The definitive diagnosis is made only from studies of the antibody status of the affected individual, with evidence of the absence of specific antibody at the time of onset of the disease followed by a 4-fold or greater rise in titer of the antibody during the following days or weeks. Complement-fixing antibody is the first to appear in most patients, but hemag-glutinating and neutralizing antibodies are usually demonstrable shortly thereafter. More recently, antibody tests using fluorescein- or enzyme-labeled antibody, or the various modifications of these, showing specific rise in titer, are sufficient to establish the diagnosis. Antigenic variation is common among viral isolates, and at least two immunotypes have been delineated; thus the serodiagnosis must be performed in laboratories that have on hand the several subtypes that may be needed for a full serologic analysis of a given case or outbreak.

The disease is one of the most fatal among arboviruses, with case fatality rates of 50 to 70 percent having been recorded in outbreaks. Recovery may be complete, or there may be residual damage to the central nervous system; Japanese B encephalitis, in contrast to other arboviral encephalitides, is accompanied by relatively high rates of complete recovery despite the high case fatality rates.

There is no specific treatment, and supportive care is the major intervention that can be offered. The protective effect of antibody suggests that convalescent serum or other sources of antibody might have some therapeutic value, but this has not been systematically investigated on a suitable scale.

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