Like many bioarchaeologists, I have a fondness for plagues. They upend the natural order of things, cutting across the normal risk factors for ending up in archaeological samples and giving a snapshot, captured in death, of not just the old and the infirm but also a sample of the whole (unlucky) population. The tragedy of mass causalities exposes lives that would, statistically, rarely be unearthed, including the adolescents and adults who form the bulk of a living population, so rarely represented in a cemetery. Calamities such as plague that knock everyone into the grave with one indiscriminate sweep are one of the few chances bioarchaeologists have to overcome something known as the Osteological Paradox, a term coined by researcher James Wood and colleagues to cover the very awkward point that, in studying past lives, the evidence bioarchaeologists actually have to go on are past deaths. Without access to modern medical care, the greatest potential for mortality comes in old age and in infancy and early childhood. Death is less of a risk for adolescents and reproductive-age adults, until something comes along to level those odds.
A giant, sweeping epidemic disease that carries away huge swaths of population, respecting neither rank nor righteousness, the phenomenon of plague holds a particular cultural fascination. The death’s heads and dancing skeletons of fourteenth-century European art reflect the macabre upending of order in the European world in the wake of the Black Death, with death itself brought front and centre in the narrative of European civilisation. Indeed, the after-effects of the incredible loss of life seen during the Black Death had far-reaching consequences, whose scope and scale researchers are only now beginning to unravel.1 The Black Death didn’t just fell kings; it felled kingship and the entire medieval way of life in the parts of Europe that it devastated. Increasingly, scholars are seeing the influence of plague in other areas as well – lesser-known consequences of the catastrophic mortality that rippled out from epicentres in Asia and Africa. But why should any one particular disease have such a virulent effect? What circumstances conspired to kill uncounted millions on three continents? What, exactly, is plague, and how did we get it?
Plague is not one disease, even though most people’s first association might be the bubonic plague caused by Yersinia pestis, popularly known as the Black Death. Plague can be any disease2 that strikes enough people with sufficient virulence to kill in large numbers. Your definition of ‘large’ might understandably vary depending on whether those numbers are made up of your friends and family, but it’s another one of those things where you would know it if you saw it. Epidemic diseases require large numbers in order to succeed in the way the Black Death did. It does the bacteria or virus no good if the host organism keels over all alone in an isolated field without transferring the infection first. Some infections have a sufficiently long incubation period, or can hang about for long enough in nearby animals, that they can bridge the gaps between little clusters of people, forming a chain of infection that can rapidly spread across the landscape. The two requisite conditions for a local epidemic disease to become a pandemic are then very much the conditions bred in cities: dense populations, and well-worn roads between them. What we still don’t perfectly understand, however, is why some infections make that jump – infectious disease is nothing new, so why does it sometimes take us so much by surprise?
The real contribution of the invention of the city to the epidemiological transition is the shift from infection to epidemic. Infections are a nuisance, maybe even fatal; epidemics will kill you and leave no one left to bury the body. You cannot have an epidemic without a large, vulnerable population to infect: that’s what makes it an urban disease. It’s not that the diseases that cause epidemics don’t strike outside cities – most of our modern epidemic diseases are actually rural infections direct from the rustic goodness of the soil. They would stay there, too, but in a networked world of roads, buses, cars and people, they now reach the dense urban populations they need to explode. It’s the ready transmission of infection that makes a disease into a plague; the networks of roads, trade and the people who link an increasingly urban world. It’s the susceptibilities of unequal city lives, however, that allow plagues to flourish.
It’s possible to break the infectious diseases that kill humans down into different categories; these might be dependent on transmission vector (what you get it from), disease agent (bacteria or virus) or even climate and geography (it’s difficult to get malaria if malarial mosquitoes aren’t around). I’m going to cheat slightly and divide the major infectious diseases by the level of terror they inspire – that and how they are identified in the archaeological record. This means that some of the most insidious killers, diseases caused by contaminated food and water like cholera, will be discussed in Chapter 13, when we talk about endemic diseases in the context of Industrial Revolution. Syphilis is sufficiently macabre and mysterious that it gets its own chapter. In the previous chapter, we covered the peculiar case of tuberculosis and leprosy as a function of population density; much of the same reasoning will be used in the discussion here: people (lots of people) offer a great opportunity for a disease on the make to become a full-fledged plague.
