The Best Australian Science Writing 2012 (15 page)

The state was being squeezed tighter and tighter and the wind kept getting stronger. But the front over the Tasman was just sitting there, saying, ‘You can keep coming all you like, but I'm not moving.' We in Victoria were caught in the pressure point between them.

The horrific 12 year drought added to the heat as well, and was doubtless the reason why so many temperature records were broken. The ground was so parched and hard-baked that there was little evaporation possible to ameliorate the conditions. In wetter years, residual moisture in the soil and vegetation would have had a moderating effect, reducing the temperature. Now solar radiation heated the ground and was returned directly back into the atmosphere in the form of high-powered dry convective thermals, which further warmed and dried the air.

The confluence of these phenomena amounted to a massive blast of sun-dried, super-heated air being driven down to the
southeast of Victoria, into what fire historian Stephen Pyne calls the ‘fire flume'.

A flume, in the common sense of the word, is a man-made structure: a deep, narrow defile through which a fluid – usually water – is channelled. A flume might be constructed to transport timber, to divert water from a dam or power a water wheel: a mill race is a flume. But in Pyne's elegant trope, it is not water that is channelled, it is wind.

The eastern ranges act like wings, shepherding heated air southwards, concentrating energy; the variable soil and precipitation produce vast amounts of fuel on the ground. Topography, botany and weather: these interwoven forces provide the dynamism that makes the great fire triangle of southeastern Australia – its corners at Botany Bay, Port Phillip Bay and the Eyre Peninsula – the most fire-prone location on Earth.

Writing as therapy

Tragedy

Weather

Under the influence

Frank Bowden

I had a little bird/Its name was Enza/I opened up the window/And in-flu-enza.

Children's skipping rhyme, c. 1918

One of the great advantages of being a well-paid specialist on the staff of a public hospital – rather than a ridiculously well-paid visiting medical officer in private practice – is that you are entitled to long-service and study leave. After ten years without much of a break, I was tired, grumpy, sick of being on call, fed up with working weekends, short with colleagues and occasionally dismissive of my students. I knew that soon I would reach that lowest of low points for a doctor – when you start to see patients as enemies and complain in the tea room about them, as if they'd contrived their illnesses just to annoy you. My family had started giving me concerned looks across the dinner table, and even my dog was keeping her distance.

So it was with considerable anticipation that I began a three month sabbatical on 27 April 2009. I was determined to make the leave count: I promised myself I would be sitting at my desk
every morning ready to write by no later than nine and, in an uncharacteristic display of planning, I had even constructed a timetable for the next 12 weeks.

On the first morning – unshaved, wearing ugg boots, tracksuit pants and a T-shirt – I drove my wife to work, returned home to a leisurely read of the paper over breakfast, had a long shower and arrived at my desk just minutes after my self-imposed deadline. I quickly scanned the top stories on the ABC News website and one item caught my eye.

‘Experts say the swine flu outbreak currently stoking fears of a global epidemic poses a greater risk to Australia, with the onset of winter bringing the peak of the flu cycle.' I checked the BBC site: ‘Schools in the capital city of Mexico are closed due to an outbreak of a disease called swine flu.'

Now this was strange. We had been expecting the next influenza pandemic to be caused by a mutation in the avian influenza virus, the H5N1 strain that mainly affects birds, not the H1N1 virus associated with pigs. I rang my wife, who works in infection control, and asked her what was going on.

‘I can't talk,' she said. ‘I have to go into a meeting with the chief health officer in a minute. There's a bit of a flap on in here.'

There were five infectious diseases specialists in our unit at the hospital at the time. Two were on duty, one was overseas working on a project, one was in the Kimberley on holidays, out of phone range and I was … ‘Oh no, you can't do this to me,' I said out loud. I put down the phone and tried to concentrate on writing, without success. I turned on the radio and listened to the 10am bulletin. The top story was swine flu.

* * * * *

There had been three influenza pandemics in the preceding 100 years: 1918, 1957 and 1968. The 1918 Spanish flu pandemic
was the greatest natural disaster of the 20th century. Estimates vary, but a minimum of 20 million – and possibly up to 50 million – people died, at least double the ten million killed on the battlefields of World War I. In a world without antibiotics, the secondary bacterial infections that followed the epidemic were often deadly. And there were no intensive care units (ICUs) to provide the care needed to allow patients time for their own immune system to win the fight against the pathogen. Around a third of the global population was infected with Spanish flu and more than 2.5 per cent of humanity died.

The other pandemics were, by comparison, not in the same league: the Asian flu of 1957 is estimated to have caused around two million deaths worldwide, while the Hong Kong flu of 1968 is thought to have killed at most one million people.

I became intimately acquainted with Hong Kong flu as an eight-year-old when it nearly killed my father. I remember my father lying in the single bed in the spare room, the bedclothes pulled up over him as he shook his way through what I now know to be a rigor. When my mother had picked him up from the train station the previous night he had been completely well, but during the three minute drive home he started complaining of chills and had started to shiver. By the time he had put his case down in the bedroom he could hardly talk because of the shaking.

The Hong Kong flu was on that evening's television news and on the front page of the day's
Sun
newspaper, so my mother had already made the diagnosis by the time our GP arrived the next morning. I remember her concern and the hushed kitchen conversations with friends suggesting that he needed to go to hospital. He coughed and spluttered for weeks after the worst was over and he always remembered the illness as one of the worst he had experienced.

For 40 years following the 1968 outbreak it was all quiet
on the influenza front. There was a false alarm for a swine flu pandemic in 1975, and virologists remained on alert, knowing the next pandemic was not a matter of if but when.

