Japanese encephalitis (japonica)

2021-01-31 12:00 AM

The onset of the disease corresponds to when the virus crosses the vascular barrier - the brain damages the brain organization and causes brain oedema.

Define

Japanese encephalitis is an acute infectious blood-borne disease caused by the Japanese encephalitis B virus. The disease is clinically characterized by severe systemic intoxication syndrome with the development of severe myelitis and high mortality.

Research history

Japanese encephalitis was known more than 100 years ago. At the end of the nineteenth century, outbreaks occurred in the mountains of Japan in the summer - autumn with many critically ill patients and 60% mortality. In 1933 Hayashi (Japanese) isolated Japanese encephalitis virus from the brain of dead patient. He took the patient's brain fluid and injected him with disease.

In the years 1933-1936 Japanese researchers demonstrated that this virus is transmitted by mosquito bites as Culex mosquito. In 1954, a vaccine for preventing Japanese encephalitis was developed in Japan for the first time.

Japanese encephalitis outbreaks have been reported in countries such as Japan, China, Korea, Burma, Indonesia, Malaysia, the Philippines, India, the Soviet Union, Thailand, Vietnam and other regions. Australia and Africa.

In Vietnam, discovered in the 60s of the 20th centuries, epidemic outbreaks occur annually in the most endemic outbreaks, especially in the areas along Day River in Ha Tay, Thanh Hoa, Thai Binh ...

Epidemiology

Pathogens

Japanese encephalitis virus, belonging to group B arbo virus, family Togaviridae, genus Flavivirus; with dimensions 15-22-50 nanometres, with RNA. Virus development in chicken embryonic cells and culture. Viruses are not heat resistant, they are inactivated at 56 ° C for 30 minutes; at 70 ° C for 10 minutes, 100 ° C for 2 minutes. In the frozen state the virus can persist for several years. Under the effect of acetone, alcohol and viral ether died after 3 days. Lysol 5% solution kills viruses in 1 minute. Some of the animals that are susceptible to the Japanese encephalitis virus are: monkeys, guinea pigs and some field mice, some mosquitoes and many birds.

Inoculum

Mainly wild birds (herons, cigarettes…) and cattle (pigs, horses…).

Japanese encephalitis is a disease with natural epidemics everywhere. Petrixepva - 1969 divided into: outbreak of grassland (steppe), outbreak of seas, outbreaks in mountainous areas and outbreaks in mountainous areas. The virus circulates in natural outbreaks among mammals and birds. In Vietnam, virus has been isolated from birds of Lieu (Garrulax parapicitlaties).

Infection

As blood sugar, through disease vectors are Culex mosquitoes.

In nature, viruses are transmitted from hosts to each other and to humans through Culex-like mosquitoes (strains of C. tritaeniorhynchus, C.pipiens, C. bitaeniorhynchus ..) are mainly, in addition, Aedes breed ( strains A. togoi, A. Japonicus), have documents mentioning Anopheless maculipennis also capable of transmitting disease.

In Vietnam, Culex tritaeniorhynchus mosquito reproduces strongly in the summer (especially from March to July), and is active in the evening. This mosquito has a high density in the plains and midlands, it is the main vector for the transmission of Japanese encephalitis in our country.

Sensory body, immune properties

Fertility is high for children under 10 years old. The proportion of adults with high antibodies is therefore less likely to get the disease.

The incidence of Japanese encephalitis is higher in the lowlands than in the mountains and in the countryside higher than in cities.

After being sick, it leaves strong and stable immunity.

Mechanisms of pathogenesis and anatomical pathology

Mechanism of pathogenesis

The course of Japanese encephalitis depends on the factors of the infected host and the Japanese encephalitis virus.

The virus is transferred into the blood by mosquitoes, they grow in the blood and travel throughout the body. Thanks to the neural direction, the virus invades nerve cells, reproduces and grows rapidly there. After reaching high densities in nerve cells, the virus again invades the blood for the second time. A second viral infection in the blood begins to cause a fever reaction. Clinically it corresponds to the onset of the acute phase of the disease. When the Japanese encephalitis virus has entered the central nervous system, they have the ability to multiply in neurons, causing inflammatory responses in the brain and local antibody production against the virus in the brain. Central nervous system as well as cellular immunity promotes neurological symptoms as well as prognosis of the disease.