What makes a plague? Dead people – and lots of them – in unusual places. As we go wandering back in time, there are few candidates to fit this description: the disease we know as Plague-with-a-capital-P, which we will get to, and the plague that came before it, smallpox. Smallpox manages to be both the oldest archaeologically known epidemic and by far the deadliest recent epidemic. It is caused by infection with one of two species of virus, Variola major or Variola minor. The latter causes alastrim, a relatively benign form of dermatological disease which is rarely fatal and is endemic to parts of Central America. The former has killed by some estimates 500 million people, and leaves a disfiguring rash in many of those who were lucky enough to survive; this is the disease we are interested in. Smallpox is a disease that acts first on the skin: there are spots, then there are fluid-filled blisters. These blisters are what cause the horrific scarring associated with smallpox.3 Subsequently, the infection can progress even into bones, causing osteomyelitis, though this occurs only in a very small percentage of cases.4
Osteomyelitis is a very broad category of pathology; the term is used to describe any infection of the bone itself. It is the one sign accessible to bioarchaeologists who work on bone of potential smallpox infections. When bone is infected, it has an inflammatory response just like other tissues of the body, met in turn by a repair response that results in characteristic changes to bone shape. The infection may simply be evident as reactive bony changes on the interior or exterior surfaces of the bone. It can form an abscess, a pus-filled lesion, which may force the formation of a channel all the way out through the bone, along which said pus can suppurate. The clinical term for this channel is ‘cloaca’, which is Latin for ‘sewer’ and every bit as disgusting as you might imagine a Roman sewer to be. New bone formation on the surface in response to the infection can change the width or thickness of the bone, so when compared to an opposite number, say from the other side of the body, the shape is very much changed.
Of course, the majority of cases of osteomyelitis are not caused by smallpox but by a host of bloodstream-borne infections, with about 90 per cent of modern infections caused by the bacterium Staphylococcus aureus.
Clinical reports from the twentieth century give us insight into the varied courses smallpox itself could take; in an epidemic involving some 1,400 cases in what is now Malawi, primarily children were affected, first by the typical skin rash but secondarily by bone infections. The infection rates varied with the ages of the children, but seemed to have no link to any concomitant conditions (malnutrition or red blood cell diseases like sickle-cell anaemia); two-thirds of the children between the ages of one and five showed that the disease affected their bones. This may be similar to the pattern of skeletal involvement in the metabolic diseases discussed in Chapter 5, where the effect changes depending on which parts of the child’s skeleton are most actively growing. In smallpox, modern clinical practice reports changes occurring in the elbows, the fingers and toes, and the ankles. The only known potential archaeological example of Osteomyelitis variola (smallpox skeletal damage) was reported by Mary Jackes from a seventeenth-century cemetery in Ontario, Canada from the bones of an older man who died around the 1650s. She traces the potential route of infection through a series of local indigenous interactions, encounters with colonial powers and all the way back to a London outbreak of 1628. It’s not clear, however, that the osteomyelitis described necessarily results from smallpox; the lesions on the man’s skeleton could well have resulted from an infection of bone picked up from other sources.
When did we get smallpox? It’s a very interesting question. Historical descriptions of a disease that seem very much like smallpox come from India in the first millennium BC; medical texts attributed to the work of the rather mythical personage Dhanvantari record a disease of fevers, pustules and skin ‘that seems studded with rice’. A further text attributed to Dhanvantari describes a process of inoculation that would not be discovered again until the middle of the second millennium AD. Reports of an inoculation – essentially, introducing the infection deliberately in a different or weaker form – process of similar antiquity in China have been suggested to be seventeenth-century exaggerations,5 but the disease seems to have been attested in text by around the same date.
The key to preventing smallpox, and the clue to its eventual eradication, was the practice of ‘variolation’. Variolation involves inoculating small children by scratching them with material taken from the blisters of cowpox, a bovine-focused relative of human smallpox, and seems to have been widely attested in Africa, Europe, India and China from at least the late medieval period, though likely practiced well before. More surprisingly, given the state disease theory was in at the time, it largely worked. A man called Edward Jenner came across the idea at the tail end of the eighteenth century from chance6 observations of milkmaids; his experimentation led to the Western medical establishment’s embrace of the inoculation concept, and eventually to the smallpox vaccine.7
Historical records are all well and good, but they suffer from a number of inadequacies. First, for the vast majority of human history no one wrote anything down. Second, diagnoses of medical traditions which rely heavily on religion, spiritual beliefs and fairly out-there theories of the human body may not be easily comprehensible to the modern researcher.8 Despite smallpox only rarely leaving telltale signs of bony infection, bioarchaeology has another avenue for detecting the disease in antiquity: mummies. In 1979 physician Donald Hopkins was granted special permission to examine the upper half of the unwrapped body of the Egyptian pharaoh Ramses V, who died in 1143 BC.9 The mummy’s skin showed evidence of a pustular rash, very akin to smallpox, and subsequently Ramses V became famous not for a perfectly sensible large-scale tax survey he carried out in his limited reign, but for being the first archaeological evidence of smallpox.
