Disability-adjusted life year for<unk>  encephalitis per 100,000 inhabitants in 2002<unk>  encephalitis (JE) is the leading<unk>  of viral encephalitis in Asia, with up to 70,000<unk> s reported annually.<unk> -fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk;<unk>  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, South Korea, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia.<unk>  encephalitis has been reported in the Torres Strait Islands, and two fatal<unk> s were reported in mainland northern Australia in 1998. There were reported<unk> s in Kachin State, Myanmar in 2013. 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. In February 2022,<unk>  encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March,<unk> s were detected in South Australia. However, the current presence on mainland Australia is minimal. There were 116 deaths reported in Odisha's backward Malkangiri district of India in 2016. Human, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Pigs act as an amplifying host and have a very important role in the 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. The natural hosts of the<unk>  encephalitis virus are birds, not humans, and many believe the virus will therefore never be completely eliminated. In November 2011, the<unk>  encephalitis virus was reported in Culex bitaeniorhynchus in South Korea. Recently, whole genome microarray research of neurons infected with the<unk>  encephalitis virus has shown that neurons play an important role in their own defense against<unk>  encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during<unk>  encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease. A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients. * The use of rosmarinic acid, arctigenin, and oligosaccharides with degree of polymerization 6 from Gracilaria sp. or Monostroma nitidum has been shown to be effective in a mouse model of<unk>  encephalitis. * Curcumin has been shown to impart neuroprotection against<unk>  encephalitis infection in an in vitro study. Curcumin possibly acts by decreasing cellular reactive oxygen species level, restoration of cellular membrane integrity, decreasing pro-apoptotic signaling molecules, and modulating cellular levels of stress-related proteins. It has also been shown that the production of infective viral particles from previously infected neuroblastoma cells is reduced, which is achieved by inhibition of the ubiquitin-proteasome system. * Minocycline in mice resulted in marked decreases in the levels of several markers, viral titer, and the level of proinflammatory mediators and also prevented blood-brain barrier damage.
medical cause of Japanese encephalitis
symptom of Japanese encephalitis
symptom of Eastern equine encephalitis
symptom of West Nile fever
symptom of Rabies
symptom of Tuberculous meningitis
symptoms of Rabies
symptom of Neuroleptic malignant syndrome