At the outset of the 2010 flu season, 16 million vials of the vaccine for H1N1, also known as swine flu, lay unused. The biggest vaccination program in our country’s history, costing an estimated $120 million, triggered a wave of inaction. The federal health minister, Nicola Roxon, sees this inertia as the palpable cost of complacency. Since the vaccine’s arrival on 1 October last year, Ms Roxon, backed by the major voices in our health system, including the Australian Medical Association, has been urging Australians to take the injection. By the end of January, only 27%, or 6 million people, had listened, a figure considered so low that it prompted the federal Opposition’s health spokesperson, Peter Dutton, to call for a review of the government’s commitment to buy 21 million doses from the pharmaceutical company CSL. Not even the alarming news that by the end of 2009 about 10,000 Americans had died from the virus and 22 million had been infected was enough to send Australians to their doctors. If the take-up rate does not increase markedly this autumn, the program will become an embarrassment for the government and a possible public-health catastrophe. But our relationship with influenza is unique among all illnesses and nothing about it has ever been simple.
Although it is an everyday virus, there is something about influenza that inspires awe. This microscopic hard-shelled parcel of genetic matter lives in aquatic birds, which have been flying it around in first-class comfort for generations. It is coughed into the air – and across the species barrier – and lodges in the lungs of mammals such as pigs and humans, where it becomes the common flu, our most cited cause for staying home from work. This bird-borne cocktail brings with it our muscle pain, headaches, chesty coughs, sore throats and fevers. It also incites some of our deepest fears, because influenza is often not just a passing illness, but a killer. More than 200,000 times per year in the US, flu develops into a lethal cascade of symptoms that require hospitalisation; death from flu, via pneumonia and organ failure, is fever-racked agony. It kills the young and the old, the pregnant and the chronically weakened; occasionally it juggles its genetic material into a new combination and kills millions.
Because flu begets fear, it can become political. Public preparedness for the flu season is a matter for the state. Vaccination is argued over, not just as a question of available dosage, but on quasi-religious terms. Due to the centrality of fear, the public argument over influenza takes the same shape as the argument over terrorism, or climate change, or immigration, or the economy: it is as much about belief as it is about scientific assessment and says much about our disposition toward fear itself.
The mysteries of the virus itself are genuine rather than warped by ideology, though. The world’s foremost influenza experts know remarkably little; they have not even known that flu was a virus for very long. To inform us about its evolutionary history, its human history and what it might do next, scientists are piecing together a narrative from the barest scraps. Great resources have been marshalled for solving the flu mystery, yet most of our knowledge is contingently held.
It is likely, says Dr Keith Horsley, that nobody in Australia had the flu before July 1820. Horsley, a former medical officer with the Australian Institute of Health and Welfare, has been working on a book about historic flu pandemics in Australia. There was a good reason Australia was flu-free before 1820, he argues: “The ships were too slow. As far as we know there was no flu in the Aboriginal population, and among the Europeans, if influenza broke out aboard a ship it would have passed through its cycle and no longer been contagious by the end of the voyage here.”
The flu virus can only live in humans for days or, at most, weeks. It needed shorter voyages than the early sea journeys that took months to get to Australia, and Dr Horsley says it probably came “after island-hopping through the South Pacific to New Zealand, and then someone from New Zealand could have infected someone here”. The evidence is circumstantial – we suspect a New Zealand origin because a flu contagion could have survived the four-day Tasman voyage – but the consequences were real. “It decimated the Aboriginal people, who had already lost 20% of their population in the smallpox outbreak after 1789,” Dr Horsley says, “and it also laid low the white population, who were immunologically naive.”
Immunological naivety (where resistance to viruses has not been developed) is at the heart of every public health debate over flu. Opponents of vaccination maintain that getting the flu this year is an insurance against getting a worse bout next year. The first wave of swine flu, which hit Australia last winter, has either prepared us for a less-severe second wave or left us vulnerable because of its mildness – we don’t yet know which.
All we can be sure of is that resistance is a product of exposure. Thirty-eight years ago the South Atlantic island of Tristan de Cunha was a human laboratory of immunological naivety. Some 300 inhabitants of the island evacuated to England after a volcanic eruption in 1961, then grew homesick and returned in 1963. For the next nine years they were isolated from diseases affecting the rest of the world. Then, says John Mathews, a population health professor at the University of Melbourne, an outbreak of influenza infected 96% of the population, a rate never seen before or since. “That says very strongly that if you haven’t seen any influenza in the population, people become highly susceptible to it,” he concludes.