Due to the antiquity of historical records and the singular case of Ramses V, which was never confirmed in the lab, many historians and archaeologists have speculated that smallpox came out of India, or possibly North Africa, and from there circulated to China and to Europe. A great number of plagues recorded by history but undiscovered by archaeology have been attributed to smallpox: one among the Hittites of Anatolia in the mid-fourteenth century BC; the Plague of Athens in 430 BC recorded by Thucydides; the plague that struck the army of Alexander the Great in the Indus Valley in 327 BC; the Antonine Plague that decimated Rome and its provinces in AD 165; and, the Plague of Cyprian, a hundred years later. Not all of these are in fact confirmed smallpox epidemics: the Hittite plague has been argued to have been Francisella tularensis, and the Athenian one typhoid. Mentions come in from Syria and France in the first half of the first millennium AD, and after that smallpox is more or less an established disease everywhere but the Americas and Australia. It was established primarily as an endemic risk and only becoming epidemic on the occasions it encountered a new, immunologically naive host.
This is precisely what happened when Variola major swept into the Americas on the back of European refugees, speculators and adventurers. In virgin territory, where the population had no inbuilt resistance to infection, smallpox became the deadliest epidemic this planet has ever seen. In the conquest of the Americas by European colonial powers, the mortality rate for the native population was anywhere between 30 and 70 per cent. Of course, immunity is relative; globally, even in regions that have had smallpox infections for thousands of years, some 300 million or more people were killed by smallpox in the twentieth century alone as populations shifted, changed and crowded together. One important question remains, however. If Variola viruses exist in a killer form that came out of Europe and not-so killer form that was already in the Americas, and you can cure the first with a related virus that doesn’t even come from humans … why did so many Native Americans die? Why did the precepts of inoculation not work between the Variola major of the Old World and the Variola minor viruses of the New?
Perhaps this is because Variola minor wasn’t a ‘New World’ version of the disease, but rather another form of the same Old World disease. It’s only recently, with aDNA, that we’ve been able to more clearly understand the interaction of infectious diseases in the past. Research into the genetics of infectious pathogens themselves can reveal an astonishing amount, including variation in pathogen genetics around the world. By calculating the molecular clocks of the change-over in that material, researchers can even estimate the point in time that different strains diverge from each other, potentially becoming more or less virulent, affecting new hosts or even being geographically isolated. The Variola virus can be opened up to reveal just this sort of information. The complicated history of smallpox is a story of multiple different strands appearing on one continent only to disappear and appear on another. The low-fatality version that causes alastrim in the Americas shares a recent common ancestor with the low-fatality version of the disease identified in West Africa, suggesting that early smallpox cases in Brazil and the Caribbean were due to contact through the slave trade. Reconstruction of the disease suggests that it switched over to human hosts at least 16,000 or so years ago, spread out of Africa and conquered Asia in epidemic form before turning back to the West and invading Europe and North Africa. Pathogen genetics are increasingly rewriting what we thought we knew about the history of disease and civilisation; this is nowhere more true than in the case of plagues.
