Japanese encephalitis
Introduction
Introduction to epidemic encephalitis Epidemic encephalitis (abbreviated as JE) is a central nervous system infection caused by a neurotropic JEV. The disease is mainly distributed in the Far East and Southeast Asia, and is transmitted by mosquitoes. It is more common in summer and autumn. It is clinically acute, with high fever, disturbance of consciousness, convulsions, tonic spasm and meningeal irritation. Aftereffects. The mortality and disability rate of JE is high, and it is one of the major infectious diseases that threaten children's health. Summer and autumn are the peak seasons of JE, and the distribution of epidemic areas is closely related to the distribution of vector mosquitoes. Some patients have severe sequelae, and the mortality rate of critically ill patients is higher. Japanese encephalitis pathogen was discovered in Japan in 1934, hence the name Japanese encephalitis. In 1939, JE virus was also isolated in China. After liberation, a lot of investigation and research work was carried out, and it was renamed epidemic encephalitis. basic knowledge Sickness ratio: 0.05% Susceptible people: no special people Mode of transmission: insect vector transmission Complications: sepsis enteritis cerebral edema cerebral palsy
Cause
Cause of epidemic encephalitis B
JEV infection (35%):
JE belongs to the Flaviviridae family. The virus has a diameter of 40 nm and a core of 30 nm. It has a icosahedral structure and is spherical. Under electron microscopy, the virus contains a positive-stranded single-stranded RNA consisting of approximately 10.9 kb. JE is a neurotropic virus. Intraplasma reproduction, sensitive to temperature, ether, chloroform, protease, bile and acid. It can be inactivated at high temperature of 100 °C for 2 min or 56 °C for 30 min. It has high resistance to low temperature and dryness. It is freeze-dried at 4 °C. It can be stored in the refrigerator for several years. The virus can be passaged in the brain of mice, growing and reproducing in chicken embryos, monkey kidneys and Hela cells. The suitable temperature for breeding in mosquitoes is 25-30 ° C. It is known that there are differences in nature. The virulence of the Japanese encephalitis virus, and the virulence can be affected by various external factors. The antigenicity of Japanese encephalitis virus is relatively stable. In addition to the strain-specific antigen, it also has more than one cross-antigen. It cross-reacts with other group B arboviruses in the complement fixation test or hemagglutination inhibition test. High specificity, commonly used in the identification of each virus in the group and each strain of Japanese encephalitis virus.
Exogenous heat syndrome (25%):
In addition, according to the onset season and clinical characteristics of this disease, Chinese medicine believes that the main cause of this disease is caused by the evil of the exogenous heat-sensitive epidemic, which is caused by the difference between the shallow depth of the evil and the individual's ability to resist disease. The condition is mild, heavy and sinister. Although the heat evil is a range of warm diseases, it is different from the general rule of the warm disease. The incidence of JE, especially in severe cases, is sharp, and there is a "children's summer temperature." Fever, that is, seeing the characteristics of horror, so the transitional boundaries between health, gas, camp, and blood are sometimes difficult to distinguish. Summer is a yang, easy to ignite (high heat), wind and oyster (Exhausted coma and phlegm and throat), ( , , , , , , , , , That is, there are a series of symptoms such as high fever, convulsions, coma, etc., even if it can cause positive internal gas loss, it is invincible, and the crisis of "internal closure and external dislocation" occurs, and the summer is often wet, so in some cases in the early stage, Because of the heat and dampness, I see a headache, and Im not hot. Chest tightness, vomiting, fascination, dampness and other symptoms of wetness and stagnation, in the late stage of the disease, due to heat and evil, injury, dystrophic dysfunction, or because the residual heat is unclear, wind, retention and obstruction Regular fever, tremor, aphasia, dementia, difficulty swallowing, quadriplegia and other symptoms, a small number of severe cases, due to qi, yin loss, viscera, meridian function failed to recover in time, can leave sequelae.
Neurocycosis (20%):
Nerve cell degeneration, swelling and necrosis, Nissl bodies disappear, the nucleus is soluble, vacuoles appear in the cytoplasm, and severe necrotic softening lesions of varying sizes are formed in the brain parenchyma, gradually forming cavities or calcinosis, necrosis Softening lesions can be scattered in various parts of the brain parenchyma, a few are fused into a block, and those with severe neuronal disease often cannot be repaired and cause sequelae.
