In 1918, the Italian-Americans of New York, the Yupik of Alaska and the residents of the Persian shrine city of Mashed had almost nothing in common – except for a virus.
It spanned the breadth of the globe and killed up to 100 million people, making it the greatest human disaster of the twentieth century – and possibly in all of recorded history. And yet, in our popular conception, the Spanish flu of 1918 exists largely as a footnote to World War I. Why?
In Pale Rider, Laura Spinney recounts the tale of an overlooked pandemic, tracing it from India to Brazil, from Persia to Spain, and from South Africa to Ukraine. Drawing on the latest research in history, virology, epidemiology, psychology and economics, she narrates a catastrophe that changed humanity for decades to come, and continues to make itself felt today.
In the process Spinney demonstrates that the Spanish flu was as significant – if not more so – as two world wars in creating the modern world; in disrupting, and often permanently altering, global politics, race relations, family structures and thinking across medicine, religion and the arts.
Laura Spinney is a science journalist. Her writing has appeared in National Geographic, Nature, The Economist and the Daily Telegraph, among others. She is also the author of two novels, The Doctor and The Quick. Born in the UK, she has lived in France and Switzerland.
BY THE SAME AUTHOR
The Doctor
The Quick
Rue Centrale: Portrait of a European City
For RSJF and the lost generations
The brevity of the influenza pandemic of 1918 posed great problems to doctors at the time . . . It has posed great problems to historians ever since.
Terence Ranger, The Spanish Influenza Pandemic of 1918–19 (2003)1
Kaiser Wilhelm of Germany abdicated on 9 November 1918 and in the streets of Paris there was jubilation. ‘À mort Guillaume!’ they shouted. ‘À bas Guillaume!’ Death to Wilhelm! Down with Wilhelm! Meanwhile, high above the city’s seventh arrondissement, the poet Guillaume Apollinaire lay on his deathbed. A leading light of the French avant-garde movement, the man who invented the term ‘surrealist’ and inspired such figures as Pablo Picasso and Marcel Duchamp, he had signed up to fight in 1914. Having survived a shrapnel wound to the head and the drilling of a hole into his skull, he died of Spanish flu at the age of thirty-eight, and was declared ‘mort pour la France’.
His funeral was held four days later – two days after the armistice was signed. On leaving the Church of St Thomas Aquinas, the mourners set off eastwards towards Père Lachaise Cemetery. ‘But as it reached the corner of Saint-Germain,’ recalled Apollinaire’s friend and fellow poet, Blaise Cendrars, ‘the cortège was besieged by a crowd of noisy celebrants of the armistice, men and women with arms waving, singing, dancing, kissing, shouting deliriously the famous refrain of the end of the war: “No, you don’t have to go, Guillaume. No you don’t have to go…’” The famous refrain was directed with irony at the defeated kaiser, but it was filled with poignancy for the friends of Apollinaire.2
The poet’s death serves as a metaphor for our collective forgetting of the greatest massacre of the twentieth century. The Spanish flu infected one in three people on earth, or 500 million human beings. Between the first case recorded on 4 March 1918, and the last sometime in March 1920, it killed 50–100 million people, or between 2.5 and 5 per cent of the global population – a range that reflects the uncertainty that still surrounds it. In terms of single events causing major loss of life, it surpassed the First World War (17 million dead), the Second World War (60 million dead) and possibly both put together. It was the greatest tidal wave of death since the Black Death, perhaps in the whole of human history.
Yet what do we see when we unravel the scroll of the twentieth century? Two world wars, the rise and fall of communism, perhaps some of the more spectacular episodes of decolonisation. We do not see the most dramatic event of them all, though it’s right there before our eyes. When asked what was the biggest disaster of the twentieth century, almost nobody answers the Spanish flu. They’re surprised by the numbers that swirl around it. Some become thoughtful and, after a pause, recall a great-uncle who died of it, orphaned cousins lost to sight, a branch of the family that was rubbed out in 1918. There are very few cemeteries in the world that, assuming they are older than a century, don’t contain a cluster of graves from the autumn of 1918 – when the second and worst wave of the pandemic struck – and people’s memories reflect that. But there is no cenotaph, no monument in London, Moscow or Washington DC. The Spanish flu is remembered personally, not collectively. Not as a historical disaster, but as millions of discrete, private tragedies.
Perhaps that has something to do with its shape. The First World War dragged on for four long years, but despite its name, the bulk of the action was concentrated in European and Middle Eastern theatres. The rest of the world felt the hot wind sucking it into that vortex but remained outside it, and in some places the war seemed very far away indeed. The war had a geographical focus, in other words, and a narrative that unfolded in time. The Spanish flu, in contrast, engulfed the entire globe in the blink of an eye. Most of the death occurred in the thirteen weeks between mid-September and mid-December 1918. It was broad in space and shallow in time, compared to a narrow, deep war.
