On January 28, an eight-year-old girl from Hong Kong visiting relatives in south China fell ill with influenza and was admitted to hospital. A week later she died. Since then her father has died of the same flu, while her nine-year-old brother lies gravely ill in an isolation ward in Hong Kong. The virus is outwardly similar to the A(H5N1) strain, also known as “bird flu”, that killed six people in the last outbreak in Hong Kong in 1997.
New strains of viruses that can kill humans generally emerge by mutation as they hop back and forth between people and domesticated animals. This exchange goes on all the time in farming areas, but it’s only when a virus crosses the species barrier and starts to pass from one person to another that the alarm bells start to ring. They are ringing now.
The “Spanish flu” pandemic of 1918 killed 20 million people in four months, twice as many as did World War I — and the majority of victims were young, healthy people who died of complications like bronchitis and pneumonia. If a flu virus like that appeared now, could it do as much damage'
Certainly, the two subsequent flu pandemics, occurring after the development of anti-viral medicines, did not cause the same carnage. The impact of the 1957 “Asian flu” pandemic was greatly reduced by mass vaccination: only one human being in six caught it, and it killed an estimated two million people worldwide. The 1968 “Hong Kong flu” pandemic killed only a million people, and as in 1957, most of the victims were elderly. But viruses are not impressed by medical technology.
Despite the higher standards of sanitation and medical care in the developed world, influenza death rates there have not been much lower than in poorer countries. Viruses mutate fast, antibiotics are no use against them, and good hygiene is no protection either. Bacterial diseases like cholera, anthrax and malaria have complex life cycles and mutate slowly, so they are easy to contain — but if the latest version of “bird flu” is transmitted between people, we could be looking at millions of deaths over the next year. Nor is that the worst that could happen.
The true nature of the “Black Death” was long a mystery, but early in the 20th century, after doctors had found and described bubonic plague in India, experts concluded that a more virulent form of that disease, endemic in rats and transmitted to humans by their fleas, was the real culprit. This was a comforting conclusion because it meant that it was a bacterial disease, easily contained by hygiene and antibiotics.
But the standard treatment for the Black Death was to quarantine affected families and villages for 40 days. That could not have worked if it were carried by rats. So two years ago Christopher Duncan and Susan Scott of Liverpool University suggested in Biology of Plagues that the Black De-ath was really an Ebola-like virus, a haemorrhagic fever transmitted directly from person to person. It is frighteningly plausible.
Another Black Death
The plague called the Black Death appeared in Mongolia in the 1320s, and killed two-thirds of China’s population between 1330-50. It reached Europe in 1347, and killed between 30 and 40 per cent of the population in the first onslaught. It returned at intervals of about a decade, with gradually diminishing lethality, until it disappeared at the end of the 17th century. The aching, the bleeding from internal organs, the red blotches on the skin caused by the effusion of blood under the skin, were all typical of Ebola-style fevers. Besides, bubonic plague, unlike the Black Death, did not disappear. There was an outbreak of bubonic plague in Glasgow as recently as the 1890s.
If Duncan and Scott are right, therefore, there is a virus out there somewhere, dormant for the moment while it tries out mutations that might break through the genetic defences that human beings evolved to defeat it last time, which could kill a significant portion of the human race in a year. The Black Death is not dead, it’s only sleeping. And in the meantime, the “bird flu” may be coming.