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VIRAL ENCEPHALITIS

Viral encephalitis and myeloencephalitis are group of acute infectious diseases. These diseases are accompanied by fever and lesion of the brain and/or spinal cord. The title "encephalomyelitis" descended from Greek word "encephalon" -brain, "myelon" - spinal cord. There are 2 groups of encephalites the primary encephalites and the secondary encephalites.

The primary encephalites are independent diseases, for example: Tick encephalitis and Japanese encephalitis.

The secondary encephalitis is syndrome of some other disease, for example: encephalitis due to measles, smallpox, herpetic infection.

Viral transmissive encephalites and myeloencephalites are diseases from group of arboviral infections. Arboviral diseases are characterized by endemic and seasonal spread, transmissive way of the transmission. All arboviral encephalites are zoonotic infections.

Arboviral encephalitis are accompanied by general toxic syndrome, high temperature and mainly by damage of the central nervous system.

The agents of this group of the diseases are arboviruses, i.e. "arthropod-borne viruses". The general characteristics of arboviruses is ability to parasite in the organism of animals and arthropods.

Arboviruses are typical parasites of the birds, rodents, mammals, reptiles. Arboviruses evoke latently persistent or subclinical infection in the organism of birds and animals. Human is included to ecological chain accidentally, and as rule he is not a source of the infection, except for some arboviral fevers, which having declination to epidemic spread (Denge fever, yellow fever, flebothomic fever and other). The group of Arboviruses is detached on the basis of their general ecology. The live cycle of viruses consists of the next stages:

1. Reproduction in the organism of vertebral hosts.

2. Crossing to attaching insects and reproduction in the organism of anthropoids.

3. Transmission by bite to new vertebrate hosts. The vertebrate hosts become the source of infection due to accumulation of virus in the blood.

The transfer of Arboviruses by anthropoids (gnats,ticks,mosquitoes) is not mechanical process. Virus, entering the insect's organism with blood is reproduced and accumulated in the cells of the salivatory glands. It enters the wound with saliva due to bite. The condition of the infection is concentration of virus in the saliva. The infection of anthropoids is also possible in sufficiently high quantity of virus in the blood of vertebrate hosts. Arboviral infection doesn't harm anthropoids. Virus is preserved in the organism of anthropoids during all life.

 

 

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In infected ticks virus is transmitted transovarially. The forming posterity becomes carrier of virus, it may be able to transmit infection to the vertebrate hosts.

The tropical countries are regarded as historical heartland of arboviruses. At the present time these countries are areas of the most spread of arboviral infections. The variety of species of insects, the considerable density of the population of vertebrate hosts and anthropoids and high temperature of air promote spread of arboviral infections.



The important factor of the activity and epidemic manifestations of the focuses of arboviral infections is activity of human and violations of ecological balance. For example, Japanese encephalitis is registered in all regions of rise fields and conditions of pigs. The irrigated rise fields are the places of replication of vectors of agents; Culex mosquitoes and infected pigs are the reservoir of infection.

All arboviral infections are natural focal diseases. There are the next groups of arboviral diseases:

I. Arboviral encephalites and encephalomyelites.

II. Arboviral systemic feverish diseases.

The next diseases are concerned to the first group:

1. Venezuelan equine encephalitis is widespread in the northern, southern and central areas of America. The birds, rodents, monkeys, mammals are the reservoir of virus. Amount domestic animals-sheeps, goats and horses may be the source of infection. The mosquito is a factor of transmission. The lethal rate is 6-9 % of cases in adult and 35 % in children.

2. Eastern equine encephalitis is widespread in the almost whole American continent. The sources of infection are the horses and some kinds of the birds. The diseases is transmitted by mosquitoes. The lethal rate is 70-75 %.

3. Western equine encephalitis is widespread in the some regions of American continent. The reservoir of infection is some kinds of the birds, snakes, frogs and horses. The disease is transmitted by mosquitoes. Lethal rate is 15 %.

