Susan Scott, Christopher J. Duncan

If the twenty-first century seems an unlikely stage for the return of a 14th-century killer, the authors of Return of the Black Death argue that the plague, which vanquished half of Europe, has only lain dormant, waiting to emerge again—perhaps, in another form. At the heart of their chilling scenario is their contention that the plague was spread by direct human contact (not from rat fleas) and was, in fact, a virus perhaps similar to AIDS and Ebola. Noting the periodic occurrence of plagues throughout history, the authors predict its inevitable re-emergence sometime in the future, transformed by mass mobility and bioterrorism into an even more devastating killer.

5 thoughts on “Susan Scott, Christopher J. Duncan

  1. shinichi Post author

    人獣共通感染症 連続講座 第159回(09/2/2004)

    第159回 中世の黒死病はペストではなくウイルス出血熱

     英国リバプール大学動物学名誉教授のクリストファー・ダンカン(Christopher Duncan)と社会歴史学の専門家スーザン・スコット(Susan Scott)は教会の古い記録、遺言、日記などを詳細に調べて「黒死病の再来」(Return of the Black Death , Wiley, 2004)を出版しました。彼らの結論では、黒死病はペスト菌ではなく出血熱ウイルスによるものであり、今でもアフリカの野生動物の間に眠っていて、もしもこれが現代社会に再び出現した場合には破局的な事態になりかねないと警告しています。その内容をかいつまんでご紹介します。

     1665年から66年にかけては、ロンドンで黒死病の大流行が起こり、ピーク時には1日に6000人が死亡するという事態になりました。その際の社会の衝撃は1772に出版されたダニエル・デフォー(ロビンソン・クルーソーの著者)の「A Journal of the plague year」生々しく語られています。なお、これのハイライト部分は「ロンドン・ペストの恐怖」という表題で和訳されています(小学館1994)。

  2. shinichi Post author


    The Surprising Link between AIDS and the Black Death

    When the Black Death struck first in 1347 and swept through Europe, it seems that almost everyone who made effective contact with an infectious person caught the disease and died. The reason for this was because nobody had been exposed to the disease before. Three hundred years later, in the seventeenth century, there is evidence that in towns where the plague had struck previously, some of the inhabitants had a form of in-built resistance. We have seen that the apprentices and servants in London, who had come from the countryside and small provincial towns where there had rarely (if ever) been a major epidemic, were often the first to be struck down. On the other hand, a proportion of the inhabitants, whose families had been in the metropolis for some generations, seemed to have some resistance to the infection.

    Detailed inspection of parish registers shows that many people must have been in close contact with infectives indoors but did not contract the plague, and this indicates that by that time a proportion of the families, particularly those long resident in London, had a resistance to the disease. Samuel Pepys continued about his business in London (although he took some elementary precautions) and was not stricken during the major outbreak of 1665^66. And we have seen that some of the people at Eyam and Penrith were in close contact with victims but never succumbed.

    What was going on here? We can obtain some clues concerning the molecular genetics of plague resistance 600 years ago from a surprisingly different and remarkable source today.

    HIV and AIDS

    Everybody has heard of the HIV pandemic, but it is not so well known that a considerable proportion of people of European origin do not catch the disease, even after continued exposure. They are resistant to HIV infection.

    When the primary human immunodeficiency virus (HIV) enters the human body, it homes in on certain white cells in the bloodstream and then gains entry via a special molecular complex in their surface membrane, which is termed in technical jargon the CCR5 receptor. This acts as an entry port (or chemical doorway) for the virus into the blood cell. Once inside, it can remain dormant for many years before its victim finally shows the symptoms of AIDS. However, once inside the virus quickly begins its dirty work and, unknown to anybody, the victim soon becomes fully infectious. Therein lies the major problem in controlling the spread of HIV. We see that the disease has an exceptionally long incubation period, which is measured in years. The CCR5 receptor also acts as the means of entry for the pox virus that causes myxomatosis in rabbits, and it is probable that several other infectious agents that use it as a doorway will soon be discovered.

    The delta-32 mutation

    Europeans who have a resistance to HIV infection have inherited a genetic mutation in the CCR5 receptors on their white blood cells that prevents them acting as an entry port. This is called the CCR5-D32 mutation, and individuals who have inherited a pair of mutated genes from both parents have nearly complete resistance to HIV infection, whereas those who have only one copy of the mutation delay the onset of AIDS.

    Although this mutation occurs at a high frequency in Eurasian ethnic populations today, it is absent among native sub-Saharan African, American Indian and East Asian ethnic groups. This might explain the rapid spread of HIV in sub-Saharan Africa, whereas possession of the mutation may have delayed its progress in Europe.

    When did the protective mutation appear?

    When and why did this mutation arise in the first place? After all, HIV=AIDS emerged to scourge the human race only a few decades ago (no time at all in evolutionary terms) and presumably, before that time, the mutation would have been of no selective advantage in the rat race of human evolution.