Pathogenesis
When the human body is bitten by mosquitoes with JEV, the virus multiplies through the skin capillaries or lymphatic vessels to the mononuclear macrophage system, and after reaching a certain level, it invades the blood circulation, causing viremia, and invading the intima and each Target organs, such as the central nervous system, liver, heart, lung, kidney, etc., cause systemic diseases. The onset of disease depends mainly on the body's immunity and other defense functions, such as whether the blood-brain barrier is healthy, etc. When cysticercosis can promote the occurrence of encephalitis, the number and virulence of the virus can also play a role in the onset of the disease, and it is closely related to the severity of the clinical symptoms of the susceptible person. When the body's immunity is strong, only transient viral blood is formed. Symptoms, the virus is quickly neutralized and eliminated, does not enter the central nervous system, manifests as a recessive infection or mild cases, but can obtain lifelong immunity; if the infected person has low immunity, the amount of infected virus is large and virulence , the virus can invade the central nervous system through the blood-brain barrier through the blood circulation, using nutrients and enzymes in the nerve cells to multiply in the nerve cells, causing changes in brain parenchyma, if the center If the nerve damage is not heavy, it will be a transient fever; if the damage is severe, the nervous system symptoms are prominent and the condition is severe.
The immune response is involved in the pathogenesis. Some people think that although patients with encephalitis have neuronal cell destruction, most patients can recover almost completely, and the pathologically characteristic vascular cuffs, etc. It suggests that immunopathology is one of the main pathogenesis of this disease. It has been shown in animal experiments that this perivascular cell infiltration is a delayed allergic reaction. It has also been reported that the acute immune complex (CIC) of Japanese encephalitis The positive rate was 64.64%, the IgG content was increased, the CIC was 42.62% in the recovery period, and the IgG was decreased. The CIC-positive patients were accompanied by C3 consumption, indicating that the pathogenesis of JE is involved in immune complexes, and the autopsy reported in brain tissue. IgM, C3, and C4 were detected in the vasculature and inflammatory lesions of the brain parenchyma. CD3, CD4, and CD9-labeled cells were observed, suggesting that cell-mediated immunity and partial humoral immunity may be involved in the pathogenesis.
Pathological anatomy: The disease is a systemic infection, but the main lesion is in the central nervous system. The pathological changes of brain tissue are caused by immune damage, and the clinical manifestations are closely related to the degree of pathological changes.
The disease has a wide range of lesions, and pathological changes can occur from the brain to the spinal cord. Among them, the brain, midbrain, and thalamus are the most severely affected, cerebellum, cerebral ventricle, cerebral palsy, brain parietal lobe, frontal lobe, and hippocampus. Significantly, the lesions of the spinal cord are the lightest.
1. Visual observation of pia mater congestion and edema in the naked eye, shallow sulci, thickening of the cerebral gyrus, visible translucent softening of miliary size, or scattered, or aggregated, even into a larger softening stove, The parietal lobe and thalamus are most prominent.
2. Microscope observation
(1) Cell infiltration and glial cell proliferation: lymphocytes and large mononuclear cells infiltrate in the brain parenchyma. These cells often accumulate around the blood vessels, forming vascular sleeves, and the glial cells are diffusely proliferating in the cerebral parenchyma of inflammation. Walks, plays a role in phagocytosis and repair, and sometimes gathers around necrotic nerve cells to form nodules.
(2) vascular lesions: brain parenchyma and meningeal vasodilatation, congestion, a large amount of serous exudation into the brain tissue around the blood vessels, the formation of cerebral edema, vascular endothelial cells swelling, necrosis, shedding, can form embolism, blocked by blood circulation, local There is congestion and hemorrhage, and the arterioles are paralyzed, which causes the blood vessels of the brain tissue to supply blood and cause nerve cell death.
Severe cases of this disease often involve other tissues and organs, such as liver, kidney, pulmonary interstitial and myocardium, and the severity of the lesions varies.
Prevention
Epidemic encephalitis prevention
prevention:
1) Early detection of the patient, timely isolation of the patient until the body temperature is normal.
2) Pay attention to changes in the condition, observe signs such as body temperature, pulse, respiration, blood pressure, big pupils, and respiratory arrhythmia.
3) Eliminate mosquito breeding grounds, do a good job of anti-mosquito, anti-mosquito measures, cut off the route of transmission.
4) Improve the immunity of the population. For susceptible people, especially children under 10 years old, they should be vaccinated on a regular basis, usually in the first 1-2 months before the popular season. If you have any convulsions, you may be given a massage to promote the recovery of your limb function.
