Japanese Encephalitis in India: Civil Services Mentor Magazine February 2013

JAPANESE ENCEPHALITIS IN INDIA

Japanese encephalitis (JE)- epidemics have been reported in
many parts of the country. The incidence has been reported to be high among
pediatric group with high mortality. The incidence of JE in recent times is
showing an increasing trend. It appears that JE may become one of the major
public health problems in India, considering the quantum of the vulnerable
pediatric population, the proportion of JEV infections among the encephalitic
children and wide scattering of JE-prone areas. JE burden can be estimated
satisfactorily to some extend by strengthening diagnostic facilities for JE
confirmation in hospitals and by maintenance of contact with the nearby referral
hospitals to collect the particulars on JE cases. Vaccination proves to be the
best to protect the individual against any disease. In the case of JE, it is
essential to immunize the pigs (amplifying host) also to interrupt the
transmission of the disease.

Japanese encephalitis—previously known as Japanese B
encephalitis to distinguish it from von Economo’s A encephalitis— is a disease
caused by the mosquito- borne Japanese encephalitis virus. The Japanese
encephalitis virus is a virus from the family Flaviviridae. Domestic pigs and
wild birds (herons) are reservoirs of the virus; transmission to humans may
cause severe symptoms. Amongst the most important vectors of this disease are
the mosquitoes Culex tritaeniorhynchus and Culex vishnui. This disease is most
prevalent in Southeast Asia and the Far East.

What is Japanese Encephalitis (JE)?

JE is the mosquito-borne virus which mainly affects the CNS
or Central Nervous System. It can be transmitted to human beings if infected
mosquito bites. Mosquitoes in turn are affected when they feed on domestic pigs
that carry this virus. JE usually affects children who are below 15 years of
age. Around 25 percent affected children usually die and among those who
survive, 30-40 percent suffers from mental and physical impairment. In 2011, it
was reported that JE had occurred in 135 districts in 17 states of India.
Japanese encephalitis has an incubation period of 5 to 15 days and the vast
majority of infections are asymptomatic: only 1 in 250 infections develop into
encephalitis. Severe rigors mark the onset of this disease in humans. Fever,
headache and malaise are other nonspecific symptoms of this disease which may
last for a period of between 1 and 6 days. Signs which develop during the acute
encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and
a raised body temperature between 38 and 41 degrees Celsius. Mental retardation
developed from this disease usually leads to coma. Mortality of this disease
varies but is generally much higher in children. Transpla- cental spread has
been noted. Lifelong neurological defects such as deafness, emotional lability
and hemiparesis may occur in those who have had central nervous system
involvement. In known cases some effects also include nausea, headache, fever,
vomiting and sometimes swelling of the testicles.

Japanese encephalitis (JE) is the leading cause of viral
encephalitis in Asia, with 30,000–50,000 cases reported annually. Case-fatality
rates range from 0.3% to 60% and depends on the population and on age. Rare
outbreaks in U.S. territories in Western Pacific have occurred. Residents of
rural areas in endemic locations are at highest risk; Japanese encephalitis does
not usually occur in urban areas. Countries which have had major epidemics in
the past, but which have controlled the disease primarily by vaccination,
include China, Korea, Japan, Taiwan and Thailand. Other countries that still
have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and
Malaysia. Japanese encephalitis has been reported on the Torres Strait Islands
and two fatal cases were reported in mainland northern Australia in 1998. The
spread of the virus in Australia is of particular concern to Australian health
officials due to the unplanned introduction of Culex gelidus, a potential vector
of the virus, from Asia. However, the current presence on mainland Australia is
minimal.

Human, cattle and horses are dead-end hosts and disease
manifests as fatal encephalitis. Swine acts as amplifying host and has very
important role in epidemiology of the disease. Infection in swine is
asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are
common sequelae. The most important vector is Culex tritaeniorhynchus, which
feeds on cattle in preference to humans, it has been proposed that moving swine
away from human habitation can divert the mosquito away from humans and swine.
The natural host of the Japanese encephalitis virus is bird, not human, and many
believe the virus will therefore never be completely eliminated. In November
2011, Japanese encephalitis virus was reported in Culex bitaeniorhynchus in the
Republic of Korea.

Increased microglial activation following JEV infection has
been found to influence the outcome of viral pathogenesis. Microglia are the
resident immune cells of the central nervous system (CNS) and have a critical
role in host defense against invading microorganisms. Activated microglia
secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha
(TNF-á), which can cause toxic effects in the brain. Additionally, other soluble
factors such as neurotoxins, excitatory neurotransmitters, prostaglandin,
reactive oxygen, and nitrogen species are secreted by activated microglia.

In a murine model of JE, it was found that in the hippocampus
and the striatum, the number of activated microglia was more than anywhere else
in the brain closely followed by that in the thalamus. In the cortex, number of
activated microglia was significantly less when compared with other regions of
the mouse brain. An overall induction of differential expression of
pro-inflammatory cytokines and chemokines from different brain regions during a
progressive JEV infection was also observed. Although the net effect of the
pro-inflammatory mediators is to kill infectious organisms and infected cells as
well as to stimulate the production of molecules that amplify the mounting
response to damage, it is also evident that in a non-regenerating organ such as
brain, a deregulated innate immune response would be deleterious. In JE the
tight regulation of microglia activation appears to be disturbed, resulting in
an auto toxic loop of microglia activation that possibly leads to bystander
neuronal damage. In animals, key signs include infertility and abortion in pigs,
neurological disease in horses and systemic signs including fever, lethargy and
anorexia.


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