Murray Valley Encephalitis in Australia, 1974: Antibody Response in Cases and Community

Abstract

Fifty-three patients accepted on clinical grounds as cases of Murray Valley encephalitis (MVE) in Australia in 1974 were examined for antibody to MVE virus. Only one (who died early in the disease and whose diagnosis was confirmed by virus isolation) did not develop antibody; 13 patients showed stationary or single convalescent titres not diagnostic of recent infection, but other evidence that infection was recent was obtained in eight; 39 showed significant rise or fall in titre confirming recent infection. Haemagglutination-inhibition (HI) was more effective in establishing a diagnosis than complement-fixation (CF) although both tests were of value. Patients varied widely in timing and magnitude of rise and fall of titre. Two showed late rises in antibody titre which raises the possibility of recrudescent persisting infection. CF titres were enhanced in some sera by increase in the number of units of antigen used and by inactivation at 56 degrees C rather than 60 degrees C. Five patients with clinically-acceptable diagnoses of MVE (and one with minor illness) showed higher HI titres to Kunjin than to MVE virus. The results in several cases suggest that Kunjin virus was the infecting agent. In others it is possible that MVE infection had occurred in patients with pre-existing Kunjin antibody. HI reactivity to MVE virus was found in IgM fractions of sera taken for at least 40 days and in some cases for over 100 days after onset of symptoms. IgM fractions gave similar titres to MVE and Alfuy virus but clearly distinguished MVE-Alfuy and Kunjin viruses. HI antibody to MVE virus was found in about 10% of sera from family contacts or neighbours of patients with encephalitis, and in a similar proportion of patients in Victoria with various febrile illnesses not accepted as MVE. One patient with minor illness had antibody response to Kunjin virus. 2589 sera from pathology laboratories in towns in the Murray Valley gave additional evidence of community immunity to flaviviruses and suggested some increase in the proportion reactive between January and May 1974. HI and plaque reduction tests on these sera also gave evidence of antibody to Kunjin virus in the Murray Valley.