The African historian Terence Ranger pointed out in the early 2000s that such a condensed event requires a different storytelling approach. A linear narrative won’t do; what’s needed is something closer to the way that women in southern Africa discuss an important event in the life of their community. ‘They describe it and then circle around it,’ Ranger wrote, ‘constantly returning to it, widening it out and bringing into it past memories and future anticipations.’3 The Jewish text, the Talmud, is organised in a similar way. On each page, a column of ancient text is surrounded by commentaries, then by commentaries on the commentaries, in ever-increasing circles, until the central idea has been woven through space and time, into the fabric of communal memory. (There may be another reason why Ranger proposed a feminised history of the Spanish flu: it was generally women who nursed the ill. They were the ones who registered the sights and sounds of the sickroom, who laid out the dead and took in the orphans. They were the link between the personal and the collective.)
At the root of every pandemic is an encounter between a disease-causing microorganism and a human being. But that encounter, along with the events that lead up to it and the events that ensue from it, is shaped by numerous other events taking place at the same time – as well as by the weather, the price of bread, and ideas about germs, white men and jinns. The pandemic in its turn affects the price of bread, ideas about germs, white men and jinns – and sometimes even the weather. It is a social phenomenon as much as it is a biological one; it cannot be separated from its historical, geographical and cultural context. The way African mothers and grandmothers recount an event gives weight to that contextual richness, even if the event it impinges on lasts no longer than a historical heartbeat. This book sets out to do the same.
The time is right. In the decades immediately after the pandemic, the only people who studied it – besides actuaries employed by insurance companies – were epidemiologists, virologists and medical historians. Since the late 1990s, however, Spanish-flu historiography has exploded, and this recent burst of attention has been noticeable by its multidisciplinary nature. Now economists, sociologists and psychologists are interested in it too, along with ‘mainstream’ historians. Each has trained their gaze on a different aspect, and between them they have transformed our understanding of it. All too often, though, their conclusions are buried in specialist journals, so this book attempts to bring them together; to weave all the different strands into a more coherent picture of the beast, in all its multifaceted glory – or horror.
The information that is available today is not only more academically diverse, it is also more geographically diverse – capturing the global reach of the disaster. Most accounts of the Spanish flu to date have focused on Europe or North America. They had to, because for a long time it was only in those places that data had been collected systematically. In 1998, when Spanish-flu experts from around the world met in Cape Town to mark its eightieth anniversary, they acknowledged that almost nothing was known about what happened in large swathes of the globe – South America, the Middle East, Russia, South East Asia and inland China. But Europe- and North America-centred accounts distort the picture for two reasons. First, those continents reported the lowest death rates, on average, so their experiences were atypical. And second, by 1918 they were both heavily implicated in a war that would devastate Europe. War was undoubtedly the main event on that continent: France lost six times more souls to the war than to the flu, while in Germany the multiple was four, in Britain three and in Italy two. But on every other continent – with the possible exception of Antarctica, which both disasters left pristine – more died of flu than war. At the time of writing – nearly twenty years on from the Cape Town summit, and as we approach the centenary of the catastrophe – it is possible to begin to reconstruct what happened in those other parts of the world.
This book takes a different approach to telling the flu. It moves in on it – from prehistory to 1918, from the planet to the human, from the virus to the idea and back again. At the heart of it is the story of how the Spanish flu emerged, swept the planet and receded, leaving humanity transformed. But that story pauses, at times, to look at what set communities apart in their experiences of it, as well as what brought them together. In 1918, the Italian-Americans of New York, the Yupik of Alaska and the residents of the Persian shrine city of Mashed had almost nothing in common except the virus, and in each place cultural and other factors moulded their encounter with it. A series of portraits therefore tracks the disaster as it unfolded in societies located at different points on the globe, highlighting the profoundly social nature of a pandemic.
These portraits shine a light into areas of the map that were previously dark, and give an indication of how the Spanish flu was experienced in parts of the world where 1918 was the year of the flu, not the year the war ended. They are not comprehensive, because millions of stories remain untold, so they come with caveats. It surely wasn’t only in Rio de Janeiro that a post-flu orgy produced a spike in births, or only in Odessa, Russia, that people performed archaic religious rituals to ward off the scourge. It wasn’t only Indians who temporarily transgressed strict social boundaries to help each other, or only in South Africa that people of one colour blamed those of another. A Catholic bishop may have frustrated efforts to contain the disease in Spain, but missionaries were often the only ones bringing relief to remote tracts of China. There is one overarching caveat: the narrator is, once again, European.