    We can put this another way. Any new mutation has a very high likelihood of being lost within a few dozen generations unless it confers a clear selective advantage on those individuals who have it. Possession of the CCR5-D32 mutation is of obvious benefit today: it confers protection against the killer disease HIV. But what could possibly have been gained by having the mutation before HIV=AIDS emerged and spread across the world in the twentieth century? It is highly unlikely that a mutation in the CCR5 receptor that conferred no selective advantage on individuals in whom it occurred could spread randomly through the people of Europe. In simple terms, if a new mutation does not provide an advantage in the struggle for survival, it will eventually disappear from the population.

    Molecular biologists, using their extremely sophisticated techniques, have estimated that the CCR5-D32 mutation may have first appeared in Europe some 2000 years ago. There is general agreement that its frequency must have been driven up to present-day values in Europe of 5-20 per cent by a historic event that occurred approximately 700 years ago, probably an epidemic of an infectious disease that, like HIV-1 today, used the same entry port on white blood cells.

    The Black Death is obviously an excellent candidate for such a catastrophe. The timing is right and it has been widely suggested and agreed that those very few fortunate individuals in Europe during the Black Death who possessed the CCR5-D32 mutation escaped with their lives and bore children who then also carried the mutant gene. The incidence of the CCR5-D32 mutation in Europeans at that time has been estimated at 1 in 40 000. All those who did not possess the CCR5-D32 (the great majority) and who made effective contact with an infected person inevitably died. In this way, the proportion of the population who carried the mutation would have been raised dramatically. Some individuals who carried the mutation may have caught haemorrhagic plague but recovered; they lived to fight another day and continued to have children, most of whom carried the D32 mutation.

    What is wrong with this suggested origin of the D32 mutation?

    Scientists who discovered that the CCR5-D32 mutation appeared around the time of the Black Death firmly believe that this was an epidemic of bubonic plague. Consequently, to make their story fit the facts, they have had to assume that the bacterium Yersinia pestis enters the white cells of the blood via the CCR5 receptor. We have already seen conclusive evidence that there never was an epidemic of bubonic plague in Europe, but there is further compelling confirmation that their theory is all wrong:

    * Bacteria like Yersinia do not penetrate via the CCR5 receptor, an entry port used by some viruses. This points to a virus, and not a bacterium, being responsible for haemorrhagic plague.
    * Mortality in epidemics of bubonic plague is always low: insufficient to have a major effect in forcing up the frequency of any protective mutation.
    * The CCR5-D32 mutation occurs only in people of European origin – the only area that was ravaged by plagues. In contrast, the mutation is not found in people from eastern Asia, sub-Saharan Africa nor American Indians, areas where bubonic plague has been rampant. Further evidence, if any were needed, that bubonic plague was not responsible for the Black Death.

    At last: the explanation of resistance to the plague

    So there is good reason to suggest that an epidemic of viral haemorrhagic plague during the Black Death suddenly conferred a strong selective advantage on those few lucky individuals who possessed the CCR5-D32 mutation and thereby sharply increased its frequency. Nevertheless, this popular explanation is much too simplistic. A single epidemic like the Black Death could not have had such far-reaching and long-lasting effects, but it did presage the age of plagues. We suggest that each successive wave of outbreaks over the next 300 years steadily increased the numbers of individuals who had inherited the CCR5-D32 mutation; if you were not carrying the mutation there was a good chance of dying when the disease next came round.

    However, this again is an oversimplification of the situation. The major epidemics of haemorrhagic plague were largely confined to communities that were above a certain minimum size, and there were vast rural areas of Europe practising a scattered agricultural economy where the disease rarely, if ever, struck. The continuing strong selective pressures forcing up the frequency of the CCR5-D32 mutation would operate only in the towns, particularly London, because haemorrhagic plague became ever-present there after 1580. Consequently, the overall distribution of the CCR5-D32 mutation in Europe must have been patchy in the seventeenth century: the frequency of resistant individuals in the towns must have been very much higher than the current 20 per cent, and in rural areas very much lower.

    The frequency of the mutant gene in Europe today is the result of a great deal of mixing and migration over the last 350 years since the plague disappeared ^ a general levelling-out process in the course of which the distinctions between rural and urban life have disappeared.

    As we have seen, plague was persistent in London in the seventeenth century, with major outbreaks at irregular intervals, albeit with a relatively low percentage mortality. Having suffered from this continuous onslaught, in addition to a low grumbling endemic level of infection, a sizeable proportion of the population of London probably carried the mutation and was resistant. Mortality levels had fallen below 15 per cent by this time, and those who died from plague in London in the seventeenth century were frequently incomers, apprentices and servants. Each epidemic or famine crisis brought fresh waves of naive immigrants from the countryside who were not resistant and who made up a substantial part of those dying in the plagues.

    The Eyam inheritance

    Remember the story of Margaret Blackwall of Eyam, who survived the plague apparently by drinking warm fat? Molecular biologists visited Eyam in 2001 and took swabs from the mouths of 100 villagers ‘who could trace their ancestry back the furthest’ and found that the CCR5-D32 mutation was present in 14 per cent of them ^ probably a little above the average European rate. Much more importantly, Joan Plant, who is living in Eyam today, is a direct descendant of the plague survivor Francis, the brother of Margaret Blackwall: she carries the CCR5-D32 mutation.

