Japanese encephalitis is a transmissible viral neuroinfection with a predominant lesion of the brain substance. It is characterized by endemic outbreaks in the period from August to the end of September. It has a general infectious origin, during the peak period, disorders of consciousness, meningeal syndrome, hyperkinesis, myoclonia, paresis, bulbar disorders are characteristic. Diagnostics involves the study of cerebrospinal fluid, IFA, ELISA and PCR studies. Therapy is carried out with specific immunoglobulin or serum, decongestant, detoxification, vascular, anticonvulsant, corticosteroid pharmaceuticals.
ICD 10
A83.0 Japanese encephalitis
General information
Japanese encephalitis is a severe neuroinfection affecting the medulla and cerebral membranes, prone to generalized spread throughout the body. The description of outbreaks of this disease in Japan is found in historical materials of the late XVIII century. In 1924, a large epidemic of Japanese encephalitis was observed in Japan with a mortality rate of 70-80%. During this period, the first detailed descriptions of the disease appeared, and it was singled out as an independent nosology. In connection with the events in Japan, encephalitis was called “Japanese”. However, natural foci of the disease are found not only in Japan, but also in the Far East, Primorsky Krai, India, Vietnam, China, Korea, and the Philippines.
In 1933-36, a virus causing Japanese encephalitis was isolated. It turned out that goats, horses, sheep, cows, monkeys, rodents and some wild birds are susceptible to it. Children under the age of 10 are most susceptible to morbidity. In pregnant women with the disease in the 1-2 trimester, spontaneous termination of pregnancy (miscarriage) is often observed. The high percentage of lethality and residual phenomena make Japanese encephalitis an urgent task of modern neurology, infectology and epidemiology.
Causes
Japanese encephalitis develops when its pathogen enters the human body — a specific neurotropic arbovirus, which has great resistance. When boiled, the virus dies only after 2 hours, in disinfectants (alcohol, acetone) — after 3 days; when frozen, it persists for more than a year. The role of virus carriers are mosquitoes Culex trithaeniorhynchus, Culex pipiens, Aedes japonicus, Aedes togoi.
Japanese encephalitis is characterized by a clear seasonality associated with the period of hatching of mosquito vectors. Encephalitis outbreaks are observed mainly in August-September and last no more than 50 days. The risk group includes mainly men working in the wetlands of the endemic area. The probability of an outbreak increases in a hot climate with heavy precipitation.
Pathogenesis
Whether Japanese encephalitis develops when a mosquito infected with the virus bites or not depends on many factors: on the amount of the virus that has entered and the degree of its virulence, on the state of the immune system and the resistance of the macroorganism. Often, the death of viruses occurs at the site of their introduction. If this does not happen, then the virus with blood flow or perineurally reaches the blood-brain barrier (BBB), penetration through which is facilitated in conditions of overheating of the body. After passing through the BBB, the virus penetrates into the substance of the brain, where it multiplies intensively, causing the death of neurons. In severe cases, infection is generalized and the virus multiplies outside the nervous system.
Symptoms
The incubation period takes 5-16 days. Manifestations of Japanese encephalitis may be preceded by prodrome: drowsiness, fatigue, a feeling of weakness and decreased performance; in rare cases — speech disorders, decreased vision, diplopia, dysuric disorders. After a couple of days, general infectious manifestations suddenly make their debut and quickly worsen: high fever reaching 41 ° C, terrific chills, intense headache, myalgia, lower back and abdominal pain, sharp weakness, staggering, sweating, nausea and vomiting. There is hyperemia of the face. Bradycardia is characteristic, which then transforms into tachycardia. On the 3rd-4th day of encephalitis, signs of central nervous system damage appear against the background of an infectious-toxic syndrome.
