IN Australia, 23 cases of Zika virus (ZKV) infection have been reported in returned travellers from South-East Asia, Pacific Islands and South America since 2012, but widespread transmission here is unlikely for a number of reasons.
ZKV infection is a mosquito-borne pathogen that has widened its geographic range from Africa and Asia to the Pacific Islands and the Americas in the last decade. Currently there is a large and ongoing outbreak in the Americas, and as of January 2016 local circulation of ZKV was widely established in several regions.
Evidence for human infection was first reported in 1952, but ZKV, an arbovirus of the Flaviviridae family, was originally identified in a rhesus monkey in Uganda in 1947. The primary vector for the epidemic transmission of ZKV is Aedes aegypti, and infection occurs after a bite from an infected mosquito. Other Aedes species are also competent vectors of transmission, including A. albopictus, A. hensilli and possibly A. polynesiensis.
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At present, the only competent vector in mainland Australia are A. aegpyti populations in Far Northern Queensland (FNQ), but sustained, widespread ZKV transmission in FNQ is unlikely for several reasons.
Firstly, the local history of dengue importations means there is a high index of clinical suspicion and reporting of viral illnesses with exanthema, so ZKV cases should be detected relatively quickly.
Secondly, a focused mosquito control program around suspected index cases would contain and eventually terminate the spread of ZKV, just as it has against dengue virus outbreaks in the same locations over several decades.
Finally, A. aegpyti populations in some parts of Cairns and Townsville now contain strains of the symbiont bacterium Wolbachia that render these mosquitoes much less competent vectors for arboviruses.
Establishment of Wolbachia in the ZKV-affected countries of Brazil and Colombia is underway.
ZKV infection generally results in asymptomatic or a mild self-limiting febrile illness, but there is now a suspected association between ZKV infection and congenital microcephaly in pregnant women. Neurological complications, including Guillain–Barré (GB) syndrome, have been identified as complications of ZKV infection. Prospective research, including cohort and case-control studies, is required to improve the quality of evidence linking congenital ZKV infection with microcephaly and ZKV with GB in adults.
The incubation period is typically 3-12 days, and infections caused by ZKV virus are mostly asymptomatic. If symptomatic, it presents as a mild to moderate illness characterised by rash, fever, arthritis or arthralgia and conjunctivitis, with symptoms lasting 7 to 10 days.
The typical rash is typically a maculopapular, with a median duration of 6 days (range, 2 to 14); arthralgia lasts for about 3 days. Other reported symptoms include headache, myalgia, retro-orbital pain and vomiting.
While there is considerable overlap between the symptoms of ZKV and dengue virus infections, none of the haemorrhagic or plasma leakage-related complications seen in severe dengue have been described in any ZKV outbreak.
Laboratory abnormalities often seen in dengue cases, such as thrombocytopenia and leukopenia, have been described less frequently in association with ZKV infection.
Laboratory diagnosis of acute ZKV infection is primarily by direct detection of viral nucleic acid by reverse transcription polymerase chain reaction (RT-PCR), usually in acute phase serum. Viraemia can be reliably detected up to 3 days after symptom onset and occasionally for as long as 11 days.
Initial studies suggest that ZKV RNA at higher load is detectable in urine samples up to 7 days longer than in serum samples.
Testing of both urine and serum is a sensible approach to diagnosis of the relatively small numbers of Australian patients anticipated. Nucleic acid testing capacity for ZKV is available in the larger Australian public health laboratories.
Detection of ZKV-specific IgM and total antibodies is possible, but complicated by potentially significant serological cross-reactions arising from earlier infection with or vaccination against other flaviviruses. Plaque reduction neutralisation assays may resolve such cross-reaction by demonstrating fourfold rises in titre between acute and convalescent serum samples. This is, however, labour-intensive and only available at a limited number of sites.
The mainstay of the clinical management of ZKV infection is bed rest and symptom relief. In regions where the vector is prevalent, individuals suspected of being infected with ZKV would be advised to seek medical advice immediately. ZKV infection is notifiable to state and territory health departments in Australia.
Prospective Australian travellers to countries reporting ZKV infection would be advised to comply with prophylaxis measures, including the use of mosquito repellent during daylight hours. While the association between infection in pregnancy and congenital microcephaly is suspected, pregnant travellers should reconsider travel to areas where ZKV is endemic.
For up-to-date recommendations for travellers and for the management of pregnant women with suspected ZKV virus infection:
Professor Cameron Simmons is with the Department of Microbiology and Immunology, Dr Irani Thevarajan is with the Victorian Infectious Disease Service, and Dr Mike Catton is with the Victorian Infectious Disease Reference Laboratory, all at the Peter Doherty Institute for Infection and Immunity, a joint venture between The University of Melbourne and the Royal Melbourne Hospital. Katherine Gibney is with the Department of Epidemiology and Preventive Medicine at Monash University.