    We interpreted this news as follows: Margaret Blackwall carried the CCR5-D32 mutation; she contracted the disease but did not die of it, as we have seen. Her brother Francis did not get the plague at all and was completely resistant. Copies of the mutation were handed on to his descendant, Joan Plant.

    But the full story of Eyam is not clear. We have been unable to trace any record of the plague striking in Eyam before 1665, so there is no evidence of an event that would force up the frequency of the CCR5-D32 mutation there. We conclude that the families at Eyam (or their parents) who were resistant at the time of the plague had been previously exposed to it elsewhere and had then moved into the village. It had struck violently at Thorpe 18 miles (29 kilometres) to the south in 1538 and at nearby Curbar 30 years before. Derby was repeatedly ravaged by plague, starting with the Black Death, which moved through the county and was recorded in the village of Crich, 17 miles (27 kilometres) to the south of Eyam. Rector Mompesson seems to have been resistant and it is reported that he had seen the plague elsewhere earlier in his life.

    A number of those who survived at Eyam thus carried the CCR5-D32 mutation and so the proportion of the population that was resistant would rise in the next generation. But they would have no selective advantage, because the disease had now gone. People would move into the village to fill the vacant niches and, during the next 300 years, there would have been a tremendous amount of immigration and emigration of both resistant and nonresistant individuals. The result of all this stirring up is the 14 per cent of resistant persons found in Eyam today.

    The people of Eyam were unlucky because the epidemic there was very nearly the last outbreak ever. They had escaped for 300 years by being small and remote, only to be caught by the final strike.

    What happened to the mutation after the plagues?

    Once the pestilence had disappeared completely from Europe by 1670, there would apparently have been no benefit to anyone possessing the mutant gene. The mutation therefore probably changed from being advantageous to being neutral and, over the next 300 years (and some 12 generations), the frequency in European populations would be expected to fall slowly. Present-day frequencies are 5^20 per cent but they were probably higher than this in the seventeenth century, unless the CCR5-D32 mutation conferred some other selective advantage on those lucky individuals who carried it …

    Fascinating and exciting news was announced in September 2003. Several earlier reports had proposed links between protection against smallpox and against HIV ^ older people who had been vaccinated against smallpox were less likely to contract HIV. Now, preliminary experiments with human blood cells at George Mason University, Virginia have shown that vaccination confers, on average, a fourfold reduction in infectivity of HIV. Myxoma poxvirus, a relative of the smallpox virus, also uses the CCR5 receptor to gain entry to its target blood cells.

    When the plague disappeared, smallpox replaced it as the dreaded scourge. Is it possible that possession of the CCR5-D32 mutation in the eighteenth century in Europeans may also have provided at least partial protection from either infection or death from smallpox? If so, then the mutation would have been maintained or even modestly pumped up until 1900 when smallpox was effectively eliminated in Europe. On this argument, non-European races, which were never exposed to plague, might historically be expected to be particularly susceptible to smallpox ^ both North and South American indigenous populations were particularly badly hit when smallpox was introduced by conquering Europeans.

    Thus those ethnic Europeans who today are resistant to HIV owe their good fortune to a chance genetic event in their ancestors, which provided them with protection against the plague.

  3. shinichi Post author


    Assembling the Jigsaw Puzzle

    Today, when a crime is witnessed and a suitable description of the felon is available, the next step is to have an identity parade. But to do that, we must decide who is to be included in our gallery of suspects.

    Of all the infectious agents, bacteria and viruses are the most important kinds for our purposes. These tiny organisms are sometimes called microbes and in the immortal words of Hilaire Belloc:

    The microbe is so very small
    You cannot make him out at all.
    But many sanguine people hope
    To see him through a microscope.


    Bacteria are single-celled organisms that are between one-half and one-ten-thousandth of a millimetre in length: too small to be seen by the naked eye. Looked at under a microscope, they may be shaped like rods, spirals or spheres but, in spite of their small size, their structure is highly complex. They are the most abundant of all organisms and have many essential roles to play in the maintenance of life on earth. However, only a minority of species can infect humans and cause serious diseases.

    Some bacterial diseases are spread by the intervention of insects, ticks or lice and these include bubonic plague (spread by a flea) and epidemic typhus, which was once a major killer in crowded conditions with poor sanitation. It is transmitted from human to human via lice and, unless treated with antibiotics, about 20 per cent of cases are fatal. Historians have (erroneously) sometimes tried to explain outbreaks of plague that could not possibly have been caused by bubonic plague as typhus.


    While viruses vary in size, they are all much smaller than bacteria and can be seen only under an electron microscope. Unlike bacteria, viruses can reproduce and multiply only within other living cells, which may belong to animals, plants or even bacteria. Since viruses cannot reproduce independently, they are not regarded as truly alive.