Because this is a chapter on plague, the reader will rightfully expect to hear a bit about the plague, the disease that caused the Black Death. Well, the plague has two black marks against it in my book: first, everyone else has written about it, and some quite well; second, infection with Yersinia pestis does not leave appreciable traces on the skeleton, and so makes for annoying bioarchaeology. Luckily for you, the third factor of plague more than makes up for all of the above: it kills a lot of people. Quickly. Faster than even smallpox, the rapid deterioration that follows infection with plague means that the epic mortality rates experienced do leave a scar in the archaeological record in the form of mass burials. They leave an even greater scar on the history and progress of society, as written and as experienced.10
The modern perception of the experience of the Black Death owes more to a cinematic imagining of biblical proportions than to the actual reality of a recurrent condition that (sorry) plagued Europe for centuries. Quite frankly, Monty Python and his Flying Circus hasn’t helped either – think of plague, and the first cultural reference you’ll have if you’re of a certain age and a certain language group is Eric Idle banging a triangle and shouting: ‘Bring out your dead!’ How true to life (or death) were the not-quite-dead corpses that John Cleese heaped on top of a plague cart? Actually, there is considerable evidence for the level of devastation portrayed in films. Much of this evidence comes from contemporary written accounts, so while it might be supposed that there was a certain degree of dramatisation, there is no argument that the sweeping plagues of the fourteenth century were lacking in drama. The Decameron by fourteenth-century Italian author Giovanni Boccaccio is perhaps the best-known contemporary account of the experience of the Black Death,11 and it mostly concerns hiding from sick people and taking potshots at the avarice and moral turpitude of the Catholic Church.12 Boccaccio relates the impact of the plague on Florence with a practical, if not clinical, air:
Not such were they as in the East, where an issue of blood from the nose was a manifest sign of inevitable death; but in men and women alike it first betrayed itself by the emergence of certain tumors in the groin or the armpits, some of which grew as large as a common apple, others as an egg, some more, some less, which the common folk called gavoccioli. From the two said parts of the body this deadly gavocciolo soon began to propagate and spread itself in all directions indifferently; after which the form of the malady began to change, black spots or livid making their appearance in many cases on the arm or the thigh or elsewhere, now few and large, then minute and numerous. And as the gavocciolo had been and still were an infallible token of approaching death, such also were these spots on whomsoever they shewed themselves. Which maladies seemed set entirely at naught both the art of the physician and the virtue of physic; indeed, whether it was that the disorder was of a nature to defy such treatment, or that the physicians were at fault – besides the qualified there was now a multitude both of men and of women who practiced without having received the slightest tincture of medical science – and, being in ignorance of its source, failed to apply the proper remedies; in either case, not merely were those that covered few, but almost all within three days from the appearance of the said symptoms, sooner or later, died, and in most cases without any fever or other attendant malady.
The Decameron, Giovanni Boccaccio, 1353
Boccaccio was truly astonished by the disease that descended on his Florentine commune; while his words are the ones that have passed down to modern readers, they would have been sentiments echoed by his contemporaries. The most shocking thing, one gathers, was not so much the piling up of the dead, though Boccaccio describes how this appeared:
Many died daily or nightly in the public streets; of many others, who died at home, the departure was hardly observed by their neighbors, until the stench of their putrefying bodies carried the tidings; and what with their corpses and the corpses of others who died on every hand the whole place was a sepulchre.
The shocking thing was that seeing a dead man, or two or three, being carried on planks to the grave through the street with no funeral procession around him occasioned all the emotion of, as Boccaccio himself put it, seeing a dead goat in the street.
The plague described by Boccaccio is the bubonic plague, or Black Death, that caused catastrophic mortality in Europe in the late 1340s. Many readers may be more familiar with the Black Death than any other subject of medieval history,13 and can recite the details well enough: Plague came to Europe on a ship from India, it infected an enormous number of people by means of fleas on rats, some of those people died horribly with swellings (buboes) in their groins and armpits alongside a spotted rash, some of those people transported plague to other places, and in the end half of Europe was dead. For reference, at least the ‘half of Europe’ part appears to be correct, and the rest is only mildly misleading. Plague actually came to Europe several times, for instance as the Plague of Justinian in AD 541, but seems to have lacked the ability to transport itself quickly across the continent to infect the whole of Europe.14 No one is really sure how it got to Europe in 541, but it may have come through Egypt via trade with India over the Red Sea. For the Black Death of the fourteenth century, there are no recorded episodes of epidemic disease in India that fit. Instead, the origin was more likely to have been via the Silk Road from northern China, which seems to have had sporadic episodes of deadly epidemics from the 1330s. Admittedly, boats did seem to feature in at least a few outbreaks, as described below. Fleas and rats, meanwhile, get a bad rap; not all plague is spread by flea bites – the last outbreak of plague in China in 2009 was marmot-based. There are three pertinent varieties of Yersinia pestis infection: bubonic (buboes!), septicaemic (in the blood), and pneumonic (in the lungs). The latter is a mechanism of direct transmission from human to human, and no fleas need apply.