According to reports, JE vaccine is the most effective way to prevent epidemic JE. At present, the main application vaccine is a dead vaccine. After 2 weeks of inoculation, neutralizing antibodies, complement-binding antibodies and hemagglutination-inhibiting antibodies appear in the serum, reaching a peak in about 1 month. A certain amount of neutralizing antibody and hemagglutination inhibitory antibody can neutralize the Japanese encephalitis virus entering the human body, thereby preventing the encephalitis virus from invading the central nervous system and preventing the brain. Newborn babies do not infect JE because the neutralizing antibodies and hemagglutination-inhibiting antibodies of JE can also be transmitted to the fetus through the placenta, allowing newborns to obtain passive immune protection from the mother. After the baby is born, the antibody gradually disappears as the baby ages. Therefore, the vaccination of the JE vaccine should begin when the baby is born for eight months. Since JE mainly sucks the blood of JE virus-carrying pigs through mosquitoes, it will cause infection again by biting susceptible people. Therefore, it is necessary to pay attention to mosquito prevention in daily life.
Complication
Epidemic encephalitis Complications septic enteritis cerebral edema cerebral palsy
First, bronchial pneumonia : more common in severe patients, cough and swallowing reflexes weakened or disappeared and coma patients, prone to pneumonia. Atelectasis can be caused when the secretions of the respiratory tract cannot be discharged smoothly.
Bronchial pneumonia: Bronchopneumonia, also known as lobular pneumonia, is the most common pneumonia in children. Pneumonia occurs mostly during the winter and spring seasons and when the climate suddenly changes, some southern China have more incidences in the summer. Indoor living is crowded, poor ventilation, air pollution, and more pathogenic microorganisms, which are prone to pneumonia. Bronchial pneumonia can be caused by bacteria or viruses. According to the pathological changes, it is divided into two categories: general bronchial pneumonia and interstitial bronchopneumonia. The former is mostly caused by bacteria, while the latter is mainly caused by viruses. Clinically, the general diagnosis is bronchial pneumonia. According to acute onset, respiratory symptoms and signs, general clinical diagnosis is not difficult. If necessary, you can do fluoroscopy, chest X-ray, or throat test, bacterial secretion of tracheal secretions or virus isolation. Other pathogen tests include antigen and antibody detection.
Second, oral infections: patients who do not pay attention to oral hygiene and do not take oral care can have oral ulcers.
Oral ulcers: Oral ulcers, also known as "mouth sores", are superficial ulcers that occur on the oral mucosa. They range in size from rice to soy, round or oval, with a concave surface and congestive congestion. Ulcers are characterized by periodicity, recurrence and self-limiting, which occur in the lips, cheeks, and tongue. The etiology and pathogenesis are still unclear. The cause may be local trauma, mental stress, changes in food, drugs, hormone levels, and vitamin or trace element deficiency. Systemic diseases, genetics, immunity, and microorganisms may play an important role in their occurrence and development. Treatment is mainly based on local treatment, and severe cases require systemic treatment. After 7 to 10 days, the ulcer can gradually heal itself without leaving scars. However, after a period of varying lengths, it can relapse. The interval between the elderly can be 10 to 20 years or longer; the short one can be one after another, the year is continuous, the patient is very painful.
Third, other infections : Staphylococcus aureus caused by sepsis and enteritis, E. coli caused by urinary tract infections.
Sepsis: Septicemia is a systemic infection caused by pathogenic bacteria invading the blood circulation and growing in it, producing toxins, which easily occurs when the body's resistance is reduced. Clinical manifestations include chills, hyperthermia, toxemia symptoms, rash, joint pain, hepatosplenomegaly, septic shock, and migratory lesions. The vast majority of patients have an acute course of disease, with severe illness and poor prognosis. It is now further believed that sepsis is a series of chain reaction processes caused by pathogens and their toxins and metabolites that activate and release inflammation mesons after entering the bloodstream. This process can lead to dysfunction and failure of multiple organs throughout the body.
Enteritis: Enteritis is gastroenteritis, enteritis, and colitis caused by bacteria, viruses, fungi, and parasites. Clinical manifestations include nausea, vomiting, abdominal pain, diarrhea, loose water or mucus pus and blood. Some patients may have fever and sensation after urgency, so it is also known as infectious diarrhea. Common enteritis has the following categories: ulcerative colitis, fungal enteritis, ischemic colitis, rotavirus enteritis, chronic ulcerative colitis, pseudomembranous colitis, acute hemorrhagic necrotic enteritis.
Fourth, hemorrhoids : patients who stay in bed for a long time, if they do not pay attention to change position frequently, it is easy to develop hemorrhoids in the posterior occipital and lumbar vertebrae.