    All viruses, then, are parasites that can wreak havoc on human populations by causing serious epidemic illnesses. They start by cleverly gaining entry to certain cells in our bodies and, once inside, the virus proceeds to take over the cell’s genetic machinery, which then has to obey its commands. We have seen how HIV can enter certain white blood cells via the CCR5 doorway, whereupon it sets about its dirty work.

    An infecting virus is simply a set of instructions, like a computer program. The working of any cell in our body is normally directed by commands encoded in its DNA, but an invading virus can introduce a new set of instructions, so that the cell stops its normal work and puts all its efforts into making copies of the introduced program. In this way, the virus makes the host cell its slave, forcing it to provide all the raw materials and energy necessary for propagation. And viruses reproduce at a phenomenal rate. A single common cold virus can create 16 million copies of itself in a day.

    The following is a small ‘rogues gallery’ of viral diseases:

    * HIV/AIDS. The HIV virus destroys the body’s immune defences and, eventually, the victim dies from another infection or from cancer. It is transmitted directly by body fluids or semen. There is, as yet, no cure.

    * Influenza. This disease is spread by direct transmission and mutates readily; in the past, some strains have been major killers. It often emerges from animals ^ the major reservoirs are ducks, chickens and pigs in Asia. Again, there is no cure, but vaccines are now available.

    * Measles. This very infectious disease is usually spread by droplet infection and can be fatal in children in developing countries with poor nutrition. There is no cure, but a vaccine is available.

    * Poliomyelitis. This was the great epidemic disease of the developed world from the late 1940s to the early 1960s. It is an acute viral infection of the central nervous system, with serious effects including paralysis and sometimes death. It is incurable, but a vaccine is now available.

    * Smallpox. In the past this was a major killer of children, but a worldwide vaccination programme has eliminated the virus completely, except for some stocks held in laboratories. Smallpox is regarded as a possible terrorist weapon. It is often fatal and there is no cure, but a vaccine is available.

    Medical science has enabled us to gain effective control of many infectious diseases (but not all ^ look at AIDS). An extensive range of antibiotics has been developed that can cure many bacterial infections, although the appearance of resistant strains of bacteria is causing problems. However, there are few really effective drugs to treat viral diseases. Nevertheless, prevention is better than cure and the development of vaccines, beginning with the work of Edward Jenner on smallpox in the eighteenth century, has transformed our ability to cope with these killer infections.

    The hidden dangers of animal reservoirs

    All animals carry parasites, which have evolved together with their hosts over hundreds of thousands of years and have established a way in which they can coexist, if not in perfect harmony, at least without causing too much harm to each other. But occasionally, parasitic viruses or bacteria escape from their normal mammalian hosts to be transmitted to other species ^ including humans. Many human diseases originated in this way.

    Some of these ^ such as Lyme disease (where the animal host is a deer) and bubonic plague (where the animal host is a rodent) ^ are not usually passed on further by person-to-person infection. Their spread is critically dependent on the animal rather than on the human population. The mechanisms of infection are therefore much more complicated than in ‘simple’ viral infectious diseases such as measles, chickenpox or smallpox ^ and haemorrhagic plague.

    Other viral diseases – such as AIDS, influenza and Ebola – have emerged from animals to infect humans and, most importantly, they can then be directly transmitted from one person to another. These pose a much more serious problem; they are often lethal and, once established in a human population, their spread is governed by the same factors as for any other directly transmitted infectious disease. Their origins in animals are immediately forgotten. These are called emergent viral diseases.

    Narrowing the field of suspects

    From our investigations, can we make an informed guess as to whether haemorrhagic plague was a bacterium or a virus? Its characteristics, summarized in the previous chapters, suggest that the causative agent was a virus. This hypothesis is supported by the observation that in the population of medieval Europe, there seems to have been very strong genetic selection in favour of the CCR5-D32 mutation, which is known to protect against the human immunodeficiency virus.

    The infectious agent also appears to have been remarkably stable. In the 300 years of plagues following the Black Death, the characteristics of the infectious agent seem to have changed very little. There may have been some minor mutations, but these had little effect on the time course of the disease, on its infectiousness, on its symptoms or on its lethality.

    Most changes in the pattern of the disease from the fourteenth to the seventeenth century can be explained as alterations in the behaviour and genetics of human populations, rather than as any change in the virus. Thus, the gradual increase in levels of the human CCR5-D32 mutation throughout Europe increased the proportion of resistant individuals and so modified the spread and mortality rate of plague epidemics.

    Many respiratory viral diseases are spread directly from one person to another by droplet infection. Dr Thomas Stuttaford, medical correspondent for The Times, explains that droplet infection is a euphemism used by doctors to describe the spread of a disease by small drops of spittle and nasal discharge which, laden with a pot-pourri of organisms, viruses and bacteria, are scattered with every cough and sneeze. A sneeze can produce millions of droplets, which can travel at anything up to 90 mph (145 kph). Kissing delivers an even larger dose. Or an infected person sneezes into his or her hand, then shakes yours and you rub your eye, a virus can travel into your nose and throat through your tear duct. We remember that haemorrhagic plague was believed to have been passed by droplet infection; it was considered to be safe if one kept at least 13 feet (4 metres) away from an infected person out-of-doors.

