8: Emerging viral infections in Australia

Hendra virus infection has been identified in three people. In Brisbane, in 1994, a 49-year-old horse trainer died after a fulminating septic pneumonic illness, while a 40-year-old worker at his stable survived an influenza-like illness. Eighteen horses in the same stable developed a pneumonic illness, and fourteen died. Serological evidence of infection was demonstrated in three other horses which were asymptomatic.1,3 A year later, a 36-year-old farmer died as a result of Hendra virus encephalitis in Mackay, Queensland.4 Two of his horses were subsequently shown to have died of Hendra virus infection 13 months earlier.

Subsequent seroepidemiological testing for Hendra virus in a large number of human contacts of these three people was completely negative.5 Seroepidemiological studies of more than 2000 horses and more than 5000 samples from 46 other animal species in Queensland also failed to identify a single Hendra virus infection.6 However, antibody to Hendra virus was found in 20 of 224 serum samples from four species of fruit bats from as far north as Madang, Papua New Guinea, and as far south as Melbourne.7 Fruit bats (Box 2) now seem a likely source of Hendra virus, although they appear to be asymptomatically infected.

Menangle virus was isolated from stillborn piglets in New South Wales in 1997, and serological evidence of infection was found in pigs, humans and fruit bats closely associated with the piggery. Two piggery workers developed an influenza-like illness with a spotty, red, non-pruritic rash.2 No further cases have been identified. The wider prevalence of Menangle virus remains to be determined.

An outbreak of encephalitis involving more than 250 pig farmers occurred in northern Malaysia in 1999, with a 40% case-fatality rate.8 At about the same time, an outbreak occurred in Singapore involving 11 abattoir workers who had fever with pneumonia or encephalitis; one died.9 Both outbreaks were shown to be caused by Nipah virus (named after the town of first recognition in Malaysia). Ribavirin therapy was used in many patients without obvious therapeutic benefit.8 More research is required to define the epidemiology of this virus, although pigs seem to be involved asymptomatically as intermediate hosts. Nipah virus infection has not yet been reported in Australia.

ABL infection should be suspected in patients who present with a progressive neurological condition and history of exposure to bats (Box 1). The diagnosis is made by polymerase chain reaction tests for ABL in cerebrospinal fluid or serum antibody tests. Examination of bat brain tissue can also be helpful but is rarely possible.

Once the disease develops, there is no specific treatment. Post-exposure prophylaxis should be given after a bite, scratch or significant salivary exposure from a bat in Australia (Boxes 2 and 4). Prophylaxis is not indicated after exposure to bat urine or faeces. As long incubation periods (over a year) have been anecdotally described for lyssavirus infection, there is no cut-off period of infectivity after exposure. However, it is suggested that rabies immunoglobulin can be omitted if exposure occurred more than a year earlier.13

Pre-exposure prophylaxis with three doses of rabies vaccine, at Days 0, 7 and 28, is recommended for expatriates and travellers spending more than one month in rural parts of endemic areas (advice on high-risk countries is found on the World Health Organization website <www.who.int/>, and on rabies-free countries in the Australian immunisation handbook13). In Australia, pre-exposure prophylaxis is recommended for people at risk of bites or scratches from bats (eg, bat handlers, veterinarians, wildlife officers and others who are liable to come into direct contact with bats).13

Although seroprevalence in enzootic areas ranges from 39% to 46%,17 clinical illness is rare. The clinical and epidemiological features of MVE in the Northern Territory, where the virus is endemic, were described for 16 of 18 identified cases between 1987 to 1996. Most cases were in children. Fever was universal, and some cases had a variable prodrome, which included diarrhoea, rash and cough. Seizures were common in children, while adults more commonly presented with headache, dysphasia, memory impairment, confusion and tremor. Several distinct clinical patterns were noted, including relentless progression to death, a poliomyelitis-like illness, cranial nerve or brainstem involvement with tremor, and a non-specific encephalitic illness. Mortality has been estimated at about 20%, with residual neurological impairment in about half the survivors.18

Kunjin virus infection presents with an acute febrile illness and polyarthralgia. The major differential diagnosis is infection with Ross River or Barmah Forest virus. Encephalitis occurs rarely.

JE has a short prodrome which may include coryza, diarrhoea, and rigors.21 Headache, vomiting, obtundation and seizures may ensue, with some individuals presenting with personality change or abnormal behaviour. Seizures are common, particularly in children, and extrapyramidal features, such as tremor, hypertonia, cogwheel rigidity, choreoathetosis, opsoclonus, myoclonus and lip smacking, are suggestive of JE.21 Upper motor neurone facial nerve palsies and opisthotonos or a clinical syndrome of acute flaccid paralysis may occur.24 Overall mortality is about 30%, with residual neurological damage in about half the survivors.

Diagnosis is usually serological, with enzyme immunoassay IgM and IgG capture assays useful for testing serum and cerebrospinal fluid (case history, Box 6).

• residents of endemic areas;

• laboratory workers potentially exposed to the virus; and

• travellers spending 30 days or longer in endemic areas, particularly if they intend to spend a lot of time outdoors in rural areas during the wet season.13

The vaccine is administered in a series of three doses, at 0, 7 and 30 days, with a booster recommended at one year. Tenderness, redness and swelling occur in up to 20% of recipients, and fever, headache, malaise and chills in about 10%. The combination of itching, urticaria, and occasionally angio-oedema of the face, which can be severe, has been recognised since 1989, with an incidence estimated at 2–10 per 1000 vaccine doses, and higher in those with a history of urticaria.