Pathological anatomy

The most pronounced pathological variation in the nervous system. On a microscope one can see the changes that are: edema of the brain and brain structure, the arteries and veins of the brain dilated and blood stasis, small spot haemorrhages in the brain and soft membranes. In the brain organization and especially the hippocampus, the striatum and the ammonium horn have cerebral foci and haemorrhage.

In internal organs there is blood stasis, there are many petechiae in mucosa and serosa. Degeneration of myocardial organization, liver, kidney and arises pneumonia. Haemorrhagic inflammation and degenerative meningitis - medulla and brain-marrow matter. In addition to edema and spotting haemorrhage, infiltrates around the blood vessels of the brain and spinal cord are also seen, creating inflammatory foci around the blood vessels, glial cells, necrosis and cerebral necrosis. small. The most severe pathological changes occur in the hippocampus, Gray matter, red nucleus, frontal body and cerebellum.

clinical

Divide the clinical form

Typical body.

Meningitis.

Hidden.

Spinal paralysis.

Specifically.

Soft polio like polio.

Symptom clinical form

Typical body

Incubation period:

Lasts 5-14 days, an average of 1 week.

Onset period:

The onset of illness is very sudden with a fever of 39-40 ° C or more. Patients with headache, especially the forehead, abdominal pain, nausea and vomiting. Right in the first 1-2 days of the disease appeared stiff neck, increased muscle tone, disturbed eyeball movement. Psychologically, confusion or loss of consciousness may appear. In the first days, the tendon reflexes increase, the pulse dilates clearly. In some young children, in addition to a high fever, diarrheal, abdominal pain, and vomiting may look like a bacterial infection - eating poison.

To summarize during the onset of disease are characterized by sudden high fever, meningeal syndrome and mild to severe consciousness disorders (dystrophy, irritability, struggles, gloominess, complete loss of consciousness.).

The onset of the disease corresponds to when the virus crosses the vascular barrier - the brain damages the brain organization and causes brain edema.

Full-play period: 

(From day 3-4 to day 6-7 of illness).

By day 3-4 of the illness, onset symptoms do not decrease but increase. From excitable delirium, initial gloom, gradually the patient enters a deep and deep coma.

Nervous plant disorders symptoms also increased: Excessive sweating, red skin, pale, dyspnoea, and increased secretion in the bronchial airway so when listening to the lungs, you can see a lot of hissing. both snoring and exploding. The pulse in the patient is usually rapid and weak.

Symptoms of general brain damage and focal nerve damage are prominent in the general phase. Delirium, hallucinations, agitation, extrapyramidal hypertonia cause the patient to lie down and have twists. In the case of severe damage to the pyramid system, spastic convulsions or tremors of facial and limb muscles may be seen or spastic paralysis. In some patients, a fixated state appears, maintaining position (catalepsia).

Due to dysfunction Hypothalamus causes rapid pulse 120-140 times / min, increasing arterial pressure and peripheral vasoconstriction.

The cranial nerves are also damaged, especially the ligaments of the eye (III, IV, VI) and the VII cord.

Disorder of the central respiratory region leads to shallow tachypnea, exudates much in the bronchial air and can see pneumonia or splenitis.

About testing: Right from the first days, white blood cells usually increase from 15,000-20,000 / mm3, in which, neutrophils increase by 75-85%, eosinophils and lymphocytes decrease. The rate of blood sedimentation in most patients increases (up to 20-30mm / hour).

Cerebrospinal fluid test: Cerebrospinal fluid pressure increased, clear fluid, Protein slightly increased (60-70mg%) slightly increased cells (less than 100 cells / mm3) and at first polymorphonuclear leukocytes and later Lymphocyte predominates, Glucose in cerebrospinal fluid has little change or increases slightly ...

Acute fundoscopy in the acute phase often shows popular congestion, sometimes with both edema and bleeding. Patients with disorders of colour and light perception, narrow their field of vision.