    We can now compare haemorrhagic plague with two other viral diseases, influenza and HIV, that have emerged from animal reservoirs to attack humans. The viruses responsible for these three diseases have evolved very different strategies to maximize their chances of survival and spread. The above table summarizes their basic characteristics.

    Influenza persists because it is highly infectious and is transmitted to many other people even during its short infectious period. HIV continues to spread slowly because of its very long infectious period, which compensates for the low infectiousness associated with its difficult mode of transmission.

    Haemorrhagic plague lies somewhere in between: its infectious period was long enough for the disease to be transmitted over long distances, and it was infectious enough for an epidemic to get going easily, given a sufficient number of susceptible people and suitably warm weather.

  4. shinichi Post author


    Is There Something more Terrible than the Black Death?

    We know that the great powers of the world have been secretly working with biological weapons for several decades. The development of the requisite technology was an inevitable consequence of the discovery in 1953 of how DNA governs heredity and controls the working of all living things, from microbes to man. An immense amount of time and money has been spent on devising ways of attacking and killing people en masse by releasing lethal organisms or their toxins, as well as on preparing defences against such attacks.

    Germ warfare is the poor man’s atom bomb because nuclear weapons are expensive to produce, difficult to deliver and easy to detect. Saddam Hussein’s resistance to stopping Iraq’s biological weapons programme, which cost him billions of dollars in forfeited oil revenues, shows the importance that he attached to this method of attack. A terrorist organization, unless it is backed by a superpower that can provide nuclear weapons and the means of delivering them, will fall back on germ warfare, and a trained microbiologist could easily teach such a group of fanatics how to make devastating biological weapons ^ ‘from a few handfuls of backyard dirt and some widely available laboratory equipment’ (noted in Germs: The Ultimate Weapon, see below).

    For the terrorist, a further advantage of biological weapons lies in the uncertainty of their effects. Once a conventional bomb has exploded, the scale of the devastation and the mortality can be determined, but in a biological attack the health authorities would know neither the nature nor the scale of the strike, and would be unable to predict future developments or the final death toll. All they could do would be to prepare for a worst-case scenario, which might be an over-the-top response to a minor attack.

    Early bioterrorists

    The history of biological warfare is a long and undistinguished one. The story told in the Old Testament (Exodus 9:8^9) of the Lord advising Moses to sprinkle ashes in the face of Pharaoh is considered to be an example of germ warfare and an account of an outbreak of anthrax: the dust must have been converted into an aerosol of bacilli because it became ‘a boil breaking forth with blanes upon man, and upon beast’.

    In the sixth century BC the Assyrians contaminated the wells of their enemies with rye ergot, a type of fungal disease. Solon, the sage of Athens, used the herb hellebore to poison the water supply of the Cirrhaeans.

    More than 2000 years ago, Scythian archers dipped arrow-heads in manure and rotting corpses to increase the deadliness of their weapons. As we have seen, the bodies of plague victims were thrown over city walls in the hope of infecting the enemy during the plague of Athens and the siege of Caffa.

    Smallpox became a way of subduing Indian tribes in North America. In one case, during the French and Indian War in Canada, Sir Jeffrey Amherst is said to have presented tribal leaders with blankets contaminated with smallpox crusts, which infected the population and aided the British advance. The British also used smallpox-laced blankets to infect tribal members at Fort Pitt on the Pennsylvania frontier in 1763.

    All this has returned to haunt us. Gregg Bourland, chairman of the Cheyenne River Sioux tribe in South Dakota, is a descendant of one of the American Indians who died of smallpox, called Blue Earrings. He claims that unlike the Europeans, the native North Americans did not build up immunity against the disease and he is demanding mass vaccination for his people in case of a bioterrorist attack.

    In 1797 Napoleon infected the citizens of Mantua with swamp fever. There are accounts of soldiers during the American Civil War poisoning water supplies by deliberately dumping dead animals in ponds.

    A present-day nightmare

    But these primitive efforts at germ warfare pale into insignificance beside today’s methods. In their book Germs: The Ultimate Weapon, Judith Miller, Stephen Engelberg and William Broad describe how during the Cold War, the USA and Soviet Union devoted enormous amounts of money and manpower to the development of biological weapons; by the early 1980s, the Pentagon was secretly spending $91 million a year on so-called bio-defence. The legacy of this secret arms race was a windfall for terrorists.

    All nations signed a treaty in 1972 that banned the develop-ment of biological weapons but, in direct conflict with the spirit of the agreement, the Soviets secretly decided to expand their programme on a vast, industrial scale. Miller, Engelberg and Broad give the following staggering industrial capacities for germ production (in metric tons per year) at peak levels:

    There were therefore two terrible consequences of the Cold War: first, a literally unimaginable stockpile of germs; second, an army of trained scientists capable of producing and manipulating microbes to order. Projects included work on making a biological attack harder to diagnose and on enabling germs to defeat vaccines.