4. Sant-Louis encephalitis. It is widespread in the countries of American continent and on the islands of Caribbean basin. The reservoirs of infection are pigeons,sparrows,chickens and cattle. The factors of transmission are mosquitoes and ticks. The lethal rate is 15-20 %.

5. Ilheus encephalitis is registered in some areas of the South and Central America. The reservoir of infection has not been determined. The factor of transmission is mosquitoes. There is no facts about lethal outcomes. Australian X-disease (Murray Valley encephalitis). The disease is observed in Australia. The reservoir in nature is wild birds. It is possible that mammals are the reservoir of infection too. The lethality is 50 - 70 %.

6. Kyansanur forest disease. This encephalitis occurs in New Guinea, in India. The reservoirs of infection are monkeys, palm squirrels, forest rats. The factors of transmission are ticks. The lethal rate is 5 - 10 %.

7. Scotland encephalitis (Scotland sheep's encephalitis). The disease is widespread mainly in Scotland, rarely in Northern England. The reservoir of

1.

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infection in nature is sheep. The factor of transmission is ticks. In human the course of the disease is light. There are no lethal outcomes.

Japanese encephalitis and tick encephalitis are widespread and more studied forms of arboviral infections.

JAPANESE ENCEPHALITIS

Synonyms: mosquito, autumn encephalitis.

Japanese encephalitis is an acute viral transmissive, seasonal zoonotic infection. The disease is characterized by development of serious meningoencephalitis, expressive general toxic syndrome, high temperature. The disease is accompanied by high percent of invalidity and firm residual manifestations.

Historic reference

 

The clinical manifestations of Japanese encephalitis was described more than 100 years ago. However, this disease was considered as epidemic cerebrospinal meningitis. Japanese encephalitis was recognized as independent disease in 1924 year.

Etiology

In 1933 Gayashi proved the viral etiology of the disease in Japan. In 1940 Shubladze and Smorodincev described virus in the Soviet Union. According to its characteristics virus is similar to virus of Sant-Louis encephalitis and West Nile-encephalitis. The agent of Japanese encephalitis is virus from genus Flavivirus, family Togaviridae, ecological group Arboviruses.

Flaviviridae are small (40 nm in diameter) enveloped viruses with single-stranded, positive-sense RNA genomes. Virions form on the endoplasmic reticulum of infected cells are released by exocytosis or cell lysis. Flaviviruses are readily inactivated by heat (56 Ñ, 10 minutes) detergents, ultraviolet irradiation, trypsin digestion, formaldehyde and chlorine and phenolic disinfectiants.

The virus is replicated in a variety of vertabrate and arthropod cells in culture with or without producing of cytopathic effects; extensive serologic relatedness, due to shared group-specific antigens links members of the family; crossing is most extensive by hemagglutination inhibition, intermediate by complement fixation and least by neutralization tests.

Outbreaks of this disease has been registered in Japan, Russia, China, Korea, Vietnam, Philippines, India, Indonesia, Taiwan, Australia and on the coast of the Eastern Africa.

Epidemiology

According to its epidemic characteristics, grassland, sea, coastal and forest forms of natural focuses are differentiated. The reservoir of infection is mammals and birds. During the epidemic outbreaks the patient may be the source of

 

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infection and also the domestic animals (horses, cows, pigs). These sources lead to formation of rural and urban focuses. The factor of transmission is mosquitoes of family Culex. The disease is registered in August - October.

 

Pathogenesis

 

After bite of mosquito,arboviruses enter the blood stream. The agents enter with blood stream the central nervous system. The agents multiply and cause the edema of the soft cerebral coverings and cerebral matter, edema and hyperemia of the cerebral vessels. The small hemorrhages are observed in the covering and in the region of the ophthalmic gyrus, striapallidaric system, where the formation of mildnessial focuses is possible. After reproduction in considerable quantity in the nervous system virus enters the blood again and affects the vessels and internal organs. There are venous overflow, hemorrhages, degenerative changes in the vessels and parenchymal organs with serous-hemorrhagic edema of the liver, kidneys, myocardium, and formed pneumonic focuses in the lungs.

