Of course, the media thrives on the unrealized threat of mortal disease that could wipe out entire, well, readerships. Bird flu is just the latest of these – after SARS, MRSA and HIV/AIDS. But in the case of H5N1 flu, august public health officials have added fuel to the flames, pronouncing that a killer pandemic is ‘inevitable’. Epidemiologists merely use the word ‘inevitable’ to mean that ‘there were several serious flu epidemic/pandemics in the twentieth century, the virus is able to evolve into new forms against which we have no effective vaccine or natural immunity, and so there is no reason to think that the twenty-first century will be different’. Or, as the Independent shrieked, ‘We face a century of viral pandemics’. Now it is possible – just about – to make out that the twentieth century was a ‘century of viral pandemics’, although few would define it in those terms despite the devastating advent of HIV. There is no reason to think that earlier centuries fared better, and so none to think that the twenty-first century should not have its share of viral outbreaks too. The question is whether outbreaks will be more frequent or more severe to earn the century this label.2
This kind of language is symptomatic of an old tendency to blame ourselves for visitations of pestilence. But here it has a modern dressing of anti-capitalism. For Mike Davis, SARS and HIV were the ‘deadly by-product of a largely illegal international wildlife trade, intimately connected with logging and deforestation, which mortally threatens human health as well as regional biodiversity’, while avian flu has prospered ‘in ecological niches recently created by global agrocapitalism’.3 The Independent’s columnist Johann Hari echoes him, saying we will be ‘plagued by pandemics because of the new virus-friendly ecology we have created across the world’. So it’s all our own fault, then. It’s our affluent lifestyles, our travelling, our migration to the cities that’s doing it.
But it is clear that modern life is not mainly to blame. It is quasi-rural backyards with small flocks of chickens where people catch bird flu, not intensive poultry sheds. On the whole we enjoy better food and personal hygiene and experience less risk of picking up an infection from a non-human source than in the past. Even where the risk is still high, the solution through measures such as clean water supply is within our grasp if we are prepared to pay for it.
It is true that an outbreak today is more likely to be global. But sheer geographic spread does not mean that the virus responsible is uncontainable. The pneumonia-like Severe Acute Respiratory Syndrome (SARS) emerged in November 2002. Over eight months, it spread to twenty-six countries. In all, more than 8,000 people were infected, of whom 774 died. In the most dramatic illustration of the way disease can spread in the global village, a doctor who had attended some of the first victims in China travelled to Hong Kong for a wedding. There he passed the infection to sixteen other guests. Within a day, those people and others whom they infected in turn distributed the virus to half a dozen countries as far afield as Ireland and Canada, ultimately accounting for 355 cases.
The SARS episode now provides an exemplary case study of how a powerful virus spreads – and may be contained. For although SARS did rapidly kill three times as many people as avian flu has done, it was contained relatively efficiently by isolation and quarantine of those infected.
Preparedness in this case did not mean laying in vast stockpiles of a vaccine since SARS was a completely new virus. Nor would some of the usual government reflex gestures such as closing borders have made any difference in time. The key was openness and rapid reporting, rather than the sort of administrative denial that can give a virus time to spread unchecked. Another lesson applicable to pandemics of all kinds is the importance of accurate diagnosis and decisively taken preventive measures. In general, even very contagious diseases may be controlled by means of appropriate education as much as by high-tech medicine.
If a flu pandemic is indeed ‘inevitable’, it is equally inevitable that it will start in Asia. It is the high ‘viral load’ here that tempts epidemiologists to use the word in the first place. All of the modern global flu outbreaks began in China, where many people live crammed into unsanitary conditions, frequently cohabiting with their ducks, chickens and other livestock. The future issue for the rest of the world may be containment; the issue in rural Asia now is domestic hygiene.
Despite this reality, western governments and media continue to play to the gallery. ‘If bird flu grips the nation, doctors will need guns,’ screamed the Sunday Times. The viral load is nowhere lower than in the United States, yet this is where some of the most hysterical coverage is seen. The New York Times alarmed its readers with news that the vaccine being stockpiled by the US ‘protects only about half the people who receive it’, making it sound for a moment as if survival would be a lottery even for the inoculated. Only later in the story came the admission: ‘The disease has not reached the Americas.’