Plague was then endemic in Europe, as it probably had been in Asia, for at least the next 400 years, with occasional outbreaks. The diaries of famous man-about-historic-London Samuel Pepys record the experience of the London outbreak of 1665, where he notes that everyone has such a deep and abiding suspicion that Londoners might be carrying plague that he has to keep telling people he’s from suburban Woolwich. For our diarist, however, plague did not seem too great a tragedy – it made him melancholic when confronted with actual corpses, but by New Year’s Eve of 1666, Pepys is able to report that he has ‘never lived so merrily (besides that I never got so much) as I have done this plague-time’.
It was in Pepys’ time that one of the greatest leaps forward in public health, the publication of weekly mortality rates parish by parish, was instituted: the Bills of Mortality. Pepys, and his potential hosts, were able to keep up with the weekly stats on London plague deaths because of the widespread publication of those Bills of Mortality, the morbid factsheets of London deaths and their causes compiled by the government and read with no small frisson of sanctimonious schadenfreude by country and town folk alike. The Bills, and what can be made from their rather idiosyncratic data, are a fascinating subject that will be explored in greater depth in Chapter 13.
More archaeological wordage has been put into this subject than I could possibly recount, so it’s enough to keep abreast of what we now know about the infectious disease caused by Yersinia pestis, a subject that has been radically transformed by the incontrovertible genetic identification of the bacteria from plague burials in the lab. In 2015 the team led by Simon Rasmussen and Morten Erik Allentoft of the Centre for GeoGenetics at the Natural History Museum of Denmark published a groundbreaking study of the genetic archaeology of the plague pathogen. Yersinia pestis, it seems, has been loitering around the steppes of Central Asia for some time. Animal and human versions have a long history in the region, with the human-infecting pathogen diverging thousands of years before the first ancient DNA evidence of infection. Their work showed that Yersinia pestis had been present for more than 5,000 years in Eurasia – but not as we know it. The Bronze Age version lacked a key genetic mutation that allows it to live in insects; it could not have been spread by fleas. The very oldest strains found may not even have been able to form buboes, but instead relied on pneumonic spread. The story is only becoming more complicated as further genomic work unveils a story of multiple origins and complex routes to infection and pandemic.
The very first allegations of biological warfare concern the deliberate spread of epidemic disease. The catastrophic epidemic that befell the Hittite Empire of Anatolia (in modern Turkey) around 1335 BC is tentatively attributed to an outbreak of Francisella tularensis. This is an infectious bacterium carried by animal vectors that can painfully and fatally affect humans. The texts of the period seem to suggest that whatever struck the Hittites went on to trouble everyone they fought. A very wandering and fanciful interpretation of the Hittite ritual release of a ram and heavily made-up woman undertaken before battle to appease the gods and stave off their hunger for human flesh has been interpreted as a mechanism (through either creature) for deliberate infection of enemy troops, which would make the Hittites the first-ever practitioners of biological warfare.15
One of the more colourful explanations for the origins of the catastrophic Yersinia pestis epidemic that ravaged the European and parts of the Asian continent in the fourteenth century AD starts with just such a story. Gabriele de’ Mussi authored a memoir of the ravages of the Black Death in the years immediately after, in which he gives a supposedly16 first-hand account of the siege of one of the great trading outposts of his native Genoa: the fortress at Caffa, modern-day Feodosia, in the Ukraine. The great Golden Horde of Mongol warriors led by Toqta Khan besieged the Italians at Caffa for some three years before eventually, according to de’ Mussi, succumbing to a ‘mysterious illness which brought sudden death’, and which was at the time endemic to their territory. This disease caught up with the Mongols at the siege of Caffa in 1346. In an act of desperation, defiance – or just plain peevishness – the dying warriors began catapulting their dead over the walls:
… in the hope that the intolerable stench would kill everyone inside. What seemed like mountains of dead were thrown into the city, and the Christians could not hide or flee or escape from them, although they dumped as many bodies as they could into the sea. And soon the rotting corpses tainted the air and poisoned the water supply, and the stench was so overwhelming that hardly one in several thousand was in a position to flee the remains of the Tartar army. Moreover one infected man could carry the poison to others, and infect people and places with the disease by look alone. No one knew, or could discover, a means of defense.