    Both the stockpiles and the scientists were available for purchase by unfriendly countries and by terrorist groups. Until 1989, US security was so lax that an American company was selling strains of anthrax to Iraq by mail order. In a recent security exercise, a team of American agents was able to set up a functioning germ warfare factory for a mere $1 million without the CIA knowing what they were doing. After the collapse of the Soviet Union in 1991, it was discovered that former Soviet scientists had helped Iraq to acquire stocks of Clostridium, botulinum and anthrax.

    The Aum Shinrikyo cult attacked the Tokyo underground in 1995 with a nerve gas, sarin, killing 11 people and injuring 5500 others. Investigators subsequently found a research laboratory for biological weapons in the cult’s compound; its adherents had already tried to unleash anthrax and botulinum toxin on the population, fortunately without success. Members of this cult had visited Zaire, during the 1992 Ebola outbreak there, in an attempt to obtain samples of the virus for cultivation and weapons development. The investigators discovered that an even more serious attack was planned, with devices that could pump biological and chemical agents into the streets of Tokyo.

    Germ warfare research, occasional bioterrorist activity and contingency planning against the risk of the deliberate release of a biological agent in the UK and USA have been continuing for many decades without attracting a great deal of public interest. However, the events on 11th September 2001 changed all that and brought home to everybody the reality of the situation. The emergence of the USA as the world’s most powerful nation made a biological attack there more likely. The technological revolution of the twentieth century (including the building of mega-skyscrapers) and the high density of people moving incessantly in cities have led inevitably to modern society’s extreme vulnerability.

    The western world reacted swiftly, at last, and the threat of a biological attack against a civilian population is now recognized as a current and ongoing danger. An analysis in 1997 estimated in some attack scenarios an economic impact of $26 billion per 100 000 persons exposed to anthrax, and the threat of biological weapons is considered sufficiently serious to warrant the creation of an unprecedented civilian stockpile of medicines and vaccines.

    US President Bush announced $11 billion of new spending in the health budget for the financial year 2003 to combat bio-terrorism, and the German army intends to triple its investment in research into protection against biological weapons. But Professor Reinhard Kurth, president of the Robert Koch Institute, believes that civilian vaccination programmes should be developed independently of what the army is doing, thereby creating a buffer of vaccinated people in a localized outbreak. He concludes,

    In my opinion, and it is the general opinion of experts in this field, the potential threat through biological weapons is worse than that from chemical and atomic weapons.

    In January 2002, the UK’s Chief Medical Officer announced plans for the establishment of a new protection agency with wide powers to streamline the services involved in the containment and control of infections, including future emergent diseases (which are regarded as inevitable) and those created by terrorists. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, wants ‘to include bioterrorism in the big umbrella of emerging and re-emerging infections’.

    However, as Madeline Drexler says in Secret Agents: The Menace of Emerging Infections, we should not underestimate Mother Nature, perhaps the most savage bioterrorist of all. Whatever the infectious agent may be, including some new microbial horror that we have yet to detect, the bottom line is that keen surveillance and rapid response are really the only weapons in our arsenal.

    Operation Doomsday

    A nightmare vision of Britain under terrorist attack was conjured up in February 2003 when the British Government unveiled the biggest shake-up of emergency planning since the Cold War. In blood-curdling detail it spelt out how the emergency services would decontaminate those caught in a chemical, biological or nuclear attack.

    Under these doomsday plans, specialist fire crew in protective suits will operate mass decontamination units in which survivors will be stripped and then walk or be stretchered through warm showers to remove traces of hazardous material at a rate of 15 seconds per person. Watches, spectacles and hearing aids will be confiscated and the victims will then don white overalls and be sent to casualty clearing stations.

    A sum of »56 million has been committed for mass decontamination and monitoring equipment and the number of gas-tight protection suits is being doubled to 4000. Police cordons with armed military back-up will be assigned to stop the inevitable panic and ensure that the injured are cleaned up before they are given treatment.

    Biological warfare

    About 25 microbes or bacterial toxins have been identified as potential biological weapons. The most serious threats are considered to be anthrax, smallpox, bubonic plague and the viral haemorrhagic fevers, either because they are easily disseminated or transmitted from person to person, or because they cause high mortality, or because they might cause widespread panic and social disruption. The Center for Disease Control and Prevention, very significantly for our thesis, has cited the viral haemorrhagic fevers as possibly posing the highest threat if used as a bioweapon, because of their potential for aerosol transmission and high mortality rates. The manufacture of these agents is now straightforward, but to produce them in a form that can be easily delivered and would harm large numbers of people is technically more difficult at present.

    The fear of anthrax

    So what happened after 11th September 2001 that completely changed everybody’s thinking and appreciation of the possibility of a bioterrorist attack and led to the reallocation of prodigious sums of money? The chosen weapon on that occasion was anthrax spores delivered via the US postal system that left five dead, with considerable attendant inconvenience and public alarm.

