West Nile virus and West Nile virus/Kunjin disease

Arboviruses are viruses that are spread by the bite of arthropods, particularly mosquitoes. They are divided into alphaviruses and flaviviruses. WNV and WNV/KUN viruses are members of the flavivirus genus.

Notification requirement for West Nile virus and West Nile virus/Kunjin virus disease

WNV and WNV/KUN infections are “routine” notifiable conditions and must be notified by medical practitioners and pathology services in writing within 5 days of diagnosis. WNV is notifiable under “arbovirus infections other”.

This is a Victorian statutory requirement.

Primary school and children’s services exclusion for West Nile virus and West Nile virus/Kunjin disease

Exclusion is not required.

Infectious agent of West Nile virus and West Nile virus/Kunjin disease

West Nile virus

WNV was first identified in Uganda in 1937. The virus was largely confined to Africa, Eastern Europe, the Middle East and West Asia. The virus was imported into New York creating a large outbreak in 1999. It caused thousands of deaths in birds and horses, and human disease, including fatal encephalitis. It then spread throughout the Americas, from Canada to Venezuela.

West Nile virus/Kunjin disease

WNVKUN virus is a strain of WNV. It was first isolated from Culex annulirostris mosquitoes collected in north Queensland in 1960 and given the name of a nearby Aboriginal clan living on the Mitchell River. It was previously included as one of the causative agents in the disease called ‘Australian encephalitis’, which also includes a disease caused by Murray Valley encephalitis virus (MVEV), another flavivirus. These viruses are now accepted as causing two separate diseases: MVE and WNV/KUN. Prior to 2010, WNV/KUN was known as Kunjin.

There are at least seven genetic lineages of West Nile virus. Kunjin virus is a small but genetically distinct sublineage, designated as 1b. The epidemics of severe disease in humans and animals during the past decade have been due to WNV sublineage 1a, which has never been found in Australia.

Identification of West Nile virus and West Nile virus/Kunjin disease

Clinical features

West Nile virus

Approximately 80 per cent of people who become infected have no illness; up to 20 per cent of people who become infected have mild symptoms; and a very small minority experience severe disease. West Nile virus disease can be described as a febrile illness of sudden onset, often accompanied by tiredness, headache, muscle pain, nausea, rash, vomiting, swollen glands and eye pain. Some patients experience gastrointestinal symptoms, including nausea, vomiting, loss of appetite or diarrhoea. Symptoms usually resolve within 7-10 days, although tiredness can last for some weeks. This virus should be considered in returned travellers from endemic areas whom have a clinically compatible illness.

West Nile virus/Kunjin disease

Serological surveys for WNV/KUN virus indicate that subclinical infection is common. Two main clinical forms of disease have been reported: mild disease and encephalitis. Mild diseases consist of lymphadenopathy, fever, lethargy and rash. Additional muscle weakness and fatigue may also be reported.

Fatalities are rare or absent. Very few epidemiological studies have been carried out to determine the life cycle, nature and frequency of WNV/KUN disease infection in Australia.

Diagnosis

Cases require laboratory and clinical evidence.

Laboratory evidence requires one of the following:

• isolation of WNV/KUN virus
• detection of WNV/KUN virus by nucleic acid testing
• IgG seroconversion, or a significant increase in antibody level, or a fourfold or greater rise in titre of WNVKUN virus
• detection of WNV/KUN virus–specific IgM in cerebrospinal fluid in the absence of IgM to Murray Valley encephalitis (MVE), Japanese encephalitis or dengue viruses
• detection of WNV/KUN virus–specific IgM in serum in the absence of IgM to MVE, Japanese encephalitis or dengue viruses. This is only accepted as laboratory evidence for encephalitic illnesses. CSF and serum (clotted blood) are appropriate samples for polymerase chain reaction (PCR) testing. Serological testing is most often performed on serum. It is important that both acute and convalescent serum samples are collected in order to demonstrate a rise in IgG as this confirms recent infection. Cross reaction of antibodies to other flaviviruses is possible.

Clinical evidence requires one of the following:

• Non-encephalitic disease: acute febrile illness with headache, myalgia and/or rash.
• Encephalitic disease: acute febrile meningoencephalitis characterised by one or more of the following:
  • focal neurological disease or clearly impaired level of consciousness
  • abnormal computed tomography (CT) scan, magnetic resonance imaging (MRI) scan or electroencephalogram
  • presence of pleocytosis in the cerebrospinal fluid.
• Asymptomatic disease: cases detected as part of a serosurvey should not be notified

Incubation period of West Nile virus and West Nile virus/Kunjin disease

West Nile virus

The incubation period is 2 –14 days.