Gabriele de’ Mussi, 1348
This seems to be a clear description of medieval biological warfare, designed not just to horrify but to kill. An even earlier example of the use of bodies to kill dates back to the tumultuous period preceding the reign of the Abbasid dynasty in the eighth or ninth century AD, in what is now Jordan. Archaeological excavations revealed the remains of at least six individuals who had been dumped in a then-full water cistern. Whether the intention was to hide the bodies or poison the city, the effect would have been the same. The very aspects of the city designed to protect its inhabitants – walls, water, stores – become engines of destruction.
The case of smallpox in the Americas could almost be excused as a terrible and naive accident, were it not clear that in a number of instances the colonists deliberately tried to spread the pandemic to the indigenous people. On 24 June 1763 the Pontiac tribe had besieged the colonial Fort Pitt (now Pittsburgh, United States), trapping a dense enough number of the European-origin population inside the fort that infectious diseases, like smallpox, began to spread. The Pontiac sued for peace on two attempts, with senior members of the tribe visiting their cornered enemies to try to convince the English to give it up already. We know this because, on that day, local merchant William Trent wrote an account of the visits, noting:
Out of our regard for them, we gave them two Blankets and an Handkerchief out of the Small Pox Hospital. I hope it will have the desired effect.
From the journal of William Trent, 24 June 1763
Trent was not alone in his hopes. The British army shared and indeed encouraged this; in a letter from about a year previously, the commander of the British forces in America, Sir Jeffrey Amherst, writes:
Could it not be contrived to Send the Small Pox among those Disaffected Tribes of Indians? We must, on this occasion, Use Every Stratagem in our power to Reduce them.
Following this up about a week later with a commendation:
You will Do well to try to Innoculate the Indians by means of Blanketts as well as to try Every other method that can serve to Extirpate this Execrable Race.17
It is interesting to note in the devastation of smallpox that none of the quiet, contemplative morality of the earlier European plagues seems to be featured. Where the Black Death inspired extensive soul-searching, moralising and what can only be described as a crisis of faith across an entire continent, smallpox by the fifteenth century seems to have been an accepted fact of life, and one that could be turned to advantage by the enterprising imperialist.
Plagues, it seems, are endemic to our world. It’s fascinating to think that plague – this terror, this awaited apocalypse that carried off such a huge number of mothers, fathers, brothers, sisters, children (and rats) – became conspicuously normal in medieval Europe. Much of the work on this chapter has been undertaken in the very pleasant German tourist resort of Überlingen, located on the northeast shore of the Bodensee (Lake Constance). I was supposed to be there recapturing family history and my sense of bewilderment at the German language, but as a sort of occupational hazard I spent quite a bit of time looking at the records of the town’s rather significantly antique hospital. During the mid-fifteenth to mid-sixteenth centuries of the Holy Roman Empire, Überlingen was a Catholic town with perhaps 3,000 inhabitants. Its Seelhaus was a ‘soul house’ for the indigent, particularly indigent women, and those struck by the ‘evil pox’ (syphilis). Überlingen is not particularly given to outbreaks of plague; indeed, its salubrious thermal baths have long been viewed as just the sort of environment to promote health. Nonetheless, even this small lakeside resort town had no less than three houses to accommodate the poor and the wretched, many of whom were, by virtue of the former characteristics, also the diseased. Überlingen, however, does not exist in a vacuum. Passing by the striking church of Birnau on a boat trip to the flowery tourist island of Mainau, my mother commented that it was there that her family went for John F. Kennedy’s memorial service, making it a more worldly village than I had previously suspected. Out running, I passed a series of derelict train stations that had welcomed passengers from the industrial cities of the north to the thermal springs. Those train tracks follow the path of a Roman road that is millennia old. Tiny, adorable Überlingen has been trapped in the weft of the urban fabric of Europe for a very long time, and has the plague deaths to prove it.