Acne: decubitus, also known as pressure sores, is a long-term compression of the body that blocks blood circulation, causing blisters, ulcers or gangrene due to ischemia of the skin and subcutaneous tissue. The prevention method is to avoid local long-term compression. To turn over regularly, it is best to turn over every 2 hours to 3 hours. Frequently massage the compression site, if necessary, use a steam pad or a sponge pad to cushion the compression site, especially the tail. When moving the patient, behave lightly to avoid pushing and pulling the patient. Always change the sheets and keep the sheets clean, flat and dry. After defecation, remove the urine and urine in time, scrub with warm water to avoid local irritation, to prevent acne.
Symptom
Epidemic type 7 encephalitis symptoms common symptoms expression apathy dysphagia typhoid face irritability uneasiness appetite loss involuntary movement response slow judgment and orientation disorder meningeal irritation symptoms central fever
The incubation period is generally 10 to 15 days, which can be as short as 4 days and as long as 21 days. After infection with Japanese encephalitis virus, the symptoms are very different, most of them are asymptomatic or mild, and only a few patients have central nervous system symptoms, which are characterized by high fever. Change of consciousness, horror, etc.
1. Course of course The typical course of disease can be divided into the following four phases.
(1) Initial stage: 3 days after the onset of the disease, the viremia period, acute onset, generally no obvious prodromal symptoms, may have fever, wilting, loss of appetite, mild sleepiness, large children may complain of headache, infants may appear Diarrhea, body temperature at around 39 ° C, continued to retreat, at this time the nervous system symptoms and signs are often not obvious and mistaken for the upper sense, a small number of patients with ambition, irritability or neck mild resistance.
(2) Extreme period: the course of disease is 3 to 10 days. In addition to the aggravation of systemic toxic blood, the symptoms of brain damage are obvious.
1 high fever: body temperature continues to rise above 40 °C and continues to not return until the end of the extreme period, high heat lasts 7 to 10 days, light is as short as 3 to 5 days, severe can be more than 3 to 4 weeks, the general fever is higher, heat Cheng Yuechang, the more serious the clinical symptoms.
2 disturbance of consciousness: the patient's systemic symptoms are aggravated, and obvious neurological symptoms and signs appear. The patient's consciousness disorder is aggravated. From sleepiness to coma, the incidence rate is 50% to 94%. The sooner the coma is, the deeper and longer the disease becomes. Heavy, the duration is mostly about 1 week, and the severe cases can be more than 1 month.
3 convulsions: the incidence of 40% to 60%, is a serious manifestation of the disease, severe cases of recurrent seizures, and even limb tonic spasm, coma deepening, can also appear pyramidal tract symptoms and limb involuntary movement.
4 nervous system symptoms and signs: the nervous system symptoms of JE appear in the course of 10 days, after the second week, there are few new neurological symptoms, often shallow reflexes disappear or weaken, deep reflexes disappear after the first hyperthyroidism, pathological cone Body bundle signs such as Babinski's sign can be positive, often with meningeal irritation, due to viral toxins invading the cerebral vascular endothelium, choroid plexus epithelial cells, arachnoid and neuroblastic epithelial cells, producing inflammation and degeneration, which occurs Different degrees of meningeal irritation, such as neck strength, Kernigger sign and Bruzinski sign positive, severe cases have horn arches, infants and young children have no meningeal irritation, but often have anterior ridge, deep coma Bladder and rectal paralysis (incontinence or urinary retention) may be associated with autonomic nerve involvement. In the case of coma, in addition to the disappearance of shallow reflexes, there may be limb tonic paralysis. Hemiplegia is more common than single sputum, or full sputum. The muscle tension is increased, and the knee and Achilles tendon reflexes first and then disappear.
5 cerebral edema and increased intracranial pressure: severe patients may have varying degrees of cerebral edema, resulting in increased intracranial pressure, the incidence of 25% to 63%, mild intracranial pressure increased pale, severe headache, frequent vomiting , convulsions, high blood pressure, the pulse first accelerates and then slows down, early conscious but indifferent, and quickly into sleepiness, convulsions, irritability or paralysis, rapid increase in breathing, severe cerebral edema is pale, repeated or Sustained convulsions, increased muscle tone, slower pulse, higher body temperature, deeper consciousness disturbance, shallow coma or deep coma, pupils suddenly and small, slow response to light, eyeballs can sink, and various abnormal breathing occurs. Progression to central respiratory failure, and even cerebral palsy, including cerebellar hernia (also known as sacral sacral hernia) and occipital foramen (also known as cerebellar tonsil sputum), the former manifested as disturbance of consciousness, gradually developed into deep coma The diseased side has large pupils, the upper eyelids sag, the contralateral limbs and pyramidal tract signs are positive; the occipital macropores appear to be extremely agitated, the eyeballs are fixed, the pupils are scattered or the light reflection disappears. Stroke slow, weak or irregular breathing, but patients often suddenly stop breathing.
