The death toll due to the Japanese Encephalitis continues to daily kill a few more people in Uttar Pradesh and seems to be spreading to the neighboring areas like Nepal.
In this special report we review encephalitis or more // commonly known as brain fever and provide some essential information on its history, its spread, its life cycle and prevention.
The first historic mention of Japanese encephalitis occurred during the “summer encephalitis” outbreaks in the late 1870’s. The virus was first isolated in Japan in 1935 from a fatal human case of encephalitis.
In 1940, JE was first identified in China. In 1954 the virus was recognized in India and a major epidemic occurred in 1978 with over 6,000 human cases occurring. Currently, the disease occurs in China, India, Nepal, the Philippines, Sri Lanka and Northern Thailand.
The geographical area affected by the virus has spread considerable over the last 50 years. Occasionally sporadic cases of disease occur in Indonesia and northern Australia. The disease has not occurred in the rest of the world. Postulated explanations include migration of birds, certain irrigation projects, animal smuggling and global warming.
Japanese Encephalitis is caused by a virus (Arbovirus). The life cycle of the virus involves mosquitoes and an amplifying host (also known as reservoir hosts). Known amplifying hosts include domestic pigs, wading bird species. Some of the incidental hosts include horses, donkeys, cattle, water buffalo, sheep, dogs, chickens, ducks and humans.
The disease is zoonotic disease, transmitted from animals to human beings. It is transmitted by mosquitoes, (Culex tritaeniorhynchus), the primary vector. In the endemic areas, only 2 to 3 % of mosquito’s carry the virus. With 50,000 cases reported annually and 10-15,000 deaths, it is the most common and the most severe form of viral encephalitis.
The infection is generally asymptomatic.
Only 1 infection in 25 to 1,000 is in fact symptomatic. Out of the symptomatic cases, 20% of clinical cases of Japanese encephalitis die, and 35% suffer permanent brain damage.
Diagnosis is based on tests of blood or spinal fluid. Treatment is largely on a conservative basis. Intravenous infusions may be given to maintain the hydration status of the patient. The main aim of therapy is to provide symptomatic relief to the patient.
The disease can be prevented by means of an inactivated vaccine given in 3 injections followed by a booster three years later. Improved management for irrigation of water resources can be undertaken to reduce the transmission of disease, in South, South East, and East Asa. Related medicine news :1
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