Dr Thomas Stuttaford
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Next year is the 90th anniversary of the end of the First World War, and doctors are still investigating the outbreak of influenza that followed it. The 1918 world pandemic had started two years earlier, when avian flu mutated and crossed the species barrier, making the virus capable of ready transmission from person to person. It initially spread among recuperating soldiers.
Among the casualties was a 22-year-old female ambulance driver. In the train on her way back to England for her demobilisation leave, which she had planned to spend with her parents in Twickenham, she suffered a sudden onset of shivering, cough and headache.
As a trained nurse she knew that flu, unlike a cold, starts suddenly. Not wanting to infect her family, she rented a room near Waterloo station, isolated herself and died alone. Only after her death did her family learn of her illness and lonely sacrifice; in tribute they paid for her to be buried in a lead-lined coffin.
John Oxford is a professor of virology at the Royal London and Bart’s hospital, and a leading flu expert. He and his team dug up the ambulance driver’s grave, and found that the dead woman’s family – who had readily given their permission for the disinterral, as they knew that she would have wanted to help others – had been cheated. The woman had been buried in a plain wooden coffin, which had disintegrated. Her skeleton may still provide useful information, but it would have provided much more if her undertaker had not been a crook.
Professor Oxford and his colleagues hope to learn from their research on the 1918 flu outbreak how the current avian flu H5N1 may behave when it has mutated, as it surely will. Once the virus crosses the species barrier it will spread readily from person to person, rather than with difficulty from bird to person.
The H5N1 virus has already mutated, though there has been scant publicity, and it has spread from person to person in a couple of families in the Far East. If the strain behaves like the 1918 virus, Professor Oxford suspects that the news will be broken by an observant journalist, who will have noticed that the local strain of H5N1 has begun spreading rapidly. However, it will be less virulent, and the mortality figures will be less startling than they were when H5N1 was caught only from birds. The usual pattern is that, after mutation, mortality drops but the rate of infection rises.
Professor Oxford thinks that the British strategy for coping with a pandemic is well planned, but he has some reservations. In contrast to other developed countries, British stockpiles of the antiviral Tamiflu are miserably low – less than half those of France and comparable to those of Slovenia and Algeria. To deal with the first wave of the pandemic, we need at least as much as France has. The Department of Health ordered 14.6 milion courses of Tamiflu in September 2006, enough for 25 per cent of the population. It would take six to nine months to raise production enough to provide adequate supplies to protect the medical and other vital services, those at increased risk, and a sufficient number of others to limit the spread of the virus.
We also need stockpiles of the antiviral Relenza, in case resistance to Tamiflu develops. But one disadvantage with Relenza is that, unlike Tamiflu, it does not penetrate the brain: in 1918 the virus left progressive, residual brain damage in some cases. It is worrying that the recent NHS spending review contains no reference to a possible avian flu pandemic or any indication of where funds could be found.
Professor Oxford feels that publicity for the standard flu injections this year lacks its usual force. This seems unwise, as there was a “pretty sharp” outbreak of Wisconsin-strain flu in Australia some months ago that caused a higher-than-average number of deaths, especially among children. There was also a worryingly high mortality rate in the US when the flu first appeared. It is likely to reach Britain, and a shortage of intensive-care beds could cause mayhem.
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