take from several months to 2-3 years. The most severe course was noted in the meningoencephalitic form with a violent onset, rapidly onset coma, and death. High mortality (up to 25%) occurs in encephalitic and poliomyelitis forms with bulbar disorders.

Diagnosis of tick-borne encephalitis

It is known that only 0.5-5.0% of all ticks are carriers of viruses. Accurate diagnosis of the disease is possible with the help of complement fixation reactions, neutralization and inhibition of hemagglutination. Of certain diagnostic value is the isolation of the virus from the blood and cerebrospinal fluid. In the blood, leukocytosis, an increase in ESR are noted, in the cerebrospinal fluid - an increase in protein up to 1 g / l, lymphocytic pleocytosis.

Tick-borne encephalitis should be differentiated from various forms of serous meningitis, typhus, Japanese mosquito encephalitis (in the Far East), and acute poliomyelitis.

Immunity after tick-borne encephalitis is persistent.

Treatment of tick-borne encephalitis

Prevention of tick-borne encephalitis

They carry out measures to combat ticks, immunize the population, exterminate rodents in endemic foci, use special clothing to prevent tick bites.

Prevention of tick-borne encephalitis includes specific and non-specific protection measures. The most effective way to prevent tick-borne encephalitis is vaccination.

The content of the article

pincer spring-summer, taiga, encephalitis is an acute primary viral disease characterized by sudden onset, fever, severe CNS damage. Refers to natural focal human diseases.
Epidemic outbreaks of tick-borne encephalitis first began to be recorded in 1933-1934. in the Far East near Khabarovsk. Later it was shown that it is found not only in the Far East, but also in Siberia, the Urals, and in many regions of the European part of the former USSR. Natural foci of tick-borne encephalitis have also been found in Czechoslovakia, Hungary, and Poland.

Etiology of tick-borne (spring-summer) encephalitis

The tick-borne encephalitis virus belongs to the group of arboviruses transmitted by arthropods. In the Far East, Siberia and the Urals, these are mainly Ixodes persuleatus ticks, in the western regions of the former USSR and central Europe, Ixodes ricinus ticks.
According to the classification of V. M. Zhdanov, two types of tick-borne encephalitis virus are distinguished: Encephalophilis silverstris, endemic to the regions of the Far East, Siberia and Eastern Europe, and Encephalopulis occidentalis, predominant in Western Europe.
The tick-borne encephalitis virus is sensitive to high temperature and, when boiled, dies within 2-3 minutes. At low temperatures and even freezing, it remains viable. The virus is sensitive to disinfectants. The virus enters the human body through the bite of a tick. It is impossible to directly become infected with tick-borne encephalitis from a sick person. The carriers of the disease are female ticks. The virus is found in all organs of the tick, but especially a lot of it is secreted through the salivary glands.

Epidemiology of tick-borne (spring-summer) encephalitis

The favorite habitats of ticks are old forests with dense undergrowth of shrubs and high grass cover.
The reservoir of the virus in nature are rodents (chipmunks, field mice, hedgehogs) and birds (thrushes, goldfinches, finches, etc.). Of domestic animals, goats are the most susceptible to the disease. Attacking wild animals or birds that are carriers of the tick-borne encephalitis virus, ticks suck up the virus along with the blood, which spreads to all organs of the insect, including the salivary glands, ovaries and eggs in them. As a result, such a tick becomes a carrier of the virus, capable of transmitting the virus from generation to generation. The virus does not die in the body of the tick and in the winter.
The disease has a pronounced seasonal character, which is directly related to the period of tick activity. For different regions of the former USSR, this period is different, but it falls on the first warm months of the year - April, May, June, July. At other times, the disease is much less common. As a rule, tick-borne encephalitis affects people who, by the nature of their work, are forced to stay in the taiga: geologists, lumberjacks, surveyors, hunters. Ticks are especially dangerous for newly arriving contingents who have not previously encountered an infection and do not have the appropriate immunity.
The tick bite is painless; the tick digs deep into the skin, can drink blood for several days, increases in size, after which it falls off and crawls away. But usually a person begins to feel itching at the site of the tick bite soon after the tick has stuck, so the tick is removed earlier. As a rule, patients remember well whether there was a tick bite or not. In rare cases, bites may go unnoticed and patients deny them when asked.
There is another way for the infection to enter the human body - alimentary - through the consumption of raw goat's milk. Infection is possible when the virus enters the mucous membranes of the mouth from contaminated hands, for example, when crushing a tick. Naturally, encephalitis is not observed after any tick bite. It has been proven that even in particularly active foci, only 0.5-5% of all ticks are carriers of the virus.