6 Respiratory failure: occurs in extremely severe cases, the incidence rate is 15% to 40%, extremely severe JE due to brain parenchymal inflammation, hypoxia, cerebral edema, cerebral palsy, hyponatremia and other causes of central respiratory failure, of which brain Substantial lesions are the main cause. When the lesions in the cerebral respiratory center occur, central respiratory failure can occur rapidly. The respiratory rhythm is irregular, double inhalation, sigh-like breathing, central hyperventilation, apnea, and tide breathing. Lower jaw breathing, etc., the last breath stops, when the central respiratory failure stops breathing, the possibility of spontaneous breathing is very small, in addition, due to concurrent pneumonia or after the spinal cord is violated, causing respiratory muscle spasm and peripheral Respiratory failure.
High fever, convulsions, and respiratory failure are serious symptoms of the extreme JE. The three interact with each other, especially respiratory failure, which is often the leading cause of death.
7 circulatory failure: a small number of patients with JE can have circulatory failure, showing decreased blood pressure, rapid pulse rate, cold limbs and vomiting brown liquid, the cause of which is mostly visceral congestion, reducing effective circulating blood volume; gastrointestinal tract Blood, hemorrhage; J brain due to metabolic disorders, toxin absorption to produce vasospasm; myocardial lesions produce cardiac insufficiency; cerebral vasomotor center damage, etc., patients with gastrointestinal bleeding can often be life-threatening, should be valued .
Most patients after the extreme course of 3 to 10 days, the body temperature began to decline, the condition gradually improved, and entered the recovery period.
(3) Recovery period: At this time, the patient's body temperature can gradually decline and return to normal in 2 to 5 days, the consciousness disorder begins to improve, and the coma patient gradually wakes up after a short period of mental stagnation or apathy, and the pathological signs of the nervous system gradually improve and disappear. Some patients recover slowly, which takes more than 1 to 3 months. In severe cases, the brain tissue lesions are heavy. The symptoms in the recovery period can be persistent low fever, sweating, insomnia, stagnation, unresponsiveness, mental and behavioral abnormalities, aphasia or In particular, dysphagia, limb tonic spasm or involuntary movements, epileptic seizures and other symptoms, after active treatment, can be restored after half a year.
(4) sequelae: sequelae are closely related to the severity of JE lesions. The sequelae are mainly conscious disturbances, dementia, aphasia and limb paralysis. If active treatment can also have different degrees of recovery, patients with coma sequelas stay in bed for a long time, can be complicated with pneumonia. Acne, urinary tract infections, and epileptic seizures sometimes last a lifetime.
2. Clinical characteristics of infant J. When it occurs, it can be characterized by laxative, salivation, mild cough, wheezing, lethargy, easyness or crying, and the incidence of convulsions is high. The proportion of people without meningeal irritation is high, but there are often anterior Uplift, cerebrospinal fluid examination is more normal, less complications.
3. Elderly patients with J-cerebral clinical characteristics of patients over 60 years old, acute onset, have high fever, serious condition, heavy and extremely heavy accounted for 86.1% and 91.7%, early coma, and long duration, some with circulatory failure and brain Hey, the mortality rate is as high as 66.6%, more complicated with intrapulmonary infection, urinary tract infection, gastrointestinal bleeding, myocardial damage and so on.
4. Clinical classification According to the severity of the disease, it can be divided into the following four types.
(1) Light type: The patient's mind is always awake, but there are different degrees of lethargy, generally no convulsions, body temperature is about 38 ~ 39 ° C, headache and vomiting is not serious, may have mild meningeal irritation, most of them recover in about 1 week, Generally no sequelae, mild central nervous system symptoms are not obvious clinically often missed diagnosis.
(2) Ordinary type: body temperature is often between 39 ~ 40 ° C, conscious disturbances such as lethargy or coma, headache, vomiting, meningeal irritation, abdominal wall reflex and cremaster reflex disappear, deep reflection hyperthyroidism or disappear, may be once or Several times of transient convulsions, with mild cerebral edema symptoms, the course of disease is about 7 to 14 days, no or mild recovery of neuropsychiatric symptoms, no sequelae.
(3) Heavy: body temperature continues at 40 ° C or higher, the mind is shallow coma or coma, irritability, often repeated or persistent convulsions, pupil diminution, presence of light reflection, may have localized symptoms or signs, such as limb paralysis, etc. Occasionally, swallowing reflexes are weakened, and symptoms of severe cerebral edema may occur. The course of the disease is often more than 2 weeks. In the coma, the brain tissue lesions recover slowly, and some patients have different degrees of sequelae.
