Forest encephalitis

Introduction to forest encephalitis Forestencephalitis, also known as tickborneencephalitis, is an acute infectious disease caused by a virus. In May-August 1934, the disease was first discovered in some forest areas in the eastern part of the Soviet Union, so it was also called the spring and summer encephalitis of the Soviet Union. Wild animals, especially voles, are the source of the disease and are the media of transmission. It is characterized by sudden high fever, meningeal irritation, disturbance of consciousness and paralysis. There are abnormal changes in cerebrospinal fluid, often with sequelae. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of transmission: voles spread Complications: pneumonia, coma, cold sore,

The cause of forest encephalitis

Forest encephalitis pathogen (25%):

The pathogen of forest encephalitis belongs to the Togaviridae family, the flaviviruses, the encephalitis virus, and the far-eastern subtype, which is a neurotropic virus. It is a 30-40 nm positive icosahedron with a reticulated lipoprotein envelope on the periphery, and a spike formed by the envelope glycoprotein E, which has an indistinct protrusion, has a villus-like appearance, and the inside of the envelope is a membrane protein (M). ), there is a protein (C) in the nucleocapsid, containing a single strand of positive-stranded RNA, the molecular weight is about 4×106, and its sedimentation coefficient is 218S. The above E, M, and C proteins are structural proteins, and the envelope glycoprotein E Containing hemagglutination antigen and neutralizing antigen, it is closely related to the virus adsorbing on the surface of the host cell and entering the cell and stimulating the body to produce neutralizing antibodies. The change of E arginine can lead to the tissue tropism of the virus, viral virulence, blood coagulation. Changes in activity and fusion activity, experiments have shown that the amino acid residue Tyr of the E protein at position 384 becomes His, which can significantly reduce the pathogenicity of the virus. If the 392 His becomes Tys, it becomes a virulent strain, and the forest encephalitis virus genome There is a single open reading frame, 5 coded virus structure eggs , 3 encoding nonstructural proteins, in addition to the above three structural proteins, and seven non-structural proteins.

Temperature (10%):

The virus is resistant to low temperature, can survive for several months at -20 °C, survives for 1 year at 0 °C in 50% glycerol, is sensitive to high temperature and disinfectant, heated to 60 ° C, inactivated for 10 min, boiled (100 ° C) Immediate death, 3% cresol soap solution 20min, 0.5% formaldehyde solution for 48h, cocoa kills the virus, in addition to ether, chloroform, acetone and bile salts can destroy the virus particles and inactivate the virus, but in 50% glycerol, 2 ~ It can be stored for at least 5 to 12 months at 4 ° C and can be stored for several years under vacuum drying.

Contagious (10%):

The virus can be isolated from the brain tissue of patients. The RNA extracted after treatment with phenol and ether is contagious and can cause infection in mice. The virus inoculates rhesus monkeys, sheep, goats, and wild mice can cause encephalitis in the brain, but home. Rabbits, rats, guinea pigs are not sensitive to this virus. The virus can breed in chicken embryos, yolk sac inoculation or chorioallantoic membrane inoculation virus can also breed, also in human embryonic kidney cells, mouse embryo cells, pig kidney cells, sheep Germ cells, Hela cells and BHK-21 cells multiply, so they are often used for virus isolation.

After infection with the virus, there may be hemagglutination inhibitory antibodies, complement-binding antibodies and neutralizing antibodies in the patient's serum, and the hemagglutination-inhibiting antibodies appear 5 to 7 days after onset, peaking at 2 to 4 weeks, and decreasing after a short-term persistence; The bound antibody appeared 10 to 14 days after infection, reached a peak in 1 to 2 months, and then gradually decreased; the neutralizing antibody rapidly increased in the acute phase, reached a peak in 2 months, and then gradually decreased to a certain level, which lasted for many years.