    In addition to the fear of another mail attack, experts suggest that the tiny airborne spores could be introduced into air-conditioning systems in apartment blocks or shopping precincts, and at government buildings such as the White House or the Capitol. Such an attack would not only kill thousands of people but could create mass panic across America.

    Patrick Kelley, director of the Pentagon’s Global Emerging Infections Surveillance Response Systems, compared the attack with the effects of HIV and malaria the world over: ‘You cannot expect them to care about five deaths from anthrax’. And yet this seemingly trivial terrorist campaign has had enormous and far-reaching consequences. A letter sent to members of the American Society for Microbiology by the FBI in January 2002 suggested that the anthrax used in these attacks may have come from a US laboratory that was conducting research into defence against biological weapons. Radiocarbon dating has now proved that the anthrax sent through the post to two senators and two prominent journalists was made and milled into a fine powder within the previous two years.

    Certainly there are thousands of tonnes of anthrax spores hidden in stockpiles around the world: more than enough to wipe out humanity if they could be appropriately delivered. Russian scientists have already produced a vaccine-resistant strain of anthrax. Only 100 kg of spores released as an aerosol upwind of a major metropolitan region could kill a million people. Furthermore, the spores are remarkably resilient and it would be very difficult to eradicate them and to disinfect the area under attack, so that the disruption to services and the normal pattern of life would be profound and long-lasting.

    In spite of the justifiable fears about the deliberate mass release of anthrax spores, the overall effects on the world would be negligible compared with the return of the Black Death or a similar emergent disease. There would certainly be a terrible loss of life, but anthrax is not an ideal weapon because it is not trans-mitted from person to person and barrier isolation precautions would be sufficient. The outbreak would be largely confined to the area downwind of the point of release and the rest of the world would not be affected. There should be no pandemic. Further-more, health authorities are now geared up to combat an anthrax attack and would be able to reduce the mortality substantially.

    Yersinia pestis

    What of bubonic plague, however? During the Second World War, the Japanese are said to have dropped fleas infected with bubonic plague on Chinese cities and may have succeeded in killing some people, presumably by initiating localized outbreaks of pneumonic plague. During the cold war, the Soviet Union invested heavily in research into Yersinia pestis as a potential weapon and it is high on most governments’ lists of infectious agents against which defences have to be prepared. But why is this?

    Nobody, but nobody, should be the slightest bit alarmed by the prospect of a terrorist attack with bubonic plague. The United States have lived with the disease for the last 100 years and it causes only a handful of cases annually. The delivery and establishment of an epidemic of bubonic plague would be very difficult because, as we show in Chapter 11, so many factors would critically affect the outcome and spread of the epidemic would be impossible. In any case, bubonic plague is readily treated with antibiotics.

    So why have governments committed so much effort and money to producing Yersina pestis as a biological weapon? The answer is obvious: they believe that bubonic plague was the cause of the Black Death, which killed half of Europe at a stroke ^ in their minds it must surely be the ideal weapon.

    Of course, this is nonsensical. There has been no consideration of the basic biology of bubonic plague. The situation has worsened considerably because mind-boggling sums of money are freely available for anyone working on anything remotely connected with bioterrorism. Consequently, several teams are now modelling the effects of an epidemic of bubonic plague that might be initiated by a terrorist. In our opinion this is a complete waste of time and resources. These research scientists should read Chapter 11. But they have a vested and financial interest in maintaining the present fiction. We believe that it is essential that everybody, particularly those needlessly handing out large sums of public money, understands the true nature of bubonic and haemorrhagic plague, and the real problems of germ warfare.

    The deadly viruses

    We should be far more concerned about the potential use of viral diseases by terrorists. They are cheap and easy to deliver and the infected people themselves do all the work of multiplication and dispersal. The virus multiplies within the victim at a fantastic rate and is soon ready for onward transmission to infect many others. With modern air travel, the result would be a global epidemic.

    The smallpox virus has long been considered as a possible biological weapon. Stockpiles are known to be ready for use and in November 2002, the USA identified four nations that have undeclared secret samples of the virus: Iraq, North Korea, Russia and France. A terrorist would only need to send one infected person travelling continuously, say on the London Underground, to start a major epidemic. This imaginary scenario was presented in a 90-minute BBC television programme broadcast in February 2002, in which the final death toll was estimated at 60 million. Governments have been working clandestinely to predict the outcome of a smallpox attack and to organize their defences via suitable public-health measures.

    We have spent several years researching historical smallpox epidemics. Although an outbreak of this disease would be dreadful, we do not believe that a terrorist strike with the standard virus would spell total disaster. The strain of the virus that existed in England in the seventeenth and eighteenth centuries killed only about 20 per cent of infected children.

    Once the disease had been identified following a terrorist attack, transmission could be greatly reduced by the use of masks and, most importantly, a protective vaccine is available. This viral, infectious disease is well understood and with forward planning, good emergency health measures, early diagnosis, rapid response and mass vaccinations, a smallpox epidemic produced in a major city by a terrorist strike could be contained and eventually controlled.