(4) extremely heavy: this type of patient begins to rise rapidly in the initial heat period, up to 40.5 ~ 41 ° C or higher, with repeated episodes of difficult to control continuous convulsions, progress to deep coma within 1-2 days, often limbs Tonic sputum, clinical manifestations of severe cerebral edema, further development of circulatory failure, respiratory failure and even cerebral palsy, high mortality, survivors often have serious sequelae.
5. Brain lesion localization
(1) Upper brain stem: lesions involving the brain and the diencephalon, not invading the brain stem, clinically slumbering or coma, pseudo-autonomous exercise when pressing the eyelids, or cortical rigidity, such as sacral leaf damage can cause hearing impairment; Leaf damage may have visual impairment, visual deformation, etc., eye movement exists, early pupil is small or normal, the pupil of the neck skin stimulation test can be dilated, the breathing is always normal, if the hypothalamic lesion, the part is a higher level of autonomic nerve The central nervous system is also the center of body temperature regulation. It can cause autonomic dysfunction such as sweating, flushing, palpitations and arrhythmia, and hyperthermia and other thermoregulatory disorders.
(2) Upper brainstem: The lesions are at the midbrain level, and some of the third to eighth pairs of cranial nerves are affected. The patient is in a deep coma, the muscle tension is increased, the eye movement is slow, and the pupil is slightly larger. The light reflection is poor or disappears, the breathing is abnormal, and the central ventilation is excessive, causing respiratory alkalosis. The cervical skin irritation test shows that the pupil is reactively enlarged, but the reaction is slow. If the central side is damaged, the pyramidal beam will descend. Impaired access, can cause quadriplegia, said to the brain tonic, if the unilateral midbrain is damaged, it is contralateral hemiplegia.
(3) Lower brainstem: The lesion is equivalent to the level of pons and cerebral ventricle, with IX~XII cranial nerve affected, deep coma, no reaction of pressure eyelid, corneal reflex and pupillary reaction disappear, no reaction of cervical skin irritation test, pupil Does not enlarge, difficulty swallowing, accumulation of throat secretions, rapid central respiratory failure.
Examine
Examination of epidemic encephalitis B
1. Blood picture The total number of white blood cells is increased, generally around (10 ~ 20) × 109 / L, individual up to 40 × 109 / L, which is different from most viral infections, neutrophils can be seen in white blood cell classification up to 80%, And there is a left shift of the nucleus. After 2 to 5 days, lymphocytes can predominate, and some patients have normal blood.
2. Serological examination
(1) Determination of specific IgM antibodies:
1 Immunofluorescence technique: The indirect immunofluorescence method was used to detect the specific IgM antibody of JE, and the positive rate was as high as 97%, which was characterized by rapid sensitivity.
2 Capture ELISA (MAC-ELISA): In recent years, the detection of JE-specific IgM by MAC-ELISA has strong sensitivity and specificity, the positive rate is 74.4%, and the positive rate on the 4th day of the disease is 93%. Can be used for early diagnosis.
3ABC-ELISA: detection of J-specific IgM antibody sensitivity, high positive rate, can reach 75.3%, for early diagnosis.
(2) Hemagglutination inhibition test: Hemagglutination inhibition antibody appears on the 5th day of the disease, and reaches the peak at the 2nd week, which can be maintained for more than 1 year. The positive rate of the hemagglutination inhibition test can reach 81.1%, which is higher than the complement fixation test. Sometimes false positives occur because the hemagglutinin antigen of Japanese encephalitis virus has weak cross-reaction with the same virus, such as dengue fever and yellow fever virus, so the double serum titer is increased by more than 4 times or the single-part titer is reached. More than 1:80 can be used as a basis for diagnosis. This method is easy to operate and can be applied to clinical diagnosis and epidemiological examination.
(3) Complement binding test: sensitivity and specificity are high, antibody appears later, and it begins to appear 2 to 3 weeks after the disease, reaching a peak at 5 to 6 weeks, so it cannot be diagnosed early, and is generally used for retrospective diagnosis. Or epidemiological investigation, antibody maintenance time is about 1 to 2 years, antibody titer is positive by 4 times or more of double serum, single serum 1:2 is suspicious, and 1:4 or above is positive.
(4) Neutralization test: Neutralizing antibodies appear in the second week after onset, lasting 2 to 10 years, and have high specificity, but the method is very complicated. It is only used for epidemiological investigation of population immunity level, and is not used for clinical diagnosis. In recent years, neutralization tests have been replaced by other methods for determining antibodies to JEV, and are rarely used.