In Britain, the Sunday Herald leaked a government study predicting the breakdown of society: ‘A minimum of 25 percent of the population will become ill over each six- to eight-week period… Mortality is likely to be high – estimated at 1 percent of the total population.’4 Not that there was much to be done about it. At home, nothing yet needed doing. For anywhere else, the precautions were elementary. The UK National Health Service advised people travelling to affected regions to avoid close contact with poultry and to wash their hands. Washing your hands is never a bad thing, of course, but the clueless advice hardly seems commensurate with the claimed scale of the looming disaster and media talk of stockpiling body-bags. It recalls that of the hygiene-obsessed economist Edwin Chadwick, who went to his grave restating his belief in ‘soap and water as a preventative of epidemics’ long after the celebrated John Snow had narrowed down the source of the 1848 London cholera outbreak to a particular street pump.5
So far, so terrifying. Perhaps it is more instructive to look at what you have to do to catch this disease rather than what to do to prevent it. What does it take to catch flu from a bird? Scientists discovered in 1974 that the avian flu virus thrives in the guts of wild birds, notably waterfowl. Unlike familiar forms of human-transmissible flu, which is a respiratory infection passed through the air, avian flu is passed on when healthy birds ingest water containing the excreta of infected birds. For a person to become infected, he or she must have intimate exposure to the excreta or intestines of an infected bird. Taking up voodoo and smearing yourself with the raw entrails of an infected chicken in a sacrificial ritual would thus be a good way to contract bird flu. Another successful method is to eat (carelessly prepared) raw ducks’ blood sausage, which is a Vietnamese delicacy and the cause of some cases in that country. Sharing your accommodation with poultry is hazardous because the birds’ excreta or remains are likely to contaminate human food. This explains the majority of human cases of bird flu – no cases have been recorded of people catching the disease from live wild birds or from cooked poultry.
In the UK, it is statistically true to say that you are more likely to die of rabies than bird flu simply because one man – a professional bat handler – died of bat rabies in 2002. This comparison may seem facetious, but both avian flu and rabies are – along with HIV, ebola and measles – zoönotic diseases, that is to say they are carried by animals but can pass to humans if the virus mutates in the right way. The comparison illustrates the fact that for both these normally animal-borne viruses a human being has to take extraordinary steps to put themselves at such a disadvantage that infection is possible.
Even then, the avian flu virus must be present in a form that is able to attack human cells. There are 144 possible combinations of the sixteen H (haemagglutinin) and nine N (neuraminidase) chemical groups that dot the surface of a flu virus. H5N1 is one particular combination. The previous flu epidemics of the twentieth century were H1N1, H2N2 and H3N2. Other combinations arise from time to time – for example, in the Netherlands in 2003 an outbreak of H7N7 led to a cull of eleven million chickens. One person died out of eighty-three infected by this less dead
ly strain. But scientists do not know what mutations are needed to produce a dangerous type of the virus. They cannot predict when mutations will appear or what they will be. This makes it impossible to prepare specific vaccines or anti-viral treatments before the new type is present in humans.
It is this mutability that makes flu dangerous. The smallpox virus, for example, has a fixed composition, which has made it relatively easy to eradicate. The H and N groups of the flu virus, on the other hand, may ‘drift’ into a different form if the amino acids within them are altered. Darwinian natural selection then ensures that the virus reappears each year in a slightly different version, although this change happens sufficiently slowly that the human immune system is generally able to cope with the new invader. But the virus can also ‘shift’ rapidly into a new type when a new H or N is introduced, for example from birds. When this happens, there is no ready immunity in the general population.