    The Government of the United States has decided to manufac-ture and stockpile enough vaccine for its entire population: a formidable task that will cost hundreds of millions of dollars. President Bush began operations on 13th December 2002, when he announced that half a million civilian health workers as well as half a million troops would be vaccinated by 15th March 2003. Fortunately, so far severe reactions have been rare. However, it seems to be unlikely that the US will reach the target of 10 million vaccinated by July 2003.

    However, there is an enormous proviso. Dr Vivienne Nathanson from the British Medical Association has warned that civil defence preparations can help counter attacks only with known biological agents.

    No medical response exists to counter unknown biological weapons or genetically engineered strains of superbugs for which there is no vaccine available. The only real defence against the use of biological or chemical weapons is to prevent their development in the first place.

    To conclude: the enormous amount of time and money currently being devoted to combating infectious diseases released in a terrorist attack are necessary and welcome. But it should be remembered that this incredible activity was stirred up only when five people died after anthrax spores had been sent via the US mail, and there is more than a hint of overkill in the response. There never has been ^ and there certainly is not now with all these welcome precautions ^ any suggestion that a bioterrorist attack or a germ warfare strike with any of the known bugs in the world today would have more than a fraction of the impact of the return of the Black Death.


    Why, then, is bioterrorist activity included in this chapter as a way in which the Black Death, or something very like it, could return? The answer lies in the biotechnology revolution. When the outbreak of SARS in the Far East was first reported, bioterrorism was considered as a possible cause and was taken seriously on both sides of the Atlantic. The UK Department of Health said: ‘The pattern of infection certainly looks like a naturally occurring illness but obviously we are keeping an open mind. It would be ridiculous for us to rule anything out at this stage.’

    There remains the frightening possibility that terrorists could manufacture something very like the Black Death. There are now many microbiologists, veterans of the Cold War, who have moved on from manufacturing bulk stocks of anthrax spores and developing vaccine-resistant variants of known diseases, to the production of designer super-germs to order. The possibilities of biotechnology are awesome and it is becoming ever easier to create new biological entities. Microbes and toxins that attack the human immune system or nerve sheaths are already available, and both the Americans and the Russians have succeeded in producing more deadly versions of anthrax, smallpox, Ebola and bubonic plague.

    In November 2003, it was announced that a scientist funded by the US government had deliberately created by genetic engineering an extremely deadly form of mousepox, a relative of the smallpox virus.

    American scientists have recently demonstrated how easy it would be to create deadly germs for biological weapons. They have assembled a man-made version of the polio virus by using DNA and a genetic blueprint for the pathogen that is available on the internet. This is the first time that a scientific team has used the available technology to make a completely artificial virus from scratch. To test its efficacy, it was injected into mice, which first suffered paralysis and then died.

    In fact, using a new emergent disease or a biologically engineered super-bug would be a cunning ploy on the part of terrorists. It might not raise suspicions for a long time during which a global pandemic could be established, whereas a smallpox outbreak anywhere in the world would be immediately recognized as being man-made.

    Inevitably, some day soon, someone, somewhere will start tinkering with the viral haemorrhagic fevers. Imagine an engineered super-germ that is even more ferocious and infectious than the Black Death. Transmission would be by droplet infection and only one person need be infected (although the terrorist would hope and work for more, preferably in different countries, to give a margin for error) for apocalyptic oblivion to beckon. That is the danger of playing with fire, and is a direct consequence of the biotechnology revolution that followed the fateful discovery of the structure of the double helix of DNA. Thus, the blueprint of life becomes the blueprint for death.

    A wake-up call

    Our quest is complete. We have turned history upside down. From our chance discovery of the record of an epidemic in a market town in the north of England, we now know that the Black Death and the plagues were caused by the most fearsome emergent infectious disease of all time. Escaping from Ethiopia about 3000 years ago, travelling as always by the movement of infected traders, haemorrhagic plague established its base in the Levant. From there it struck at the Greek and Byzantine civilizations and the early Islamic Empire. Flourishing city states were its preferred victims.

    Finally, in the mid-fourteenth century, haemorrhagic plague devastated the population of Europe, the greatest human tragedy in history. In the days of very limited transport, it was able to make these long-range strikes only because of its remarkably long incubation period. For the next three centuries, Europe was held in its relentless grip and it is probably only the presence of a genetic mutation in a few lucky individuals that led eventually to its disappearance.

    We must realize and take on board the terrible dangers of emergent infectious diseases. These occurred only rarely until about 1970, when our way of life changed rapidly and completely and a new disease was reported every year. Nevertheless, while these are serious and lethal, at present they in no way approach the ferocity of our medieval serial killer. The accounts that we have uncovered show all too clearly the devastating mortality ^ nearly half of the western world was killed in the single epidemic of the Black Death, an event that is without parallel. The descriptions of the agonizing and lonely deaths make our hair stand on end and send shivers down our spines.

    We owe it to ourselves and to those who died to be continually on our guard against the reappearance of haemorrhagic plague, to make sure that it is not allowed to establish a stranglehold once again through ignorance and misrepresentation. In this way, the suffering and deaths of millions will not have been in vain.


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