The disease presents in 3 stages, first is the acute stage (1-2 weeks), second subacute stage (more than 2 weeks) and the third stage lasting for several weeks to months .
Initially, patients present with fever with chills and rigors, malaise, and headache lasting for 1 to 6 days. Thereafter, there is an encephalitic stage in which there is marked neck stiffness, cachexia, reduced levels of consciousness. The third stage includes flaccid paralysis, features of Parkinson’s such as masked face, tremors, hypertonia, cogwheel rigidity.
In some reported cases there has been death due to brain death or respiratory arrest. There are many residual symptoms which patients suffer lifelong even after recovery from active infection such as language impairment, altered mental status and cognitive impairment .
After clinical research done on affected patients it was found that the diagnosis for virus cannot be obtained through clinical specimens and thus is done by testing the serum or the cerebrospinal fluid (CSF) for virus specific IgM antibodies. This is the standard test to confirm Japanese encephalitis .
Other tests include complete blood counts showing leucocytosis along with thrombocytopenia. MRI scans shows lesions in the thalamus with abnormalities in the basal ganglia, putamen, cerebellum and spinal cord.
Electroencephalography (EEG) reveals changes in the spike pattern and slowing of delta waves.
There is no specific treatment for Japanese encephalitis. The reason for mortality in children is delay in immediate nursing care. The aim is to restore airway, breathing and circulation. Basic life support and nutrition is taken care through intravenous fluids. Special care is necessary to avoid any rise in the intracranial pressure.
Mannitol is administered in a lower dose especially in children having a Glasgow coma score (GSC) less or equal to 8. Control of seizures is done by giving antiepileptic drugs such as phenobarbitone. Rectal diazepam also can be administered if necessary. Fluids and sodium infusion or feeds are given amply to restore the hydration and nutrition .
Japanese encephalitis has a high mortality rate especially in children. Several studies showed that children with high fever, leucocytosis in CSF and coma had a bad prognosis. Cases which had a tumor necrosis factor (TNF) concentration of more than 50 had a fatal outcome as opposed to those who had a high concentration of Japanese encephalitis virus antibodies in the CSF.
Japanese encephalitis is caused by a flaivirus. Flavivirus belongs to the family flaviviridae. The shape of this virus is spherical and is 40-50 nm in diameter. It is a single stranded RNA virus. It has 3 structural and 7 non structural proteins. These proteins have an outer layer of a domaine which does the attachment, haemagglutination and neutralization.
This virus is transmitted to humans through a bite of an infected mosquito. The mosquito usually breeds in marshy areas or rice fields. It is a non contagious infection.
Japanese encephalitis (JE) – has been frequently found in Asian countries, its incidence has been increasing in India as well. The pediatric age group of 5-10 years has been most widely affected. The Japanese encephalitis infection is suspected to be one of the major health problems across India with a mortality rate of 20 to 50 %. Statistics show that in southern India, children less than 15 years are affected and in northern India, children affected are above 15 years of age.
It is necessary to provide vaccines to protect the individual from the disease; while it is also necessary to immunize the pigs (hosts) to prevent the disease transmission . It has been observed that in all epidemics, males are affected more than females.
Japanese encephalitis is a type of infection in which the host in unable to produce any antibodies against this virus, thereby allowing it to cross the blood brain barrier and produce brain infestations. Japanese encephalitis develops after an incubation period of 5-15 days in patients during which the virus multiplies within the leucocytes of the host .
In the acute stage, there is congestion, thrombus formation, severe damage to the nerve cells, injury to the brain parenchyma such as minute necrosis, softening and perivascular cuffing. The areas of the brain affected are the diencephalon, mescencephalon, parts of the brain stem, cerebral cortex and the cerebellum.
In the subacute stage, the congestion and inflammation is less but the degeneration of nerve cells and proliferation of the glial cells is more dominant and the lesions are more localized. In the final or the chronic stage, there is marked destruction resulting in disappearance of the nervous tissue, local necrosis, vascular thickening especially in the substania nigra .
Protection from mosquito bites by using an insect repellent, mosquito nets, pesticides and environmental sanitation.
Vaccination is encouraged in children of the age group of 2 to 15 years. The Japanese encephalitis vaccine is a formalin inactivated vaccine obtained from the brain of mice. Studies say protective immunity is achieved after numerous doses. Two doses are given at an interval of 7-14 days. Thereafter a booster injection is given after a gap of 4 weeks.
This disease was first discovered in India in the year 1955, in Tamil nadu. It is still prevalent there, along with other states like from Uttar Pradesh, Karnataka, Assam, Bihar, Pondicherry, West Bengal, Andhra Pradesh, Manipur, and Goa and recently new cases have also been reported from the states of Kerala and Maharashtra.
Japanese encephalitis infection is a viral infection caused by Japanese encephalitis virus. It is transmitted to humans via infected mosquito. This infection is commonly found in Asian countries and children of 2 to 15 years are largely infected.
There is no specific treatment of this infection. The patient requires immediate hospitalization to secure his breathing and circulation. Vaccination and protecting from mosquito bites is the main step for preventing such a disease.