‘Mutation’ is also a word made for scare stories. It seems to leap straight from the pages of John Wyndham, where some malevolent biological slime manouevres for world domination using processes clearly outside human understanding or control. Mutation is an evolutionary process, but it is not directed. The flu virus is not out to get us, it is simply out to survive, which it already does in the bird population. A sequence of mutations is required for H5N1 to be able to thrive not in a bird’s gut but in the quite different conditions of the human respiratory tract. These mutations may or may not occur. And if a human-adapted virus does result, it may or may not turn out to be highly pathogenic.
Paradoxically, a virus that is both highly infective (i.e. it spreads efficiently) and highly pathogenic (i.e. it kills a high proportion of those whom it infects) may not be very dangerous on a global level because it quickly kills too many of its host species to be able to continue spreading. The pandemic threat comes from a virus that is only moderately pathogenic but highly infective. The 1918 flu was such a virus, infecting more than half the world’s population but killing only one in twenty of those it infected. The H5N1 virus circulating today is highly pathogenic (it has killed more than half the humans it has infected) but much harder to catch. If it mutates into a highly infective form, that in turn is likely to make it ultimately less lethal worldwide.
Recorded outbreaks have claimed single victims or small groups of people, almost all of whom can be directly linked to birds. All this means that it is extraordinarily unlikely that, for example, Princess Diana’s driver was suffering from bird flu on the night of her fatal car crash, a theory reportedly entertained by the Daily Express. Bird flu remains essentially a disease of birds even though it may have taken the New York Times eight paragraphs in its story about the virus ‘spreading rapidly through Asia, Europe and Africa’ to remind its readers of this basic fact.
There are other reasons to worry less about bird flu. The media has repeatedly said that a pandemic is ‘overdue’ or even ‘long overdue’. This claim is not based on any virological dictum, but simply on the historical pattern of outbreaks – one every ten to fifteen years or so from 1918 to 1977 and then a pregnant pause until now. But in fact the longer H5N1 ‘tries’, the less likely it is to succeed in adapting into a human-transmissible type. Some scientists now believe H5N1 has had its chance. A virus is not like a volcano, where pressure may build up gradually, leading to an eventual eruption. And a continued non-outbreak doesn’t make a future outbreak more likely or more deadly.
It seems these truths are at last being acknowledged. In February 2007, H5N1 avian flu rampaged through a Bernard Matthews turkey shed in Suffolk, requiring the swift destruction of 160,000 birds. Media talk of an inevitable human pandemic promptly vanished, replaced by a new Dunkirk spirit. When push came to shove, the outbreak was simply something that had to be – and could be – dealt with.
While bird flu has yet to claim a single human victim in Europe or the Americas, and has killed fewer than 300 people worldwide, it is perhaps worth adding that the familiar winter flu that nobody panics about claims at least 30,000 American and 12,000 British lives each year.
It’s Amazing What They Can Do
‘Superbug “apocalypse” warning’ Guardian
Where would you go to catch a dangerous infection? A crowded commuter train, an aeroplane, an infants’ school, a brothel? How about a hospital?
‘Hospital bug that kills in 24 hours’, warned the Daily Mail in December 2006 as an apparently new strain of the by now familiar ‘superbug’ MRSA claimed its latest victims, a nurse and a patient in Staffordshire. ‘Hospital crisis as PVL bug kills tot’, added the Sun five days later as a premature baby boy died in Norwich.
PVL (Panton-Valentine leukocidin) is a toxin sometimes produced in association with MRSA. It destroys the white blood cells which the body needs to fight infection and can quickly kill by causing pneumonia and other conditions.
MRSA (methicillin-resistant Staphylococcus aureus) was identified in the 1960s as a variant of the Staphylococcus aureus bacterium that had developed resistance to methicillin, an antibiotic introduced after the bacterium had already begun to show resistance to penicillin. Occasional MRSA infections were observed from this time, but newspapers began to use the word ‘superbug’ to describe MRSA in the 1980s, when outbreaks began to increase, especially in American and British hospitals. In 1995, in New York City alone, 7,800 people became infected with drug-resistant Staphylococcus; 1,400 of them died.1 In Britain, MRSA became a major issue in the 2005 general election campaign. Staphylococcus aureus mainly infects open wounds, causing boils and abscesses, and is therefore especially dangerous to surgical patients. It is this that makes it a hospital disease.