West Nile virus/Kunjin disease

The incubation period is usually 7 – 28 days

Public health significance and occurrence of West Nile virus and West Nile virus/Kunjin disease

WNV/KUN virus has many similarities to MVE virus, and identification of these two viruses can only be distinguished by virological tests. This distinction is important during periods when weather patterns and other surveillance indicators suggest that an outbreak of MVE virus may be imminent in south-east Australia. MVE has a higher mortality rate and can be more prevalent.

West Nile virus

WNV has not be found in Australia. The National Arbovirus and Malaria Advisory Committee (NAMAC) classifies the risk of transmission as potential local transmission through an animal host, causing significant morbidity and mortality. The necessary mosquito vectors and avian species are present to allow the establishment and spread of permanent mosquito–bird transmission cycles. There is potential for high economic impacts should the virus spread to the equine population.

West Nile virus/Kunjin disease

WNV/KUN is found in parts of Australia, particularly the Northern Territory and northern Western Australia. WNVKUN virus is less virulent than the current United States strain of WNV. Serological surveys have shown that WNV/KUN virus infection has occurred over wide areas of Australia. The virus has infected humans, and wild and domestic animals, including cattle, sheep and horses. Similar to the MVE virus, one theory is that WNV/KUN virus occasionally spreads southwards from the tropical north to central and south-eastern Australia after heavy rains.

WNVKUN virus has been detected in Victoria on several occasions since 1974. There have been two confirmed cases in Victoria since 2010, with the latest case reported in 2017.

Reservoirs for West Nile virus and West Nile virus/Kunjin disease

West Nile virus

WNV virus is maintained in nature in a mosquito-bird-mosquito transmission cycle. In Europe, Africa, Middle East and Asia, mortality in birds associated with WNV infection is rare. In striking contrast, the virus is highly pathogenic for birds in the Americas. Members of the crow family (Corvidae) are particularly susceptible, but the virus has been detected in dead and dying birds of more than 250 species.

Horses, just like humans, are “dead-end” hosts, meaning that while they become infected, they do not spread the infection. Symptomatic infections in horses are also rare and generally mild, but can cause neurologic disease, including fatal encephalomyelitis.

West Nile virus/Kunjin disease

The virus is endemic in the tropical north of Australia, where it has cycles of infection between wading birds, such as herons and mosquitoes in enzootic foci.

Mode of transmission of West Nile virus/Kunjin disease

The virus is spread by the bite of an infected mosquito. In Australia, the most common carrier of WNVKUN virus is the freshwater mosquito Culex annulirostris. This is a fresh water breeding mosquito, that bites around dusk and dawn.

Period of communicability of West Nile virus and West Nile virus/Kunjin disease

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

Susceptibility and resistance to West Nile virus and West Nile virus/Kunjin disease

People with antibodies to WNVKUN virus may be immune to infection with WNV. Infection confers lifelong immunity.

Control measures for West Nile virus/Kunjin disease

Preventive measures

There is no preventive vaccine available.

WNV and WNV/KUN virus infection can be prevented by:

• personal protective measures, such as wearing long, loose-fitting, light-coloured clothing
• using personal repellents containing diethyltoluamide (DEET) or picaridin
• avoidance of mosquito-prone areas especially at dusk and dawn, which are peak biting times.
• mosquito control measures

Control of case

There is no specific treatment for WNV and WNV/KUN and care is largely supportive. Cases with encephalitis disease should ideally be managed in hospitals with intensive care facilities and expertise in the management of complicated neurological disease.

Control of contacts

If others are unwell, it is advisable that they see their own doctor for testing.

Control of environment

To reduce or prevent virus transmission, it is necessary to interrupt human-mosquito contact by:

• avoiding mosquito-prone areas.
• preventing mosquitoes from entering the home or accommodation
• suppressing the mosquito population, through removal of stagnant water, using knockdown sprays or long-acting surface sprays if mosquitoes are particularly bad.

Outbreak measures for West Nile virus/Kunjin disease

In addition to prevention activities, outbreak measures for WNV/KUN virus may include:

• community education campaign promoting use of personal protection measures
• conducting a survey to determine the species of the vector mosquito involved, identify their breeding places and promote their elimination
• enhanced human surveillance through increased testing and notification