This period corresponds to the period when the virus invades brain cells, causing damage to nerve cells.

In summary, the full eradication period of Japanese encephalitis is short. Due to damage to the nerve cells in the brain, Hypothalamus and disorders of the subcortical medias put the patient into a deep coma with a disturbance of life functions. So, patients usually die within the first 7 days. Patients who pass this period have a better prognosis.

Recovery period:

With complications and sequelae (from day 7, 8 onwards).

Normally, in the 2nd week of illness, the patient gets better, the temperature decreases from a high fever to a mild fever, and from day 10 onwards the temperature returns to normal if there is no other bacterial superinfection. Along with temperature, the pulse also slows down to normal, breathing is not disturbed. The brain-meningeal syndrome also gradually disappears: the patient gradually awakens from coma; the muscle tone decreases and there is no spasticity. The patient stopped vomiting and headache, soft nape, and meningeal signs returned negative.

While infectious syndrome and encephalitis-meningeal syndrome diminish, the nerve damage is more localized than before. Patients may have paralysis and limb paralysis or cranial nerve palsy or motor coordination disorder, etc. This period may appear early complications such as: bronchitis, pneumonia or bronchitis - lung due to superinfection; pyelonephritis, bladder due to urination or drainage; ulcers and thrombophlebitis due to lying and nutritional disorders ... The possible early complications are: Paralysis or paralysis, loss of language, dancing, movement coordination, memory loss serious, psychosis, spastic brain loss ...

Complications and sequelae:

From the end of week 2 onwards is the period of late complications and sequelae. The possible late complications are: Lung inflammation, pyelonephritis - bladder, septic ulcer, sympathetic disorder, metabolic disorder. Late sequelae can appear after a few years or even decades with epilepsy and Parkinson's common.

Prognosis of the disease:

The disease has a high mortality rate (25% in tropical countries) and neurological sequelae is about 50%. In our country, according to reports of a number of treatment facilities (neurology department - Bach Mai hospital and infectious department - Institute for the protection of children's health) the death rate has decreased to about 10%. Death usually occurs in the first 7 days when a patient has deep coma, convulsions and symptoms of brain damage leading to severe respiratory and cardiovascular disorders. Death in the later stage is mainly due to special complications such as: pneumonia, exhaustion ...

Those who do survive may have lifelong sequelae, which is more common with mental disorders.

Some may not be atypical

Hidden:

Not every case of virus entering the body causes disease. It is found that after the epidemic the number of people who do not have the disease and still have an immune response is very high (hundreds of times higher than the number of people infected).

Specifically:

Only the syndrome of toxic infections (high fever, congestion of the skin, mucous membranes, headache). Besides, there was no symptom of brain-meningeal syndrome.

Meningitis:

 Meet in older children and young adults. The disease progresses like another viral meningitis.

Other models:

Paralysis of the medulla, soft paralysis (due to inflammation of the anterior pulp keratinocytes)

Implementing the quadrants

Clinical 

Severe systemic poisoning syndrome: sudden and continuous high fever, severe headache, confusion of consciousness, coma. Leukocytes increased (polymorphonuclear leucocytosis).

Neurological Syndrome: Initially, there are signs of diffuse brain damage with consciousness disturbances in varying degrees, later manifestations of focal neurological syndrome. Has meningeal syndrome and cerebrospinal fluid changes.

Severe vegetative neurological disorders: The skin is congested at first and after erratic changes in red to cyanosis, sweating, respiratory and circulatory disorders.

Specific test

Isolation of the virus (in the first 2-3 days) from blood, cerebrospinal fluid or cerebral fluid (just died in 2 hours).

Serum reactions: May cause complement fusion (positive from week 2) or erythrocyte agglutination and neutralization (positive lasting for many months). The enzyme immunoassay method (ELISA) is a widely used method with high sensitivity and specificity.

Imaging diagnosis: Computerized tomography and magnetic resonance imaging showed a decrease in diffuse density, wide cerebral coils, slightly deflated ventricular system, no sign of displacement mass.