The sputum encephalitis (forest encephalitis) virus that is prevalent in China and the Russian Far East and the rumored encephalitis that is prevalent in western Russia, Central Europe, and Northern Europe (such as Austria, Bulgaria, Germany, Denmark, Finland, etc.) The virus isolated from the encephalitis acarina occidentalis, also known as the Central European tick-borne encephalitis (CETE), has similar morphological and antigenic properties, but the antigenic structure is somewhat different. Clarke believes that the latter is the same Another subtype of the virus (central European subtype), its incidence area, vector, clinical features and prognosis are different from forest encephalitis. The media of western sputum encephalitis is mainly for scorpion hard sputum (Ixodes) Ricinus), followed by Dermacentor reticulatus, Haemaphysalis punctuta, showed mild symptoms, low mortality, and few sequelae.

(two) pathogenesis

Through the bite of the forest encephalitis virus into the human body, after contacting the local lymph nodes or mononuclear-macrophages, the viral envelope E protein binds to the cell surface receptor, then fuses and penetrates into the cell, and the virus is in the lymph nodes and The nuclear macrophage system replicates, and the replicated virus is continuously released to infect the liver, spleen and other organs. 3 to 7 days after infection, the copied virus is released into the blood to form viremia, which may manifest viremia symptoms. The virus flows into the capillaries with the blood, and finally invades the nerve cells. It can also reach the central nervous system through the lymphatic and neural pathways, producing a wide-ranging inflammatory change, which is clinically characterized by obvious symptoms of encephalitis.

The incidence of sputum encephalitis virus after invading the human body depends on the number of viruses invading the human body and the immune function of the human body. If the amount of virus invading the human body is small, the virus enters during the replication of the virus into the mononuclear macrophage system or after the replication. In the course of the central nervous system, it is inactivated by the body's cell-mediated immunity, complement, antibody and other human immune functions. If only a small number of viruses invade the central nervous system, and the virulence is weak, it is not enough to cause serious pathological damage. At this time, it does not cause the disease or the symptoms are very light. If the cellular immune function is low or defective, a large amount of virus invades the human body, and the virus is highly toxic, and a large number of nerve cells can be destroyed after invading the central nervous system. In addition, the human immune function is Anti-viral antigen reaction can also cause the loss of nerve myelin sheath and the destruction of peripheral blood vessels and vascular tissues. The vascular damage caused by vascular damage further causes damage to the corresponding nerve tissue. Thus, clinical symptoms and typical diseases occur. through.

Forest encephalitis has a wide range of pathological changes, cerebral hemisphere gray matter, white matter and meninges can be involved, spinal cord neck, pons, midbrain and basal ganglia lesions are often more serious, because the vascular network is particularly distributed in the network structure Therefore, unlike Japanese encephalitis, the spinal cord of this disease is also obviously damaged. The neck is heavier than the chest and the lumbar segment. The gray matter is heavier than the white matter. The brain and spinal cord lesions are mainly inflammatory exudative lesions, which are characterized by hemorrhage and congestion. , perivascular lymphocyte invasive infiltration, neuronal degeneration, necrosis and glial cell hyperplasia, degenerative lesions can also occur, internal organs, liver, kidney, heart, lung can appear exudative and degenerative lesions.

Forest encephalitis prevention

The disease has strict regional characteristics. Before entering the epidemic area, it is necessary to actively take precautionary measures: do a good job of environmental sanitation around the living area, and strengthen the work of rodent control and beekeeping. Those who enter the epidemic area for the first time should be vaccinated with a forest encephalitis vaccine. Wear five tight protective clothing when working in an infected area, ie tighten the cuffs, neckline and trousers to prevent biting. The patient's clothes should be disinfected and sterilized.

(1) Strengthening the prevention of cockroaches.

(2) Wearing five tight protective clothing and high boots while working in the forest area, wearing an insect-proof cover; the coat cap can be immersed in dimethyl phthalate, each set of 200g, valid for 10 days.

(3) The vaccination is vaccinated before March every year. The first time is 2ml, the second time is 3ml, and the interval is 7-10 days. After that, 1 needle is strengthened every year, and good immune effect can be obtained.

Forest encephalitis complications Complications, pneumonia, coma, cold sore

Common complications are bronchial pneumonia, more common in patients with coma or medullary paralysis, in addition to myocarditis and cold sore rash, mental disorders, aphasia, dementia, epilepsy, etc., muscle spasm is the most common, mostly upper limb paralysis or upper limb paralysis .

