Factsheets

Murray Valley encephalitis virus infection - Fact Sheet

Murray Valley encephalitis virus (MVEV) is a flavivirus. It has the capacity to cause severe human disease, with encephalitis being the most notable clinical feature.

Infectious Agent

Murray Valley encephalitis virus (MVEV) is a flavivirus. It has the capacity to cause severe human disease, with encephalitis being the most notable clinical feature.

MVEV was first isolated from patients who died from encephalitis in the Murray Valley in Victoria and South Australia in 1951. It was previously included as one of the causative agents in the disease called Australian encephalitis, which also included disease caused by Kunjin virus, another flavivirus. MVEV is now recognised as causing the disease Murray Valley encephalitis (MVE).

Identification

Clinical features

MVEV can commonly infect humans without producing apparent disease (subclinical infection), or it may cause a comparatively mild disease with features such as fever, headache, nausea and vomiting. In a small percentage of all people infected, mild disease may be a prodrome to disease progression and involvement of the central nervous system, causing meningitis, or in the worst scenario, encephalitis of variable severity. Signs of brain dysfunction, such as drowsiness, confusion, fitting, weakness, or ataxia, indicate the onset of encephalitis.

Method of diagnosis

Infection is confirmed by a significant rise in antibody titre to the virus in two blood specimens taken seven to ten days apart. Sera for diagnosis should be sent to the specialist diagnostic laboratories.

A diagnosis of MVEV disease should be considered in any patient who presents with encephalitis or central nervous system symptoms and who has been in the MVEV endemic area within the incubation period of the disease, especially in the period between November and July.

Laboratory evidence

• Isolation of MVEV from clinical material;
  OR
• Detection of MVEV RNA in clinical material;
  OR
• IgG seroconversion or a significant increase in antibody level or a fourfold rise in titre of MVEV specific IgG proven by neutralisation or another specific test;
  OR
• MVEV-specific IgM detected in the CSF in the absence of IgM to Kunjin, Japanese encephalitis or dengue viruses;
  OR
• MVEV-specific IgM detected in serum in the absence of IgM to Kunjin, Japanese encephalitis or dengue viruses. This is only accepted as laboratory evidence for encephalitic illnesses.

Confirmation of laboratory result by a second arbovirus reference laboratory is required if the case occurs in areas of Australia not known to have established enzootic/endemic activity or regular epidemic activity.
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Clinical evidence

Non-encephalitic illness
Acute febrile illness with headache, myalgia and/or rash
OR
Encephalitic disease
Acute febrile meningoencephalitis characterised by one or more of the following:

• focal neurological disease or clearly impaired level of consciousness
• an abnormal CT or MRI scan or EEG
• presence of pleocytosis in the CSF
  OR
  Asymptomatic disease

Incubation period

Usually seven to 28 days.

Public Health Significance and Occurrence

MVEV is endemic (always present) in northern Australia (WA and the top end of the NT) and probably in PNG. In nature MVEV is amplified in bird-mosquito-bird cycles and humans become infected if bitten by infected mosquitoes. MVEV activity increases after heavy rainfall and flooding. In northern Australia sporadic cases or small outbreaks of MVE occur every few years, usually during the wet season.

There have been seven major outbreaks of MVE in Australia since 1917. The last was in 1974 when 58 cases were reported from all mainland states. Since 1974 nearly all cases of MVE have occurred in north of Western Australia and the Northern Territory, with occasional cases in Queensland, central Australia and central regions of Western Australia. Serological studies show that only 1 in 800-1000 of people infected develop clinical disease. Of these 25% have died and a further 25-50% have been left with permanent neurological damage.

MVEV is thought to move from endemic areas in northern Australia to epidemic areas by the movement of infected native birds or infected wind-blown mosquitoes. However, there is also evidence that the virus is able to survive in these new areas for at least one or two seasons, possibly within mosquito eggs or by other unidentified mechanisms. MVEV activity occurs only occasionally in south-eastern Australia, usually after heavy rains and flooding in northern and central Australia, and it is likely that these epidemics have also resulted from reintroduction of the virus.

Reservoir

The primary hosts of MVEV are water birds. Ardeiformes (herons), particularly the Rufous Night-heron, and the Pelicaniformes (cormorants/ darters) are the most commonly infected.

Mode of Transmission

The primary mosquito vector during epidemics is Cx. annulirostris. Other mosquitoes such as Cx. australicus and some Ochlerotatus species may be involved in other aspects of MVEV ecology.

Period of Communicability

There is no evidence of person-to-person transmission.

Susceptibility and Resistance

Infection with MVEV confers life-long immunity.

Control Measures

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Preventive measures

Patients can be managed at any hospital, but facilities for providing intensive care, particularly artificial respiration, must be available. There is no preventative vaccine available.

Control of case

Investigate the source of infection. Search for unreported or undiagnosed cases of encephalitis from the Murray-Darling drainage basin.

The patient with suspected infection [or friend or relative] should be asked to recall if, in the month prior to onset of symptoms, he or she had:

• Been bitten by mosquitoes; or
• Visited regions where MVEV is endemic; or
• Participated in recreational or other activities involving exposure to bushland or other mosquito habitat (as in, for example gardening, bushwalking, camping and picnicking)

Control of environment

To reduce/prevent virus transmission, interruption of human/mosquito contact is required by:

• suppression of the vector mosquito population
• avoidance of vector contact (vectors usually bite in the first few hours after sunset.)
• apply mosquito control measures (local municipalities).
• use personal protection measures (long sleeves, long trousers, mosquito repellents).
• avoid mosquito-prone areas;

Outbreak Measures

Following notification of a seroconversion to MVEV or information of human notification:

• An emergency meeting of various health bodies in each state.
• The presence of MVEV in the area will be notified to relevant regional offices and local health council personnel, and nationally to the Commonwealth and NAMAC.
• Suitable media releases will be made available.
• Appropriate members will visit the area to consult and advise local councils, health and tourism authorities.
• Depending on the actual or potential severity of the outbreak, meetings of relevant personnel will be arranged in the affected area to consider control measures et cetera.

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