(5) Other serological methods: such as specific leukocyte adhesion inhibition test (LAIT), plaque reduction and neutralization test (PRNT) to check the serum of acute patients, the positive rate is relatively high.
(6) JE virus antigen determination: The positive rate of JE antigen in serum in the acute phase was 71.5% by reverse passive hemagglutination method of McAb, which is a good rapid diagnosis method.
3. Cerebrospinal fluid examination
(1) routine examination of cerebrospinal fluid: except for increased pressure, the appearance is colorless and transparent, even slightly turbid, and the white blood cell count is mostly slightly increased, mostly between (50-500)×106/L (about 80%), a few Up to 1000 × 106 / L or more, there are very few normal, the white blood cell count is not related to the prognosis, neutrophils mainly in the first 2 to 5 days of the disease, followed by lymphocytes, the protein is slightly increased The sugar is normal or high, occasionally reduced, chloride is normal, about 2% to 4% of patients with JE have normal and biochemical examination of cerebrospinal fluid, in addition, cerebrospinal fluid aspartate aminotransferase (AST) within 1 to 2 days of onset The activity is often increased. It is useful for judging the prognosis of the disease and brain tissue damage. It takes 10 to 14 days for the cerebrospinal fluid to change to normal. Individual cases take 1 month.
(2) JE antigen determination: The antigen in the early cerebrospinal fluid was measured by reverse indirect hemagglutination (IRHT), the positive rate was 66.7%. The method is sensitive, simple, rapid and requires no special equipment.
(3) Specific antibody assay: The JE virus IgM and IgG antibodies in the cerebrospinal fluid of patients were determined by MAC-ELISA, and compared with the occurrence of the above two antibodies in serum, it was found that IgM antibodies in cerebrospinal fluid appeared in the serum before the course of disease. It can be measured on the second day and lasts longer than the serum antibody, which can be used for early diagnosis.
4. Virus isolation JEV is mainly found in brain tissue . The virus is isolated from the blood and cerebrospinal fluid at the beginning of the disease. The positive rate is very low. JE virus can be isolated from the brain tissue of the early death.
5. Blood gas analysis can be used for blood gas analysis in critically ill patients, in order to detect early pathological changes such as respiratory failure and acid-base metabolic disorder. In recent years, some patients with JE respiratory failure have been tested and found to have respiratory acidosis. Mainly, followed by respiratory alkalosis.
The CT and MRI features of JE are characterized by bilateral symmetric distribution of the thalamus. The lesions on CT are low-density. The low-density sites are mainly found in the thalamus, midbrain and basal ganglia. Cerebral edema is also seen, accompanied by ventricular enlargement. Brain atrophy, etc., some patients with acute early CT can be normal, brain MRI showed that all cases have bilateral thalamic lesions, T1 weighted lesions mostly mixed signal or low signal, T2 weighted image showed high signal or mixed signal, most Commonly, low signals of different widths surround the high signal center, and the proton density weighted images are mostly high signals, except for bilateral thalamic damage, cerebral cortex, cerebellum, midbrain, pons, bilateral basal ganglia, white matter around the ventricles and There is at least one part of the cervical spinal cord with an abnormal signal.
6, CT, MRI examination
The CT and MRI features of JE are characterized by bilaterally distributed lesions of the thalamus. The lesions on CT showed low density, and the low-density sites were mainly found in the thalamus, midbrain and basal ganglia. Brain edema and brain atrophy with enlarged ventricles were also observed. Some patients with acute early CT can be normal. MRI of the brain showed that all cases had bilateral thalamic lesions. The T1-weighted lesions showed mixed signals or low signals, and the T2-weighted images showed high or mixed signals. The most common low-density signals of different widths surround the high-signal center. Proton density weighted images are mostly high signals. In addition to bilateral thalamic damage, there are abnormal signals in at least one part of the cerebral cortex, cerebellum, midbrain, central pons, bilateral basal ganglia, periventricular white matter and cervical spinal cord.
7, microbiological examination
Blood or cerebrospinal fluid was collected from patients in the acute phase, and JEV-specific IgM was detected by ELISA. The sensitivity, specificity and reproducibility of this method are good, and the results can be reported within 4 hours, which can be used for rapid (early) diagnosis and differential diagnosis of Japanese encephalitis.
Diagnosis
Diagnosis and identification of epidemic encephalitis
diagnosis
Diagnose based on:
1. There is obvious seasonality, mainly in 7 to 9 months, the patients are mostly children and adolescents.
2. Rapid onset, sudden fever, headache, vomiting, disturbance of consciousness, and gradually worsened after 2 to 3 days, severe cases can quickly appear coma, convulsions, difficulty swallowing and respiratory failure.