Epidemiology

The place where the epidemic is circulating (pay attention to the area along Day river). The disease usually arises in the summer (May 5,6,7,8) and in young children (from 2-3 years old to 10-12 years old).

Differential diagnosis

With secondary encephalitis

Some infectious diseases can cause secondary encephalitis such as measles, flu, chickenpox, whooping cough ... On the basis of the main disease, then appear more symptoms of encephalitis, but usually only spread discharge has no localized symptoms and when it goes away, it leaves little sequelae.

With acute brain syndrome

Due to metabolic disorders leading to hypoglycaemia (hypoglycaemic coma), due to severe water and electrolyte disturbances (Na, K, Ca), severely malnourished children have acute cerebral circulatory disorders. Acute brain syndrome due to metabolic disorder also has coma, but localized syndrome is rarely seen, cerebrospinal fluid rarely changes.

With meningitis or tuberculosis meningitis

Without brain syndrome, cerebrospinal fluid has pathological changes.

Ap x and no, u no

Based on brain CT scanner

Treatment

Currently, there is no specific treatment, so the content of treatment is: Anti-cerebral edema, symptomatic treatment and superinfection.

Against brain edema

Infusion of hypertonic fluids to increase osmotic pressure, withdraw water in the cell structure and intercellular space into the lumen. Intravenous infusion of 10-20-30% Glucose solution. Glucose only causes a short time decrease in pressure in the cerebrospinal cavity (no more than 35-40 minutes). Therefore, if not alternating using other diuretic fluids, it will cause the "re-edema" phenomenon of the cell organization worse than before.

Diuretics: Reduces stronger edema and lasts for 2-10 hours. Mannitol can be infused 20% dose from 1-2g / kg body weight, infusion at a large speed (can flow into a stream).

In severe brain cases with seizures, corticosteroids are used to help normalize the osmosis of blood vessels against the accumulation of water and salt in the brain organization.

It is better to use dexamethasone, which is a slow-acting synthetic Glucocorticoid with constant efficiency. Dexamethasone is effective against cerebral edema after 12-18 hours. Dosage 10mg intravenously, every 5 hours, inject 4mg muscle.

Sedation cut the jerking attack

Valium can be given through the catheter or intramuscularly and intravenously. Can use drip intravenous lymphadenopathy: Aminazin + Thiantan + Spartein (Aminazin dosage 3-7 mg / 1kg body weight / 24 hours).

If the patient has severe seizures, use Cardenal.

Hypothermia

Undress the patient, apply ice to the groin, armpits, neck ... fan, rub camphor alcohol. Antipyretic drugs can be taken by mouth through the tube or rectal enema ...

Aspirin 0.25 - 1g / 24 hours. It is best to use efferalgan solution (5 ml / time, 2-3 times / 24 hours), or efferalgan suppositories (1-2 suppositories / 24 hours - when the fever is high).

Respiratory and cardiovascular resuscitation

Oxygen, wipe up sputum, ready to respire when severe breathing disturbance or stop

Promptly replenish electrolyte water according to Haematocrit and electrolytes. Using cardiovascular aids ouabain, sparteine, when necessary can use vasomotor drugs such as aramin, noradrenalin, dopamine.

Prevent superinfection and nutrition, anti-ulcer

Use a broad-spectrum antibiotic such as ampicillin or 3rd generation Cephalosporine depending on body weight. Regularly clean the skin, clean the mouth, put the urinal, use the inflatable rubber pad to enter the pressure points or lie on the water cushion and often change positions for the patient. Nutrition for patients must ensure enough protein and vitamins, through the sonde 4 times/day.

Prevention

The main measure is Japanese encephalitis vaccination. Can be used for all ages, preferably for children from 1-5 years old in endemic areas. Injection dose: <36 months: 0.5 ml / dose; > 36 months: 1 ml / dose. Basic immunization is 3 doses: The second dose is 2 weeks apart from the first dose; 3rd dose 1 year from 2nd dose. Repeat injection: 3 years injected 1 ml dose to maintain immunity (injected under the skin into the muscle). In addition, combining to kill mosquitoes, causing immunity to pigs.