The Tristan de Cunha outbreak of the virus known as H3N2 was not particularly lethal. But a similar yet fatal unintended experiment on an isolated population had taken place in 1918–19, when, says Professor Mathews, “virtually the entire population of Western Samoa fell ill with influenza, and as many as 20% died. In Alaska, another isolated place, the mortality rate [for the same outbreak] was even higher.” Throughout the rest of the world – although 20 million people died in the pandemic – the mortality rate was a much lower 0.2%. “From these experiences we can conclude that any sort of flu provides some protection against later exposure.”
The years 1918–19 are the most critical to our knowledge of flu, and the pandemic from that time still forms the basis of our knowledge of how an outbreak shapes itself. The 1918 outbreak, nicknamed ‘Spanish flu’ – though we are uncertain of its origins – spread in military camps and on troop ships at the end of World War I, reaching Australia in early 1919. In January of that year, it broke out almost simultaneously in Hobart, Melbourne and Sydney. Its onset was devastating, says Dr Horsley. “Many people were, literally, healthy today, gone tomorrow.”
More than 12,000 Australians died from the flu in the 1919 pandemic. Symptoms included severe forms of common flu afflictions, as well as gastrointestinal bleeding and haemorrhaging from the nose, ears, anus and vagina. It killed so swiftly that newspapers reported the disease not as flu but as the Black Death. So little was known about viruses that the Spanish flu was widely thought to be caused by bacteria.
Uniquely, the 1918–19 flu killed populations in an “M-wave”; that is, it decimated those in their early twenties as well as the vulnerable infants and elderly who are generally most susceptible. The reasons are believed to be twofold. Firstly, the Spanish flu created a “cytokine storm” in the body of the sufferer. Cytokines are pro-inflammatory chemicals produced by influenza-infected cells as part of the body’s immune response. Among healthy young adults, the cytokine response was over-stimulated, leading to inflammations that closed down vital organs. Secondly, complacency was believed to be highest among young adults. While the wearing of masks was widespread, and cinemas, restaurants, clubs and train stations were soon deserted, young adults were the last to change their social habits, which meant they continued to spread the contagion. Young men contracted the illness more often than their female counterparts, probably because they were more likely to be exposed to it at work or at the pub.
Among the general populace, ignorance created its own kind of storm. Leaflets propounded theories triggered by ideology and fear: the flu was a visitation from God, punishment for the Russian Revolution or a result of excessive ozone. Groups calling themselves “firefighters” would rush to the scene of an influenza outbreak and measure ozone levels. Quack cures abounded, from Bonox and tobacco (which the cigarette companies did little to dispel) to snake oils such as Dr Morse’s Indian Root Pills. “Inhaling machines” were set up in public places, such as the lobbies of department stores, so shoppers could breathe in a powder disinfectant before entering. It is likely, says Dr Horsley, that the machines actually helped to spread the virus.
Although the level of precaution did limit Australia’s mortality rate to below the global rate, Dr Horsley says that “if Australia ever came close to war between the states, it was in 1919. If New South Wales had a standing army, it would have declared war on Victoria.” New South Wales police were stationed along the Murray to enforce the closure of the border, as the government believed the flu was migrating north from Melbourne. (In fact it was radiating out from all of the eastern port cities.) Queensland, Western Australia and South Australia soon closed their borders too; food shortages ensued, and trade, tourism and the economically vital sport of horseracing came to a standstill. More than 600 South Australians who had been stranded in Victoria when the border closed were taken on a special train to Adelaide and put up in a tent city on Jubilee Oval for four days. By then, ironically, the flu had broken out elsewhere in Adelaide, and it is possible that “Camp Jubilee” was the most flu-free location in the city.
While the Australian Sir Frank Macfarlane Burnet – whose later virological work led to the development of a flu vaccine – is justly famous for his contribution to this area, John Cumpston’s work during and after the 1918–19 pandemic was no less influential. A former quarantine and military doctor and a specialist on the 1789 smallpox epidemic, Cumpston was at the forefront of the public health response to the 1918–19 flu pandemic. When Australian servicemen returned from World War I and were put into quarantine against the flu outbreak, Cumpston personally supervised them. He played a key role in delaying the arrival of the virus until 1919.
In 1921, Cumpston was appointed Australia’s first Commonwealth director-general of health. As well as being a doctor and administrator, Cumpston was, says Dr Horsley, “a historical epidemiologist of particular fanaticism”. While assuming the highest position in the new health bureaucracy, Cumpston was also combing library records; from an 1834 clipping from the Australian Almanack & Sydney Directory he began to compile a record of the 1820 arrival of flu in Australia, which he wrote up in his book Health and Disease in Australia: a History (1928). Cumpston also wrote about Australia’s first large-scale flu pandemic, the Russian flu episode of 1889–90, when 2362 deaths were recorded. He found that the lethality of the Russian flu was increased by the confusion of the populace. Nobody knew how the illness moved from one person to another: people speculated that it stemmed from diet, sunspots and ozone. In a similar pattern to the 1919 pandemic, the virus spread right through Sydney within just a week of its arrival from Russia and the first cases were not correctly diagnosed as flu.