The sequelae are mainly muscle spasm, mental disorders, aphasia, dementia, epilepsy, etc. left behind after brain and medullary lesions. Muscle spasm is the most common, mostly on one side of upper limb paralysis or double upper limb paralysis.

Symptoms of forest brain inflammation Common symptoms Irregular heat expression indifferent low heat involuntary movement fatigue relaxation heat dementia nausea

1. The incubation period is generally 10 to 15 days, the shortest 2 days, and the elderly can reach 35 days.

2. The prodromal period is usually from several hours to three days. The prodromal period of some patients and severe patients is not obvious. The prodromal period is mainly characterized by low fever, dizziness, fatigue, general malaise, limb pain, and most patients are acutely ill. .

3. The course of acute phase is usually 2 to 3 weeks.

(1) fever: general onset 2 to 3 days of fever peak (39.5 ~ 4l ° C), most patients last 5 to 10 days, then stepped down, after 2 to 3 days down to normal, more hot type Hot, some patients may have a heat of exclusion or irregular heat.

(2) symptoms of systemic poisoning: high fever with headache, body muscle pain, weakness, loss of appetite, nausea, vomiting, etc., and due to damage of the vascular movement center, patients may also have facial, neck flushing, conjunctival congestion, slow pulse, Some patients with severe myocarditis have manifestations of myocarditis, often with low heart sounds, increased heart rate, and T-wave changes in electrocardiogram. Severe patients may have sudden cardiac insufficiency and acute pulmonary edema.

(3) Disorder of consciousness and mental damage: About half of the patients have different degrees of consciousness, changes in consciousness, such as lethargy, indifferent expression, confusion, coma, and paralysis and insanity.

(4) manifestations of meningeal involvement: the most common symptoms are severe headaches, which are more common with persistent dull pain in the ankle and posterior occipital region, sometimes explosive and pulsating, with a tear-like full headache, with nausea, vomiting, and neck stiffness. Meningeal irritation, usually lasts 5 to 10 days, can exist at the same time as coma. When the consciousness is awake, it can still exist for about 1 week.

(5) Muscle spasm: the most common combination of the neck muscles and the scapular muscles and the upper limbs, the lower limb muscles and facial muscle spasm are less, and the sputum is more flaccid, which is different from Japanese encephalitis, generally occurring in the second stage of the disease. In most days, most patients recover gradually after 2 to 3 weeks. A few of them have sequelae and muscle atrophy becomes disability. Due to the neck muscles and scapular tendons, the disease has a characteristic head sag. When the scapular tendon is paralyzed, the arm swings. No dependence.

(6) Other manifestations of damage to the nervous system: Some patients have signs of extrapyramidal system damage, such as tremors, involuntary movements, etc. Occasionally, language disorders, dysphagia, and other symptoms of medullary paralysis, or lightness of the central facial nerve and hypoglossal nerve Hey.

4. The recovery period lasted for an average of 10 to 14 days, the body temperature decreased, the limbs gradually recovered, the mind turned clear, and various symptoms disappeared.

Forest encephalitis usually lasts for 14 to 28 days, but a small number of patients can have sequelae, such as aphasia, dementia, difficulty swallowing, involuntary movement, and a few cases can be delayed for several months or 1 to 2 years, patient performance For flaccid paralysis, epilepsy and mental disorders.

In recent years, domestic reports have shown that the clinical symptoms of patients in the acute phase have been alleviated compared with the past, and the mortality rate has also been significantly reduced, which may be related to the use of immunization and strengthening symptomatic treatment.

5. Clinical classification is divided into the following 4 types according to the severity of the disease.

(1) Heavy: sudden high fever, headache, coma, rapid meningeal irritation and cervical muscles and limb muscle spasm, or ascending paralysis in the short-term onset, critical patients, such as rescue is not timely, can die within 1 to 2 days, A few 5 to 10 days or a few months of death due to respiratory failure.

(2) Ordinary (medium): high fever, headache, vomiting and meningeal irritation, accompanied by varying degrees of muscle spasm, and the body temperature drops to normal in 7 to 10 days.