Pathogenesis of tick-borne (spring-summer) encephalitis

After the virus enters the body through the skin during a bite, it begins to multiply in the skin and in the subcutaneous fat layer in the immediate vicinity of the bite site.
With alimentary infection, the virus multiplies in the tissue of the gastrointestinal tract, then it penetrates into the bloodstream and spreads throughout the body via the hematogenous route (viremia stage). In the brain tissue, the virus can be detected 2-3 days after the bite, its concentration reaches a maximum by the 4th day. In the future, it gradually decreases.
The incubation period for tick-borne encephalitis lasts 8-20 days. With the alimentary method of infection, the incubation period is shorter - 4-7 days. The disease is possible at any age. More often people of the most able-bodied age - 20-40 years old get sick.
The severity of clinical symptoms, the severity of the course of the disease in the eastern regions of the Union, in Siberia are to some extent more significant than in the western regions of the former USSR and other countries. Therefore, there is an idea of two variants of tick-borne encephalitis - eastern with a more severe course and western with a benign course. This concept was confirmed by virological studies that found two different strains of tick-borne encephalitis virus [Zhdanov V. M.].

Morphology of tick-borne (spring-summer) encephalitis

Macroscopically, swelling of the hard and soft membranes of the brain, plethora of blood vessels is detected. Edema of the substance of the brain, its flabbiness, numerous hemorrhages, mainly in the region of the brain stem are noticeable. These changes are especially pronounced in the region of the cervical thickening of the spinal cord. Histological examination reveals the phenomena of acute non-purulent inflammation with a pronounced reaction from the vessels, proliferation of glia and severe degenerative changes in ganglion cells. The inflammatory reaction is most pronounced in the anterior iporax at the level of the cervical thickening of the spinal cord and the motor nuclei of the trunk. Inflammatory changes, but expressed to a lesser extent, are also noted in the cortex, subcortical formations, and the cerebellum. Inflammatory changes such as interstitial neuritis are found in the roots and peripheral nerves.

Clinic of tick-borne (spring-summer) encephalitis

The disease, as a rule, begins acutely with a sharp rise in temperature to 39-40 ° C, chills, severe headache, nausea and vomiting. General weakness, weakness, pain all over the body develop. Consciousness is preserved, but in more severe cases, stunnedness is possible, sometimes arousal, accompanied by delirium, auditory or visual hallucinations. These general infectious phenomena on the 2-4th day of the disease are joined by pronounced meningeal phenomena - neck muscle stiffness, symptoms of Kernig, Brudzinsky, then peripheral type paralysis occurs in the muscles of the neck, shoulder girdle and proximal arms. Their occurrence is due to the predominant lesion of the anterior horns of the spinal cord at the level of the cervical thickening. The movements in the arms are sharply limited, the patient cannot lift them up, spread them apart, bend and unbend in the elbow joints. Due to the weakness of the neck muscles, the patient's head "falls" on his chest. "Dangling" head is one of the most characteristic symptoms of the paralytic form of tick-borne encephalitis. It is possible to limit movements in the legs, but the knee and Achilles reflexes are increased, and pathological reflexes can often be caused, which indicates the involvement of the pyramidal tracts.
Among the rather frequent signs of tick-borne encephalitis, especially its Far Eastern variant, are disorders of the functions of stem formations. Speech, swallowing are disturbed in patients, and atrophy of the muscles of the tongue is noted in the future. In the acute period of the disease, pronounced vegetative symptoms are noted - hyperemia of the skin of the face, neck, general sweating; persistent red dermographism, increased pilomotor reactions.
In the blood, moderate leukocytosis with neutrophilia and a shift to the left, increased ESR are noted. The cerebrospinal fluid is clear, moderate lymphocytic pleocytosis and a slight increase in protein are noted.
The decrease in temperature begins on the 5-7th day of illness. Headache, muscle pain decrease, meningeal symptoms gradually disappear. By the end of the second week, a recovery period begins, which can have a different duration. In some cases, the restoration of motor functions can be complete, while in others, significant motor defects remain, causing the disability of patients. Most often, weakness and atrophy remain in the muscles of the neck, shoulder girdle, and proximal arms. A “hanging” head is one of the typical symptoms not only of the acute stage, but also of previous tick-borne encephalitis.
In addition to the so-called polio form of tick-borne encephalitis described above, there are many other clinical forms. There are meningeal, meningoencephalitic, erased forms. In some patients, the disease may have a progressive course.

meningeal form

The meningeal form is a serous meningitis caused by tick-borne encephalitis virus. A feature of this form of the disease are pronounced meningeal symptoms: neck stiffness, Kernig's symptom, upper and lower Brudzinsky's symptoms. The cerebrospinal fluid is transparent, its pressure is increased, cellular-protein dissociation is clearly expressed. Cytosis reaches several tens or hundreds of cells, mainly lymphocytes. Protein within the normal range or slightly elevated. There is a pronounced pain syndrome, but motor disorders are not detected. Recovery occurs in 2-3 weeks and, as a rule, complete, without motor defects. In some cases, a long-term pronounced asthenic syndrome remains.