The story of the Spanish flu is told in Parts Two to Six of the book. But that story is embedded in a larger one – the one that tells how man and flu have cohabited, and co-evolved, for 12,000 years – so Part One, ‘The Unwalled City’, recounts that story up to 1918, while Part Seven, ‘The Post-Flu World’, explores the traces of the Spanish flu with which we live today. Since man and flu are still co-evolving, Part Eight, ‘Roscoe’s Legacy’, looks forward to a future battle – the next flu pandemic – envisaging what new weapons we will carry into it, and what is likely to be our Achilles heel. Together, these stories comprise a biography of the flu – a human story, that is, in which the fil conducteur is flu. An afterword addresses the question of memory, asking why, when its impact was so profound, we call it ‘forgotten’.
It is often said that the First World War killed Romanticism and faith in progress, but if science facilitated industrial-scale slaughter in the form of the war, it also failed to prevent it in the form of the Spanish flu. The flu resculpted human populations more radically than anything since the Black Death. It influenced the course of the First World War and, arguably, contributed to the Second. It pushed India closer to independence, South Africa closer to apartheid, and Switzerland to the brink of civil war. It ushered in universal healthcare and alternative medicine, our love of fresh air and our passion for sport, and it was probably responsible, at least in part, for the obsession of twentieth-century artists with all the myriad ways in which the human body can fail. ‘Arguably’ and ‘probably’ are indispensable qualifiers when discussing the Spanish flu, because in 1918 there was no way of diagnosing influenza, and hence no way of knowing for sure that that was what it was – any more than we can be certain that the bubonic plague (or one of its variants, pneumonic plague) caused the Black Death in the fourteenth century. What isn’t arguable is that the 1918 pandemic accelerated the pace of change in the first half of the twentieth century, and helped shape our modern world.
If all of this is true, how come we still think of the Spanish flu as a footnote to the First World War? Have we really forgotten it? Terence Ranger thought we had, but if he were still alive today he might hesitate before repeating that claim. If so, then credit must go to a vast collaborative effort. The Spanish flu can no longer be told without the contributions of both historians and scientists, including social scientists. Science tells the tale up to the threshold of history, across the acres of prehistory that look empty but are, in fact, covered in an invisible scrawl – and that moulded events in 1918 just as much as what came later. History takes it up where the scrawl becomes legible, and science sheds some light back from the present. In another hundred years, science and history will themselves have been transformed. There might even be a science of history, in which theories about the past are tested against computerised banks of historical data.4 That kind of approach will likely revolutionise the way we understand complex phenomena such as pandemics, but it’s still in its infancy. There is one thing we can already say for sure, however: by the bicentenary of the 1918 pandemic, historians will have filled in more of the blanks, and the light shed by science will be brighter.
Sometime around the winter solstice of 412 BC, a cough wracked the people of Perinthus, a port city on the Sea of Marmara in what was then northern Greece. The Perinthians reported other symptoms too: sore throat, aches, difficulty swallowing, paralysis of the legs, an inability to see at night. A doctor called Hippocrates jotted them all down, and the ‘Cough of Perinthus’ became the first written description – probably – of influenza.
Probably, because certain of those symptoms don’t seem to fit: impaired night vision, paralysis of the limbs. Their inclusion troubled historians of medicine, until they realised that Hippocrates defined an epidemic differently from us. Indeed, Hippocrates was the first to use the word epidemic (literally, ‘on the people’) in a medical sense. Before that, it had referred to anything that propagates in a country, from fog to rumour to civil war. Hippocrates applied it specifically to disease, and then he redefined disease.
The ancient Greeks thought of disease as spiritual in origin, a punishment from the gods for any kind of misdemeanour. Doctors were part priests, part magicians, and it was their role to mollify the irascible divinities with prayer, spells and sacrifices. Hippocrates argued that the causes of disease were physical, and that they could be divined by observing a patient’s symptoms. He and his disciples introduced a system for classifying diseases, which is why he is often referred to as the father of western medicine: he was responsible for the notions of diagnosis and treatment that still underpin medicine today (he also left us with a code of medical ethics, the Hippocratic Oath, from which we have the promise made by newly qualified doctors to ‘do no harm’).
Hippocrates thought that disease was the result of an imbalance between the four ‘humours’ or fluids that circulate in the human body – black bile, yellow bile, phlegm and blood. If you were lethargic, you had too much phlegm, and the treatment was to eat citrus fruit. Galen, another Greek physician who lived about 500 years after Hippocrates, elaborated on that model, suggesting that people could be categorised by temperament according to which humour dominated in them. Black bile was associated with melancholy types, yellow bile with choleric or hot-tempered ones. A phlegmatic person was laid-back, a sanguine one hopeful. We retain the adjectives, but not the understanding of anatomy and bodily function that produced them. And yet, the Galenic concept of medicine dominated in Europe for a good 1,500 years, and his notion that ‘miasma’ or noxious air could trigger a humoral imbalance was still popular, in some parts of the world, in the twentieth century.