Disorders of consciousness accompanying Japanese encephalitis during the peak period include confusion, amentia, delirium with psychomotor agitation and delirium, sopor, coma. Meningeal syndrome develops with a typical patient’s posture, hyperesthesia, meningeal signs. Convulsive seizures, hyperkinesis, oculomotor disorders, paralysis and paresis of the extremities (mainly by hemitype), central paresis of the facial nerve, bulbar disorders can be observed. Myoclonic twitching of various muscles is often noted, tremor of the extremities increasing during movements. Pathological drowsiness (hypersomnia), resembling manifestations of lethargic encephalitis, is possible.
Japanese encephalitis has an acute course. Fever persists for the first 7-10 days. The peak of the severity of clinical manifestations is usually noted on the 3rd-5th day of encephalitis. During this period, Japanese encephalitis can be complicated by infectious and toxic shock, cerebral edema, pyelonephritis, bacterial pneumonia, pulmonary edema, sepsis. Then there is a gradual reverse development of symptoms, but the convalescence occurs rather slowly (up to 1.5-2 months), asthenia persists for a long time, many patients have residual phenomena.
Diagnostics
Cases of endemic outbreaks of Japanese encephalitis do not cause difficulties in diagnosis. The epidemiological history, seasonality, duration of the incubation period, and features of the clinic are taken into account.
- Acute infectious changes (leukocytosis, acceleration of ESR) are observed in the clinical blood test.
- Lumbar puncture is performed to take cerebrospinal fluid for analysis. The study of the latter reveals lymphocytic pleocytosis characteristic of serous meningitis and a slight increase in protein concentration.
- Ophthalmoscopy reveals hyperemia of the optic disc, sometimes its swelling and petechial hemorrhages.
- Neuroimaging methods (CT, MRI) are used to exclude other cerebral pathology (intracerebral tumor, hematoma, stroke).
- In clinical practice, the determination of antibodies to the virus using IFA or ELISA is used, as well as the detection of viral RNA using PCR studies. Serological reactions with the study of paired sera are mainly of retrospective significance, since the second serum is taken at the 3rd-4th week of encephalitis.
In the initial period, Japanese encephalitis is difficult to differentiate from other acute infections: influenza, measles and other acute respiratory infections. When the picture of meningoencephalitis unfolds, differentiation from other viral encephalitis is required — tick-borne encephalitis, lethargic encephalitis Economo, secondary encephalitis, two-wave viral meningoencephalitis.
Treatment
Treatment of Japanese encephalitis is carried out by joint efforts of neurologists, infectious diseases specialists and resuscitators. In the first week of encephalitis, a specific immunoglobulin or serum taken from convalescents is injected three times a day. In parallel, pathogenetic and symptomatic treatment is carried out, aimed at detoxification, prevention of brain edema, maintenance of the activity of the main organs and systems, and the fight against complications. If necessary, ventilators and resuscitation measures are carried out. Glucocorticosteroids, diuretic pharmaceuticals, vascular agents, anticonvulsants are prescribed.
Forecast
According to various data, in 30-70% of cases, Japanese encephalitis leads to death. In some cases, mild and abortive cases are noted. Convalescents may have persistent neurological disorders (paresis, hyperkinesis, hearing loss, vision loss, speech disorders, ataxia) and mental disorders (hebephrenia, dementia, manic-depressive state), requiring further constant monitoring by a neurologist or psychiatrist.
Prevention
Measures to reduce the incidence of Japanese mosquito encephalitis in endemic foci include the use of mosquito nets and protective clothing, treatment of exposed skin with repellents. Specific prevention is carried out by vaccination. It is carried out in endemic foci and persons traveling there. Children can be vaccinated starting from the age of 1. As a rule, vaccination is not required for the adult urban population of endemic regions.
The standard vaccination regimen consists of three injections of the vaccine at intervals of 7 and then 21 days. There is also an accelerated schedule in which the third injection of the vaccine is carried out 7 days after the second. It is believed that the first 2 doses of the vaccine provide sufficient protection in 80% of cases. The last administration of the vaccine should be carried out 10 days before moving to the endemic zone. Revaccination is carried out at intervals of 2-3 years.