* * * * *

There are three types of influenza virus: A, B and C. Pandemics are always caused by influenza A. Infection with influenza B can be severe but is rarely fatal and infection with C is uncommon and usually mild. All three types have two main proteins on their surface, haemagglutinin (H) and neuraminidase (N), which are responsible for the confusing nomenclature. There are 16 H and 9 N subtypes but only H1, H2, H3, N1 and N2 commonly cause human disease. The Spanish flu and the 2009 swine flu were H1N1, the Asian flu was H2N2 and the Hong Kong flu was H3N2. Bird (avian) influenza is H5N1.

To understand why pandemics occur we need to know a little about the way the influenza virus reproduces and how our immune system responds to it. Viruses commandeer the proteinmaking machinery of the body's cells to generate tens of thousands of copies of themselves. Every time a flu virus replicates (or copies) itself there is the potential for an error (mutation) to occur, resulting over time in significant changes to the structure of the virus and altering the way the host's immune system ‘sees' it.

When your body first encounters a virus it takes days or weeks for the immune system to produce specific antibodies against it. If the same virus is encountered in the future, your body's reaction time is much faster because the antibodies can destroy the virus before it has time to invade your cells, replicate and cause disease. If a virus has mutated, however, the antibodies are unable to recognise it, giving the virus time to invade, replicate and cause disease all over again.

Some viruses mutate very little during replication. The measles
virus that we are exposed to in childhood will be almost identical to the one that we may be re-exposed to decades later, so immunity is life-long. Influenza A, however, is notable for its sloppy proofreading, and at least one mutation occurs with every copy. Most of these mutations are minor, but enough of them can accumulate, by successive passages through infected human hosts, at the end of the flu season to make the structure of the virus quite different from what it was at the beginning.

This is known as antigenic drift and is a gradual process that allows the human immune system to almost keep pace with viral evolution; you might be susceptible to next year's strain, but you are likely to have at least partial immunity.

Antigenic drift won't lead to a pandemic: for that you need a sudden and profound change in the viral structure. This produces a virus strain that no one in the population has previously encountered and developed immunity to – a seismic phenomenon called antigenic shift. A shift requires more than just a few typos while transcribing the viral genetic code; it requires viruses to have ‘sex' with each other.

Higher-order organisms, such as us, combine half their genetic material with half that of a member of the opposite sex to increase the genetic diversity of their offspring. Lower-order organisms mainly reproduce by making identical copies of themselves, but occasionally they display the traits of sexual reproduction. Sex between consenting viruses is more accurately, if less evocatively, known as reassortment.

A human influenza strain can reassort with a bird or pig strain and the resulting hybrid may have properties that produce a very severe disease in humans. The frequently cited doomsday scenario is a reassortment of the bird flu strain H5N1 with a human influenza strain, allowing bird flu to be transmitted from human to human. The reason infectious disease specialists worry so much about such an event is that the world's insatiable appetite
for poultry has produced a chicken population explosion, particularly in Asia. With so many birds living in close proximity to humans, viral reassortments are occurring all the time and the emergence of a deadly flu strain is considered inevitable.

* * * * *

All epidemics start quietly. Their early stages are usually undetectable by the routine surveillance mechanisms health departments have in place. By the time you know something is going on, the infectious agent is well established in the population. The swine flu strain responsible for the 2009 pandemic was first detected in Mexico in April of that year, in four-year-old Edgar Hernandez. This little boy recovered completely, but the viral strain would have been circulating in the community for weeks or even months before.

Within a few days of Edgar's highly publicised diagnosis dozens of other people across Mexico were reporting fevers, muscle aches and coughs. As I read the news bulletins each morning over the next few weeks it became clear to me that an antigenic shift had occurred. By the time the virus causing their symptoms was identified as swine flu (H1N1) in the US Centers for Disease Control and Prevention laboratory in Atlanta, Georgia, thousands more had been infected.

While the new strain was very similar in composition to the 1918 Spanish flu, it wasn't immediately clear if it possessed the same virulence as its 20th century predecessor. But the World Health Organization (WHO) had been preparing for this event for more than a decade and an elaborate influenza pandemic plan had been formulated. By the end of April 2009, cases of swine flu had been reported in the US, Europe, India, Pakistan, Bangladesh and New Zealand. On 11 June Margaret Chan, the WHO's Director-General, told a press conference in Geneva: ‘We are all
in this together, and we will all get through this, together.' She had just declared the beginning of the first influenza pandemic of the 21st century.

* * * * *

Influenza is an autumn and winter disease, so although the virus was already circulating in the northern hemisphere in early 2009 it was not expected to take off there until later in the year. The European and US public health communities were, therefore, closely watching the behaviour of the epidemic when it reached Australia and New Zealand during our winter, mid year. As had been predicted, attempts to contain the virus proved futile in a world interconnected by air travel, although many jurisdictions, including some in Australia, attempted to create a
cordon sanitaire
(a quarantine line), reasoning that slowing the tempo of the epidemic by even a small degree would buy some time to get local plans in place.

One of the planks of the pandemic plan is the use of antiviral prophylaxis – taking steps, such as the administration of drugs to people exposed to the virus, to reduce the spread of the illness and break the chain of transmission. The pharmaceutical antiviral agents that work against influenza, zanamavir (an Australian discovery with the trade name of Relenza) and oseltamivir (known commercially as Tamiflu), don't have anything approaching the potency that antibiotics have against severe bacterial infections. These anti-flu drugs inhibit the neuraminidase enzyme of the virus (the N of H1N1) and, as they have few side effects on human cells, they are quite safe.