So are hospitals now places to be feared rather than places of healing? The British media have widely quoted a figure of 5,000 deaths each year due to MRSA estimated by the National Audit Office. But another government organization, the Health Protection Agency (HPA), calls this figure ‘incorrect’, pointing out that it describes deaths from all hospital-acquired infections. Many people thought that MRSA was the major, if not only, such infection, hence the confusion. It is cold comfort that the death toll stands and that there are simply other infections to worry about.
Nevertheless, it was MRSA that first captured the attention of the media. The number of death certificates specifying MRSA as a contributory factor at first rose by about a hundred a year. The records start from a low base of fifty-one deaths in 1993, allowing the BBC to note ‘Superbug deaths increase 15-fold’ when the figure reached 800 in 2002.2 The figure for 2004 was 1,168. For 2005, it was 1,629.3
However, deaths are not a very reliable indicator of the prevalence of MRSA. The numbers may be an underestimate if death is still ascribed to a familiar killer such as pneumonia rather than MRSA where both are present. On the other hand, better diagnosis undoubtedly accounts for some of the rise in recorded MRSA, while the fact that MRSA is much more likely to be mentioned on death certificates of people who died in hospital than on those of people who died elsewhere could arise from an excessive readiness to name MRSA because it is already associated with hospitals.
Meanwhile, the newspapers have grown shriller as nature has come up with new tricks. Unlike ordinary MRSA, which affects the most vulnerable, PVL has the impressive property that it afflicts the ‘young and healthy’ – among them therefore perhaps even more of their readers. ‘Remember these initials,’ intoned the Independent, putting them in letters 86 millimetres high on its front page just to make sure that we did. The first PVL fatality during this period was an eighteen-year-old who died after infection of a leg injury sustained while he was on a commando training exercise.
Microbiologists had long warned that consequences were to be expected from doctors’ enthusiasm for prescribing antibiotics, as the bacteria they were designed to combat gradually developed resistance. At first, the fear was of one ‘doomsday superbug’, probably MRSA.4 But more recently, it has seemed that we will come under attack by a whole range of bugs. Entero
cocci, Clostridium difficile and tuberculosis are among the new or resurgent bacteria that have acquired resistance to antibiotics. National statistics reported in the Independent under the headline ‘Deaths from “dirty hospital bug” double in five years’ show that Clostridium difficile has emulated the rise of MRSA and now overtaken it. The bacterium was linked to 2,247 deaths in 2004 and 3,807 in 2005 – twice as many as MRSA.
In January 2007, the Guardian issued a ‘Superbug “apocalypse” warning’. The article that followed quoted Professor Richard James, the director of a new Centre for Healthcare Associated Infections at Nottingham University: ‘We are facing a future where there will be no antibiotics and hospital will be the last place to be if you want to avoid picking up a dangerous bacterial infection – in effect, cut your finger on Monday and you’ll be dead by Friday if there’s nothing to prevent it.’
This pessimistic vision carries with it a sense of the medical profession’s profound dismay that the antibiotic revolution trumpeted as a miracle scarcely half a century ago now seems to lie in ruins. Yet some of the reasons for this are to be found with the medics themselves. Like the rest of us, many doctors believed that antibiotics were indeed a miracle cure. The use of antibiotics in major surgery as well as in the treatment of infections of many kinds has unquestionably contributed to the public’s grateful awe of doctors found in the popular expression ‘It’s amazing what they can do.’
Although it had been anticipated – and later was shown to be true – that bacteria would respond to hostile antibiotics by adaptation to produce more vigorous strains, it was easy to hope that antibiotics would remain good for all time like ordinary chemical medicines. Frequent indiscriminate and precautionary prescribing of antibiotics merely hastened this process of evolution. In hospitals, meanwhile, according to Laurie Garrett’s book, Betrayal of Trust, ‘ “Typhoid Mary” doctors’ have also been directly responsible for spreading infection from patient to patient because they are too hurried or too arrogant to wash or submit to testing.5
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