On June 24, 1918, the young poet Wilfred Owen crawled into an Army-issue bell tent at a camp in Scarborough and began composing a letter to his mother, Susan. Then a 20-year-old officer in the Second Manchesters, Owen had just been deemed fit for duty after a lengthy convalescence in Scotland following an attack of a nervous condition brought on by the stresses and strain of the war. But, as Owen waited in North Yorkshire for the orders that would return him to the Front, his thoughts were on another disease entirely.
“STAND BACK FROM THE PAGE! and disinfect yourself,” he begins his letter. “Quite 1/3 of the Batt and about 30 officers are smitten with the Spanish Flu. The hospital overflowed on Friday, then the Gymnasium was filled, and now all the place seems carpeted with huddled, blanketed forms. The boys are dropping on parade like flies.”
At first, Owen’s remarks read like genuine alarm. But, as the next passage makes clear, Owen is being ironic and, far from taking the disinfectant measures seriously, considers the flu something of a joke. “The thing is much too common for me to take part in. I have quite decided not to! Imagine the work that falls on unaffected officers.”
No doubt Owen’s remarks will resonate with many Britons waking up today to the latest casualty count from Mexican swine flu, or H1N1 as the World Health Organisation now insists on calling the virus out of concern for the plumeting price of pork bellies. In a world seemingly gone mad over the “Montezuma’s revenge” virus, humour will strike many as the only rationale response. “Doctor, doctor, I think I have swine flu,” runs one joke doing the rounds. “Try oinkment.”
However, with calls to the NHS flu hotline doubling each day, and increasingly dire predictions from the WHO about the imminence of a pandemic that could dwarf the Spanish influenza of 1918, such jokes may not inoculate us for long. Owen never lived to rue his words, dying at the Sambre-Oise canal in France in one of the last skirmishes of the First World War. However, within weeks of the Armistice on November 11, men who had survived the killing fields of Flanders would find themselves turning a ghastly purple colour as the Spanish flu, which was also an H1N1, burrowed deep into their respiratory tract, causing their lungs to fill with choking fluids.
Between September and December of 1918, about 12,000 Londoners died in the second wave alone, and, by the time the third wave of infections had subsided in May 1919, about 225,000 Britons were dead. With half the nation’s doctors and nurses serving at the Front, and in a world without antivirals or antibiotics, there was little anyone could do. “So many were ill that only the worst could be visited,” recalled a GP’s son from Lancashire. “People collapsed in their homes, in the streets and at work. All treatment was futile.”
Worldwide, the mortality from the Spanish flu – so-called because Spain, not being a party to the war, was one of the few countries openly to report the spreading depredation – was simply inconceivable, with as many as 50 million dead according to conservative estimates.
But that was then. The world is no longer at war and Britain is not Mexico, point out the sceptics. On Radio 4’s Today programme on Friday, the Guardian columnist Simon Jenkins laid into Professor John Oxford, a virologist at Barts hospital and one of the world’s foremost experts on influenza, for referring earlier in the week to H1N1 as an “Armageddon sort of virus”. Scientists were “mad” to use such emotive language, Jenkins ranted, and journalists who failed to exercise judgment by quoting official government projections of as many as 94,000 London dead, were madder still.
The novelist and Evening Standard columnist Will Self has been similarly scathing, describing the predictions of imminent Apocalypse – or “Aporkalypse”, as some wags put it – as so much media “squealing”. Meanwhile, Michael O’Leary, the embattled boss of Ryanair, in a desperate effort to stave off a further catastrophic fall in passenger numbers in a business only just beginning to recover from the credit crunch, claims that only people “living in slums” in Mexico and Asia are at risk.
Behind the backlash is the sense that we have been here before – in 2005 to be precise, when Prof Oxford and experts such as David Nabarro, the head of influenza planning at the United Nations, made similarly apocalyptic predictions about the bird-flu virus, H5N1. The subtext is that they cried wolf once, so why believe them now?
Pandemics are the viral equivalent of perfect storms. In order to trigger an event on the scale of 1918, three things have to happen. First, a new influenza virus – one against which people have no or few antibodies – has to emerge from a “hidden” animal reservoir. Second, the virus has to make people sick. Both these conditions have already been met by the new H1N1 sub-type from Mexico. The third thing that needs to happen is that the virus must be able to spread efficiently between people, preferably via a cough, sneeze or handshake.
With the announcement yesterday that a 24-year-old Falkirk man, who plays on the same football team as Iain Askham, one half of the Cancún honeymoon couple who introduced the flu to Britain, has been diagnosed with the virus after a night out with Askham in the pub, the third condition has now been fulfilled.