(3) Light type: more fever, headache, dizziness, loss of appetite and body aches and other symptoms of systemic infection and meningeal irritation, brain symptoms are not obvious, more than 5 to 7 days, body temperature begins to decline, gradually reduced to normal, no sequelae .

(4) Frustration type: only mild headache, nausea, vomiting, body temperature around 38 °C, maintain a rapid decline after 1 to 3 days.

6. Classification according to clinical neurological manifestations and pathological features

(1) meningitis type: mainly the clinical manifestations of meningeal involvement such as headache, nausea, vomiting and neck stiffness, and no sputum or disturbance of consciousness.

(2) Meningoencephalitis type: In addition to meningitis symptoms, different degrees of disturbance of consciousness may occur, which may be accompanied by convulsions, pyramidal tract signs or extrapyramidal signs.

(3) brainstem type: in addition to meningeal cerebral inflammatory symptoms, as well as brain stem motor nucleus damage manifestations, such as facial nerve and hypoglossal nerve spasm, language disorders and dysphagia.

(4) polio type: mainly manifested as muscle flaccid paralysis.

(5) Ascending type (Landry type): The initial symptoms are mild, and the lower extremities appear paralyzed. After that, the lesions rise to the neck with the nerve pathway, which can cause peripheral respiratory paralysis, and finally medullary paralysis.

(6) Mixed type: It is the most serious type of clinical symptoms, with the above-mentioned clinical comprehensive manifestations, and the mortality rate is extremely high.

Forest encephalitis check

1. Blood picture: The total number of white blood cells in most patients is increased, mostly between (10 ~ 20) × 10 ⁹ / L, the classification of neutrophils is significantly increased, can be as high as 90% or more.

2. Cerebrospinal fluid examination: color clear, transparent, cerebrospinal fluid pressure increased, the number of cells increased, between (50 ~ 500) × 106 / L, lymphocytes, sugar and chloride no change, protein normal or increased.

3. Virus isolation: Conditional units can take cerebrospinal fluid for virus isolation, but the initial positive rate is low. After death, brain tissue can be used to isolate the virus.

4. Serological test: Complement binding test (CFT) and hemagglutination inhibition test (HLT), double serum titer increased by more than 4 times has diagnostic significance, or CFT single serum titer > 1:16; HIT single serum The titer>1:320 can be diagnosed. Because the operation is difficult, the neutralization test is generally only used for epidemiological investigation. Currently, ELISA is used to detect the IgG antibody of forest encephalitis virus, which is 50-200 times more sensitive than CFI and HIT, respectively. ~80 times, specificity and reproducibility are good, no cross-reaction with JE immune serum was found, and indirect immunofluorescence was used to detect specific IgM antibodies in serum and cerebrospinal fluid for early diagnosis.

5. PCR check: RT-PCR technology is used to detect viral RNA in serum or CSF of early patients, with high sensitivity and specificity.

EEG examination: Most of them are diffuse slow waves or scattered slow waves, and the electrocardiogram changes T waves.

Diagnosis and identification of forest encephalitis

diagnosis

According to the epidemic season (from May to July in spring and autumn), there was a history of bite in the epidemic area, or a history of drinking milk. The clinical manifestations were high fever, headache, nausea, vomiting, and cervical tendon; white blood cells increased, and cerebrospinal fluid pressure increased. The number of cells and protein increased slightly; serological detection of complement binding, hemagglutination inhibition, positive ELISA test, or positive by RT-PCR.

Differential diagnosis

Need to identify with tuberculous meningitis, purulent meningitis, epidemic encephalitis, mumps, poliomyelitis, Coxsackie and Echovirus and other central nervous system infections.

1. The epidemic season of Japanese encephalitis is summer and autumn. The age of onset is mainly children under 10 years old. The affected areas are mainly in temperate zone and subtropical zone. The clinical manifestations are increased in the acute phase, and the tonicity is more common. Relaxed sputum and muscle atrophy.

2. Poliomyelitis is more common in young children, usually flaccid paralysis of the limbs, while the cervical muscles, scapular tendons make the head sagging less common, and there are few conscious disturbances.

3. Infectious polyneuritis can also have muscle flaccid paralysis, but generally symmetry, and often accompanied by sensory disturbances.

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