The patterns Cumpston was able to observe in the Russian and Spanish flu pandemics remain central to the current study of flu. Flu spreads so rapidly (and in fatal cases kills so swiftly: usually within about ten days) that quick identification remains a problem. Dr Barry Gilbert, a public health physician who consults to government and business, says that last June he “was talking to the Australian Industry Group about swine flu and nobody had heard of it. It had last been seen in the 1970s. Yet within days it was known about in every household. Flu hits that suddenly.”
Diseases live in a Darwinian kind of world and the Spanish flu’s greatest enemy, in the end, was itself. “The survival advantage for any virus is that it has lower lethality,” Dr Horsley says. Flu survives and prospers when the carrier goes out in public and spreads it. But the 1918–19 flu killed, so by 1920, it had effectively burnt itself out.
It was not until the turn of this century that the genetic nature of the 1918–19 flu was conclusively identified. Frozen bodies of victims were disinterred and pathology slides were produced at the Centers for Disease Control and Prevention in Atlanta. They showed that the virus was H1N1; the worst pandemic of last century was a cousin of what we know today as swine flu.
Those Hs and Ns may need explaining. There are three types of the influenza virus, of which one, type A, is most relevant to humans. The virus is spherical, about 100 nanometres in diameter, and contains eight genes that act independently of each other and are collectively coded for 11 different proteins. Most viruses, by contrast, have just one gene that performs all the virus’s functions. Flu is comparatively complex in both structure and behaviour.
“There is no Linnaean evolutionary tree for viruses,” says leading Australian virologist Professor Gregory Tannock, of Melbourne’s Macfarlane Burnet Institute, so we cannot say with any certainty where the flu virus evolved or what animals hosted it in the distant past. It’s tempting to speculate that, as birds are phylogenetically descended from dinosaurs, the giant reptiles were flu carriers. But there is no evidence to say that flu, in its current viral form, has been around that long.
Genetically, influenza is an RNA virus (like polio), whereas many common viruses (such as herpes) are composed of DNA material. One of the characteristics distinguishing the flu virus, says Professor Tannock, is its complicated method of replication, in which carbon copies of genes are produced rather than the genes themselves being reproduced. Because this copying process is imperfect, the consequent errors produce mutated versions of the virus, which will have an initial resistance to existing antibodies.
The virus’s hard outer shell contains glycoproteins in different combinations; these create flu variants that each have different symptoms and their own contagion rates. The main glycoproteins are haemagglutinin and neuraminidase: the now infamous H and N. Haemagglutinin helps the virus bind and break into host cells, while neuraminidase assists the spread of viral material into other cells.
The current H1N1 virus (swine flu) is a mixture of avian flus that passed through pigs to humans. Though related to the Spanish flu of 1918–19, it is more complicated, with “a triple re-assortment of genes including two pig genes and one bird gene”, says Professor Tannock. Other combinations are H2N2, which caused the Asian flu of 1957; H3N2, which caused the Hong Kong flu outbreak of 1968; and H5N1, commonly known as bird flu, which is a matter of serious concern worldwide because of its lethality. Although H5N1 has seldom crossed the species barrier to humans, it is believed to be fatal to more than 50% of those who contract it. The infection and mortality rates of these flu types are measured against the “background”, or ambient, rates of seasonal flu, which thrives in cooler weather and spreads at the onset of each winter.
The weakness in our preparation for flu is in what Donald Rumsfeld might have called the “known unknowns”. “A virus can appear out of left field that we don’t have a vaccine for,” says Professor Tannock. “The time lag in developing a vaccine is usually about six months, and in that time [the virus] can do a lot of damage. There is some work being done on developing universal vaccines, but it’s doubtful that those will be able to counteract a new flu virus.”
The 2009 swine flu, the first wave of which hit Australia last winter, appears to have had a similar mortality rate to seasonal flu. “There was already a good deal of cross-immunity because the virus was similar to seasonal flu,” says Professor Mathews. “The optimistic scenario for the future is that because most people in most parts of the world are exposed to seasonal flu, while the virus can be contagious, future pandemics won’t have the severe mortality rates of the 1918–19 flu.” The pessimistic scenario is that something like the H5N1 virus could cross the species barrier in high numbers.