 

 

Anatomic pathology

The most severe morphologic changes take place in the brain and spinal cord: differentiated serous-hemorrhagic inflammation of the covering and of the matter of the cranial and spinal cord. Perivascular infiltrations and granular infiltrations around vessels, nervous cells and zones of necrosis are observed. The most expressive changes occur in ophtalmic gyrus, substancia nigra, red matter, olivia, cerebellum.

Clinical manifestations

The next periods of the disease are differented: incubation period, initial, climax period and reconvalescence. Incubation period is from 5 till 21 days, in average - 8-14 days.

The duration of initial period is 3-4 days. The onset of the disease is acute with increase of the temperature till 40-41 Ñ. The temperature is accompanied by chill and severe headache, especially in the area of forehead. At the same time the severe pain in loin, stomach, extremities, nausea, vomiting are observed. There are hyperemia of the face, sclera, upper part of the chest, increased sweat. The pulse rate is accelerated till 120-140/min. The arterial pressure increases. The pain of muscles is frequently marked. Rigidity of occipital muscles, increase of muscle's tonus and increase of tendon reflexes are observed. In severe course of the disease death of the patient may occur.

Climax period is characterized by progressive symptoms of the local brain damage. Meningeal syndrome increases. The depression of consciousness till coma is marked. Psychial disorders appear frequently: delirium,hallucinations.

Muscular tonus of pyramidal and extrapyramidal character increases. Muscular hypertension spread on masticatory and occipital muscles. In case of severe damage of pyramidal system spastic hemipareses, monopareses and paralyses may arise.

 

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In severe course of the disease clonic and tonic cramps develop. In some patients stereotonia is marked - frequent repetition of identical motions.

During examination of the blood neutrophilic leukocytosis with shift of the formula to the left is observed, ESR accelerates. During cerebrospinal puncture, liquor is transparent. The mild lymphocytic pleucytosis is observed. The pressure of cerebrospinal liquor increases.

The duration of the period of reconvalescence is 4-7 weeks. The temperature is usually normal or subfebrile. Some signs of the organic damage of the brain are preserved (hemi paresis, disorder of the motions coordination, muscular, weakness, psychical violations). The late complications occur (pneumonia, pyelonephritis).

Complications

The most common complication is syndrome of brain edema. It may be also pneumonia. In the case of the recovery the residual manifestations such as firm paralyses of the limbs are observed. Sometimes psychical changes occur with considerable decrease of intellect till to idiotia.

Japanese encephalitis is severe disease with lethal rate from 25 % till 80 %. Death becomes more frequent during the first 7 days in state of coma, bulbaric manifestations and cramps.

lagnosis

The diagnosis is based on the epidemiological data, season, typical clinical signs. Diagnosis is confirmed by isolation of virus from the blood and cerebrospinal fluid at the first days of the disease. The serological methods of diagnostics may be used from the second week of the disease (complement fixation, indirect hemagglutination, reaction of neutralization of virus).

Differential diagnosis

The differential diagnosis is performed with tick encephalitis, serous meningitis and enceph^lites of the other etiology.

Treatment

Specific treatment is performed with use of hyperimmune horse's serum and gammaglobulins. Pathogenetic therapy includes desintoxicative therapy, diuretics, hyperbaric oxygenation. During of the period of the recovery the massage, physiotherapy are indicated. Dibasol, prozerin, galantamin are also prescribed.

Prophylaxis

Specific prophylaxis in the endemic regions is performed by means of killed vaccine. It is necessary to vaccinate both people and domestic animals in focuses of infection. During epidemic outbreaks passive immunization of the people is performed with specific; gammaglobulin. The methods of prophylaxis are use of repellents and the defense from the mosquitoes.

 

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Date: 2014-12-21; view: 205


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