My point here is that plagues are diseases of contact. Contact between different environmental reservoirs for diseases – and that’s all we are to a bacterium – provides an opportunity for infectious disease to blossom into a full-scale pandemic in the absence of host immunity. To the Variola virus or the Yersinia pestis bacterium, our species are essentially little ambulatory nurseries – meals on wheels. The level of contact that preceded the transmission of the major plagues discussed here is very closely linked to the rise of cities and the push-pull effect they have on goods, the people who carry them and the armies that fight over them. The plagues of the second millennium BC arrive at the dawn of interconnected regions, when the Near East connects to Central Asia, the Eastern Mediterranean and possibly beyond. The age of big Eurasian empires (in the first millennium BC: think Persia, Rome, Mauryan India or Qin/Han China) that brings a wider circulation of goods, ships, people and attack elephants expands the range of diseases further still, and we see it in the accounts of the plagues of Athens, Rome and beyond. The devastation of the fifteenth and sixteenth centuries in the Americas is a clear extension of Old World plagues to New World bodies. And what we see in the modern day are the last bastions of infectious isolation blown away by globalisation, by the quest for intensive resource extraction in even the most obscure parts of the world. The microscope I use for my digital slides is made in Japan using American science, assembled in Germany and sold by Brits. This year alone I will go to Turkey, the US, France, Germany, Spain (twice),18 Austria, Switzerland, Lichtenstein, Luxembourg, Belgium, Finland and Japan (twice). Our modern plagues are a product of our global network of cities and the states they represent. Like the plagues of the past, though, our modern plagues will probably fall into a pattern of cursory appearances and growing immunity, until they too are replaced by whatever new plagues await over the horizon when we find a way to expand our connected cities beyond their current range.19
Bioarchaeologically, we uncover evidence of plague from the genetic material locked in ancient bone; from collagen that remains trapped, usually in teeth, long after the body has skeletonised. Molecular archaeology is our primary weapon in understanding the pandemics that have shaped our population history, and in so doing shaped our political, social and economic history. A number of scholars have argued that the depopulation of Europe by the Black Death was an underlying reason for the uptick in the value of labour that finally freed many of Europe’s peasants from their ties to the land. High labour value meant wages, which meant mobility, and mobility meant opportunity. The population of Europe did eventually recover from the fourteenth-century Plague, but it did so unevenly. The major cities drew in newly mobile workers while many rural enclaves shrivelled to nothing and disappeared. The disappearing towns of England and Denmark – DMVs or ‘deserted medieval villages’ – are well-known examples of how population movements away from rural life changed the character of the medieval world. Plagues may have spread through cities and because of cities, but in the end it is plague, with its attendant economic and social crises, that built cities into the truly monstrous sizes we see in the proto-industrial, early modern period.
1 This is an academic translation of ‘argue violently about’.
2 Or, in some slightly less credible accounts, rains of vertically dislocated amphibians, grasshoppers, etc.
3 I do not recommend image-searching this.
4 Though variable, 2 to around 35 per cent.
5 Fabrications.
6 Apparently, also prolonged and deeply contemplative.
7 ‘Vaccine’ was originally the term for only the smallpox vaccination; it derives from the Latin for ‘cow’.
8 This even applies to diagnoses less than 500 years old; it took a chance encounter with deer-hunting terminology for me to realise that the frequently recorded early modern British cause of death termed ‘rising of the lights’ was a description of lung disease, and not some sort of beatific spiritual event.
9 He has more names, all of which translate to variations on the theme of ‘honourable’, ‘rich’, ‘long-lived’ and ‘strong like a bull’.
10 They do not affect nursery rhymes; the popular misconception that ‘Ring Around the Rosy’ was about the Black Death only appeared around 1951, alongside other novel inventions like the nuclear family and the H-bomb. Apparently the atomic future inspired fairly apocalyptic interpretations of the past.
11 Also the most amusing; and, as the only book I took on a three-month field season at Çatalhöyük, rewardingly long.
12 There is also a lot of sex, quipping and combinations thereof.
13 Except for the large proportion of colleagues from archaeology and history who I expect will buy this book. At full price.
14 So it seems the collapse of the Roman Empire and the intransigence of the northern frontier were actually quite helpful, in that respect.
15 If the ritual did occur as recorded, my sympathies are entirely with the woman and the ram.
16 There seems to have been some confusion about de’ Mussi’s account, which his editor originally put forwards as an eyewitness testimony from the refugee ships that had spread the Plague back at home. It was later revealed that the medieval lawyer-notary had in fact spent the Plague at home in Italy. The amount of confusion owing to our best account of the European spread of the Plague being written by a lawyer, I leave to the reader’s estimation.
17 Humans, as I may have mentioned previously, can be terrible people.
18 Missed Andorra by a literal mile. Disappointing.
19 Michael J. Crichton may have been a visionary.