Meningoencephalitic form

The meningoencephalitic form is more severe than the meningeal form. There is a severe headache, nausea, vomiting. Patients become lethargic, lethargic, drowsy. Delusions, hallucinations, psychomotor agitation, general or partial epileptic seizures often develop, sometimes status epilepticus occurs.
Meningeal symptoms are determined. The temperature stays high for a long time. The meningoencephalitic form of tick-borne encephalitis is characterized by the development of motor disorders not of a peripheral, but of a central nature: spastic hemiparesis, subcortical hyperkinesis, 1kozhsvnikovskaya or Jacksonian epilepsy.
In the last 15-20 years, tick-borne encephalitis has been milder than in the 30s or 40s. Currently, meningeal and obliterated forms of the disease predominate. The latter are accompanied by fever, but occur without severe neurological symptoms. Light meningeal signs are possible, but with a normal composition of the cerebrospinal fluid. In the blood, moderate leukocytosis is sometimes noted. The outcome of the disease in most cases is favorable, but in rare cases, a progressive development of the disease with an increase in focal symptoms is possible.

Diagnosis of tick-borne (spring-summer) encephalitis

In the diagnosis of tick-borne encephalitis, a significant role is played by the clarification of epidemiological data, information about the patient's stay in the endemic focus in the spring and summer. The presence of indications of a tick bite directs the search in the right direction. The acute stage of the disease should be differentiated from various forms of serous meningitis, influenza, acute poliomyelitis (in children), Japanese encephalitis (in the Far East). Clarification of the diagnosis is carried out by carrying out serological reactions: complement fixation reaction (RCC), neutralization reaction (RN), hemagglutination inhibition reaction (RTGA). RSK gives a positive result from the 2nd week of the disease, RN - from the 8th-9th week.

Treatment of tick-borne (spring-summer) encephalitis

Treatment of a patient with tick-borne encephalitis must be carried out in a hospital with strict adherence to bed rest until the signs of intoxication disappear. Careful care is needed for the condition of the skin, oral cavity, constant monitoring of the state of cardiac activity, blood pressure, respiration, bowel and bladder functions. To reduce the effects of intoxication, parenteral administration of electrolyte and glucose solutions is indicated. In severe cases of the disease, prednisolone is administered (60-100 mg per day). Etiotropic treatment of tick-borne encephalitis is the use of gamma globulin titrated against tick-borne encephalitis virus. Gamma globulin is recommended to be administered 5-6 ml intramuscularly, daily or every other day for 3-5 days. The earlier the introduction of gamma globulin from the onset of the disease, the more pronounced the therapeutic effect.
In addition to gamma globulin, ribonuclease is used to treat the acute stage of tick-borne encephalitis. Ribonuclease is recommended to be administered intramuscularly in physiological saline (the drug is diluted immediately before injection) in a single dose of 30 mg every 4 hours. The first injection is done according to Bezredka. The daily dose of the enzyme introduced into the body is 180 mg. Treatment continues for 4-5 days. Ribonuclease easily crosses the blood-brain barrier. This is its advantage over gamma globulin, which inactivates the viral particles circulating in the patient's blood. Dehydration therapy (mannitol, furosemide, glycerol), repeated lumbar punctures are shown. In order to prevent pneumonia, broad-spectrum antibiotics are prescribed. For the treatment of the chronic stage of the disease, physiotherapeutic agents, dehydrating and resolving therapy, massage, exercise therapy, vitamins, and sedatives are used.

Prevention of tick-borne (spring-summer) encephalitis

Preventive measures include preventive vaccinations, protection against tick bites and tick control.
Persons who, due to the nature of their work, are forced to stay in the taiga in the spring and summer, are subject to vaccination. Vaccination is carried out in January-March with a tissue culture vaccine, which is administered three times, according to the instructions attached to it. A single revaccination is performed in a year. To protect people working in the forest from the attack of ticks, special overalls are used that hermetically cover the entire body, leaving only the face and hands open. When occasionally visiting the forest in endemic areas, for example, when conducting excursions, mutual examinations of the body surface in order to detect and remove ticks are mandatory. If the tick has already managed to stick, it is carefully removed, trying not to tear off the head and proboscis.
To facilitate this operation, it is recommended to apply a drop of vegetable oil to the tick. In the next few hours after the bite, the bitten person should be injected intramuscularly with anti-tick gamma globulin at a dose of 3 ml.
In tick-borne encephalitis-endemic areas, raw goat's milk should be avoided.