The<unk>  encephalitis virus (JEV) has an incubation period of 2 to 26 days. The vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis. Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific 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 . Mental retardation is usually developed. Mortality of this disease varies but is generally higher in children. Transplacental 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<unk> s, some effects also include<unk> a, headache, fever, and vomiting.<unk>  encephalitis virus enters the brain through two ways and leads to infection of neurons and encephalitis Increased microglial activation following<unk>  encephalitis 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-α), which can<unk>  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, the number of activated microglia was significantly less when compared to other regions of the mouse brain. An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive<unk>  encephalitis infection was also observed. Although the net effect of the proinflammatory 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 nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial 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.
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