3. There are no obvious signs in the early stage. After 2 to 3 days, the common meningeal irritation sign, abdominal wall reflex, cremaster reflex disappeared, Babinski sign positive, and limb muscle tension increased, etc. should consider the disease.
4. The diagnosis depends on serological diagnosis. The specific IgM can be positive on the 4th day after the disease, and reaches the peak 2 to 3 weeks after the disease. Domestic research confirmed that reverse transcription-polymerase chain reaction (RT-PCR) can help. In the rapid diagnosis of clinical JE patients, the sensitivity is high, the specificity is reliable, and the combined application with the RHPT method will greatly improve the diagnosis rate of current J brain patients.
Conventional serological tests (complement binding test, neutralization test) have auxiliary diagnostic significance and can be used for clinical retrospective diagnosis.
Differential diagnosis
1. Toxic bacteria caused by JE occur in summer and autumn, and more common in children under 10 years old, so it needs to be identified with more toxic bacillary dysentery in this season. The latter has a rapid onset and develops rapidly within 24 hours of onset. High fever, convulsions, coma, shock, and even respiratory failure. At this time, there are no intestinal symptoms such as diarrhea and pus and blood in the clinic. It is easy to be confused with JE. However, patients with J brain generally do not have the above-mentioned dangerous symptoms, and are toxic. Bacterial sputum generally does not show signs of meningeal irritation. If necessary, it can be enema with normal saline. If pus blood sample is obtained, microscopic examination and bacterial culture can be used to confirm the diagnosis. In special cases, cerebrospinal fluid examination can be performed, and there is no change in toxic sputum cerebrospinal fluid.
2. Suppurative meningitis The symptoms and signs of central nervous system are similar to those of JE, but the epidemic cerebrospinal meningitis in purulent meningitis is more common in winter and spring. Most of them have skin mucosal sputum, cerebrospinal fluid opacity, and leukocytosis. From thousands to tens of thousands, more than 90% of neutrophils, sugar content is reduced, protein content is significantly increased, cerebrospinal fluid smear and culture can obtain pathogenic bacteria, JE has fashion needs and other early purulent meningitis and The identification of suppurative meningitis that is not completely treated requires reference to the onset season, age, and primary infection site, and the cerebrospinal fluid is reviewed several times according to the condition, and blood and cerebrospinal fluid culture is performed, and combined with clinical diagnosis.
3. Tuberculous meningitis is not seasonal, with a history of tuberculosis or exposure to tuberculosis. Infants and young children have no history of vaccination with BCG. The onset is slow, the course of disease is longer, the meningeal irritation sign is more significant, and brain symptoms such as disturbance of consciousness are lighter. Later, the appearance of cerebrospinal fluid is ground glass, white blood cells are classified mainly by lymphocytes, sugar and chloride content are reduced, protein content is increased, and M. tuberculosis can often be found when film smears are used. X-ray examination is performed when necessary. Fundus examination and tuberculin test to identify it.
4. Other viruses cause encephalitis
(1) Meningoencephalitis caused by enterovirus: At present, the incidence rate is increasing. 20% to 30% of the summer and autumn brains are encephalitis caused by other viruses. The main pathogens are Coxsackie and Echovirus. The onset of meningoencephalitis caused by these two enteroviruses is not as good as that of JE, the clinical manifestations are lighter than that of JE, the central nervous system symptoms are not obvious, no obvious brain edema and respiratory failure occur, the prognosis is good, and most of them have no sequelae after recovery. .
(2) Cerebral poliomyelitis: a rare clinical type in polio, its clinical manifestations resemble JE, acute onset, high fever, coma, convulsions, dilated pupils, unresponsiveness, increased muscle tone in the extremities, and may appear Quadriplegia or tonic convulsions, rapid progression, high mortality, and the season is also in summer and autumn, therefore, serological or virological examination is needed for identification.
(3) Mumps encephalitis: more common in viral encephalitis, mostly in winter and spring, most have a history of contact with mumps, encephalitis often occurs 3 to 10 days after parotid swelling, a small number of swelling in the parotid gland Pre-occurrence, no swelling of the parotid gland, serum amylase determination and serum antibody detection can help differential diagnosis.
(4) Herpes simplex virus encephalitis: severe disease, rapid development, often localized symptoms of frontal and temporal lobe damage, EEG shows localized slow wave, herpes simplex encephalitis still has a mortality rate of 30% Above, most survivors have different degrees of sequelae, and antibodies to cerebrospinal fluid are helpful for diagnosis.
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