But this is not the only reason why England’s chief medical officer Sir Liam Donaldson is now saying we will see “many” more cases or why Robert Madelin, director general for EU consumer health policy, is predicting that deaths are inevitable, the only question being whether the toll will be in the “thousands, tens of thousands, or hundreds of thousands”. At the root of their concern is a scientific understanding of the way that influenza viruses evolve and recombine with the genes of other viruses, including avian-flu genes – knowledge that, for the most part, is denied their critics. Another factor is that they know that it is better to be proven wrong than to be accused of failing to keep the public properly informed, as occurred during the BSE crisis.
Indeed, one reason why even normally cautious commentators, such as Dr Alan Hay, director of the World Influenza Centre in Mill Hill, north London, are using words such as “ominous” is that the majority of the deaths recorded so far in Mexico have been in adults between the ages of 20 and 40, a mortality pattern that mirrors that of the 1918 Spanish influenza. Similar concerns motivate Prof Oxford, who has spent most of his career studying the Spanish influenza, and it is also why, on Wednesday, Angus Nichol, head of the Influenza Programme at the European Centre for Disease Control in Stockholm, informed The Independent: “Influenza viruses are very slippery creatures. The relatively few deaths we have seen so far could be the tip of the iceberg.”
In 2005, I came face-to-face with what was then also being billed as an “Armageddon” strain when I travelled to Vietnam. On an isolation ward at Hanoi’s Bach Mai hospital, I watched as doctors struggled to ventilate a young man who had caught the H5N1 virus after slaughtering an infected duck for a family meal. Pencil-thin and breathing heavily, Sy Tuan drifted in and out of delirium, gasping for air. He had waited too long to seek treatment, and the virus had burrowed deep into his lungs, sparking an auto-immune reaction. Dr Nguyen Tuong Van, the director of Bach Mai’s intensive care unit showed me Sy Tuan’s chest X-rays. There were white shadows everywhere. It was like looking at a patient with advanced tuberculosis.
Sy Tuan survived and, though there have been subsequent human H5N1 infections, H5N1 never became a “super spreader”. Indeed, since the current outbreak began in 2003, there have been only 421 cases and 257 deaths, the majority in south-east Asia. By contrast, the Mexican H1N1 subtype has already infected about 3,000 people and been reported on every continent on the globe.
It is too early to say how or where the critical mutations occurred. Some newspaper reports have pointed the finger at a pig-farming facility near La Gloria, in Veracruz, operated by the US company Smithfield, the world’s biggest pork processor. It was at La Gloria, about 12 miles from the farm, that, on April 2, a five-year-old boy, Edgar Hernandez, became ill with what the Centers for Disease Control in Atlanta has since confirmed as the first human infection with the swine flu.
However, other reports suggest that the index case may have been a census-taker from Oaxaca, who lived nowhere near the pig farm.
But what cannot be denied is that Mexican H1N1 is primarily a pig flu and a dangerous one at that: what is known in the trade as a “quadruple reassortment”, consisting of two swine flu strains, one human strain, and an unidentified avian strain. Moreover, according to preliminary analysis from human cases in California and Texas, six of the eight viral segments are closely related to a North American swine flu strain that emerged in 1998, killing hundreds of sows at a pig breeding facility in North Carolina.
Some of the most worrying parallels, however, are historical. Although the 1918 pandemic was blamed on the Iberians, “Spanish” influenza is a misnomer. Then, as now, the earliest reported case came from the Americas, from Haskell County, Kansas, where doughboys at a US army base were being fattened on chickens and pork grown on local farms before being marched on to transports to join Wilfred Owen in northern France. And then, as now, the first cases occurred in the spring, a highly unusual time of year for an outbreak in the northern hemisphere.
The last observation is particularly worrying and explains why scientists have been advising governments to activate their pandemic plans now, rather than waiting for the WHO to declare a level-six alert – the formal signal that a pandemic has started.
It is argued that, if the current outbreak is mirroring the 1918 pandemic, then we should expect the first wave to be mild. It is when Mexican H1N1 returns in the autumn that we could see a sudden ratcheting up of its virulence and a spike in mortality, as occurred in 1918.
Such questions may soon be answered by genomic analysis already underway at the CDC in Atlanta. Once epidemiologists have a better handle on the true level of infections in Mexico and whether the deaths reported so far are due to H1N1 and not some other strain of flu, or even bacterial pneumonias, we will also be in a better position to gauge the attack rate and in which direction the virus is evolving. There is even a possibility that Mexican H1N1 could recombine with H5N1 when it reaches south-east Asia, thus becoming both highly transmissible and highly pathogenic, a combination that surely would be a formula for “Armageddon”.
In 1918, Britain’s medical authorities buried their heads in the sand, reasoning that there was little doctors could do to prevent influenza or to treat it and that, besides, the needs of war dictated the nation “carry on”.
Today, we do not enjoy the bliss of ignorance, as Wilfred Owen did, and no amount of shouting at scientists will make it so.
- Mark Honigsbaum is a researcher at the Wellcome Trust Centre for the History of Medicine at UCL, and the author of Living With Enza: The Forgotten Story of Britain and the Great Flu Pandemic of 1918