The H5N1 virus is believed to have killed only about 263 people, mostly in South-East Asia. It can spread from birds to humans, but is not believed to have the ability to spread from person to person, because, Professor Mathews says, “the molecule grabs onto the host cell and is adapted to spreading among birds, which have a receptor for it, but the vast majority of human cells don’t have that receptor and so the species barrier is hard to negotiate. The alarming prospect is if the virus mutates in a way that enables it to spread from human to human.”
The 1918–19 outbreak is still the benchmark against which contemporary factors are measured. The globalising effect of World War I and the mass movement of returned soldiers by sea in late 1918 was humanity’s first experience of such rapid migration. “But we are much more highly connected now,” says Professor Mathews. “Due to air travel, everyone is only a couple of handshakes from London and Washington. What this means is that a virus can spread extremely quickly, but it also means that immunity spreads quicker.”
While H5N1 flu is obviously lethal, some milder flus pose a greater societal threat, Professor Mathews says. “These flus can spread through the population without showing symptoms. Therefore people won’t stay home and will spread it, until it finds high-risk groups.” This is what took place in the winter of 2009. It is believed that 191 Australians – mostly belonging to the highest-risk groups – died from the effects of H1N1 last year. They were not the very young and the very old, but were rather Indigenous people, who are at risk because of isolation and the immunological naivety that is a consequence of this, as well as the health effects of poverty; pregnant women, whose vital organs are already under the mechanical pressure of an enlarged uterus and the immunological pressure of pregnancy; and people already suffering from chronic diseases. The elderly, Professor Mathews speculates, probably got off lightly “because the antigens in this new virus could have been recycled from when [they] were young, and their bodies had already seen them and developed a relative immunity”.
With so much to fear about influenza, you might expect that Australians would have rushed to their doctors after 1 October 2009 when the swine flu vaccine became available to every one of us. Yet the relationship between fear and inaction is always closer and more perplexing than we would like to think. Dr Barry Gilbert says, “the biggest issue is the apathy of the population and its wilful desire for ignorance. Maybe it’s the inherent optimism of humanity, but it’s astonishing how much indifference, even hostility, there is towards the vaccine at a time when we are the only country who can supply a swine flu vaccination to every man, woman and child.”
Sometimes the opposition does not come from apathy or indifference. The anti-vaccination movement is strong in the Byron Bay area of northern NSW, where the Australian Vaccination Network lobby group is based. A Canberra doctor, Ian Griffith, who has advised the federal government on pandemic prevention, attacked the AVN last November, saying: “I’d like to put all those unvaccinated people into a leper colony, because they’re a threat to me and my children.” Dr Gilbert says such groups have “a barrow to push”.
Meryl Dorey, the past president of AVN, has said the group’s opposition to the vaccine is based on doubts about its effectiveness and safety. She cites a study by the British-based Cochrane Collaboration (an Australian branch of which, based at Monash Medical Centre, is funded by the federal government), which, she says, showed low effectiveness of flu vaccines among children and the elderly. The safety concern relates to the swine flu vaccine’s mercury content and anecdotal reports of pregnant women suffering miscarriages after taking it.
“Our concern is that the vaccines are not studied fully before being released into the population and then the claims of adverse reactions are not taken seriously,” Dorey says. “There has been a panic over swine flu here, and there doesn’t seem to be a lot of logic in what the federal government is doing. We take heart from the low take-up of the vaccine, because perhaps it shows people’s real doubts. If the take-up remains low, Nicola Roxon is going to have to explain why the government has spent so much money on a knee-jerk reaction.”
The view of virologists such as Gregory Tannock is that the current swine flu will prove to be only a small part of an ongoing portrait of the virus, which will take decades to put together. “The situation is always moving quickly around us, but we are quite blessed in having more handles on the virus now than we used to.”
Professor Mathews is also sanguine: “My guess is that the [current swine flu] won’t be too much of a problem.” However, he believes the production of data from hospitals and death certificates is too slow and imprecise. “I’ve told the government that they should expedite the process of pulling data together, because they can’t respond quickly or appropriately if they don’t have a clearer picture of what’s going on.”
For Barry Gilbert, the issue is one of wise risk-management. “We had a first wave of swine flu last year, and it was quite mild. In public health terms that was a tragedy, because it lulled people into complacency. History has shown that second waves, if the virus has adapted sufficiently, can produce severe illness and death among a great many people. The next wave might or might not cause that level of sickness, but I believe the outcome will be appallingly bad if we have the expected rate of mortality while millions of doses of the vaccine lie idle.”
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