Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F). The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement. Increased microglial activation following Japanese 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 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, the number of activated microglia was significantly less when compared to other regions of the mouse brain.
Vernal keratoconjunctivitis (VKC) is a recurrent, bilateral, and self-limiting inflammation of conjunctiva, having a periodic seasonal incidence. Vernal keratopathy
Corneal involvement in VKC may be primary or secondary due to extension of limbal lesions. Vernal keratopathy includes 5 types of lesions. Punctuate epithelial keratitis. Ulcerative vernal keratitis (shield ulceration). Vernal corneal plaques. Subepithelial scarring. Pseudogerontoxon. Sign and symptoms
Symptoms- VKC is characterised by marked burning and itchy sensations which may be intolerable and accentuates when patient comes in a warm humid atmosphere. Associated symptoms include mild photophobia in case of corneal involvement, lacrimation, stringy discharge and heaviness of eyelids. Signs of VKC can be described in three clinical forms (Cameron Classification):Palpebral form- Usually upper tarsal conjunctiva of both the eyes is involved. Typical lesion is characterized by the presence of hard, flat-topped papillae arranged in cobblestone or pavement stone fashion. In severe cases papillae undergo hypertrophy to produce cauliflower-like excrescences of giant papillae. Bulbar form- It is characterised by dusky red triangular congestion of bulbar conjunctiva in palpebral area, gelatinous thickened accumulation of tissue around limbus and presence of discrete whitish raised dots along the limbus (Trantas spots). Mixed form- Shows the features of both palpebral and bulbar types. Cause
VKC is thought to be an allergic disorder in which IgE mediated mechanism play a role. Such patients often give family history of other atopic diseases such as hay fever, asthma or eczema, and their peripheral blood shows eosinophilia and increased serum IgE levels. Risk factors
Age and sex – 4–20 years; more common in boys than girls.