Hippocrates’ definition of an epidemic didn’t survive either. For him, an epidemic was all those symptoms experienced in a given place over a given period of time, during which its population was in the grip of sickness. In those circumstances, he did not distinguish between separate diseases. Later the term epidemic came to be associated with one disease, then with one microbe, then with one strain of microbe, but this process of refinement didn’t get underway until the Middle Ages, when the great plague epidemics forced a rethink. In modern terms, therefore, the people of Perinthus were probably suffering from influenza, diphtheria and whooping cough combined – perhaps with a deficiency of vitamin A thrown in.
Why should we care about a 2,400-year-old outbreak of flu in Greece? Because we would like to know how long flu has been a disease of humans, and what caused it to become one in the first place. Understanding more about its origins might help us to pinpoint the factors that determine the timing, size and severity of an outbreak. It might help us to explain what happened in 1918, and predict future epidemics.
The Cough of Perinthus probably wasn’t the first flu epidemic. And though the historical record is silent on the subject before 412 BC, that doesn’t mean there’s nothing to be said about flu in earlier times. Like humans, flu carries information about its origins within itself. Both of us are living records of our evolutionary past. An example is the human tail bone or coccyx, which is a vestige of our tree-dwelling ancestors. As the tail became less useful, natural selection favoured individuals in whom a chemical signal during embryonic development switched off spinal elongation before the tail grew. Very occasionally, a glitch occurs and that signal doesn’t get turned off in time. The medical literature contains around fifty reports of babies born with tails – a glimpse of the arboreal primate in all of us.
The flu virus has no tail, but it harbours other clues to its origins. It is a parasite, meaning that it can only survive inside another living organism, or ‘host’. Unable to reproduce on its own, it must invade a host cell and hijack that cell’s reproductive apparatus. The offspring of the virus must then leave that host and infect a new one. If they don’t, then the virus expires with the original host, and that is the end of flu. Just as our ancestors’ survival depended on their ability to swing through trees, so flu’s survival depends on its ability to jump from one host to another. This is where the flu story becomes interesting, however, because being a parasite, its survival depends both on its own behaviour and on that of its host. And though for a long time scientists were in the dark about flu’s past, they knew a few things about what humans were doing before 412 BC.
Flu is transmitted from one person to another in tiny infected droplets of mucus that are flung through the air by coughs and sneezes. Snot is a fairly effective missile – it should be, it was designed in a wind tunnel – but it can’t fly further than a few metres. For flu to spread, therefore, people must live fairly close together. This was a crucial insight, because people didn’t always live close together. For most of the human story they were hunter-gatherers and far apart. That all changed about 12,000 years ago, when a hunter somewhere in the vastness of Eurasia erected a pen around a couple of wild sheep and invented livestock. Plants were domesticated too, for crops, and these two developments meant that the land could now support a higher density of people, who could thus come together to compete, collaborate, and generally display all the ingenuity characteristic of human societies. The hunter’s innovation, known as the farming revolution, ushered in a new era.
The new collectives that farming supported gave rise to new diseases – the so-called ‘crowd diseases’ such as measles, smallpox, tuberculosis and influenza. Humans had always been susceptible to infectious disease – leprosy and malaria were causing misery long before the farming revolution – but these were adapted to surviving in small, dispersed human populations. Among their tricks for doing so were not conferring total immunity on a recovered host, so that he or she could be infected again, and retreating to another host – a so-called ‘animal reservoir’ – when humans were scarce. Both strategies helped ensure that they maintained a sufficiently large pool of susceptible hosts.
The crowd diseases were different. They burned rapidly through a farming population, either killing their victims or leaving them immune to re-infection. They might infect other animals, but not as well as they infected humans, and some of them were so well adapted to humans that they became exclusively parasitic to our species. They needed a pool of thousands or even tens of thousands of potential victims to sustain them – hence the name, ‘crowd disease’. They would not have survived prior to the farming revolution, but after it, their evolutionary success was index-linked to the growth of human populations.
But if they would not have survived before farming, where did they come from? The clue is those animal reservoirs. We know that there are disease-causing microbes that only infect animals. There are forms of malaria, for example, that infect birds and reptiles but can’t be transmitted to humans. We know that there are microbes that infect both animals and humans (influenza falls into this category), and we know that there are microbes that infect only humans. This is the case, for example, with measles, mumps and rubella. According to current thinking, these different categories of infectious disease represent steps on the evolutionary path by which an exclusively animal disease becomes an exclusively human one. To be precise, scientists recognise five steps that a disease-causing microbe has to go through to complete this transition.1 Some diseases, like measles, have gone all the way; others have stuck at intermediate points on the path. But we shouldn’t think of this process as fixed. It’s highly dynamic, as illustrated by Ebola.
Ebola virus disease is primarily a disease of animals. Its natural reservoir is thought to be fruit bats that inhabit African forests, and that may infect other forest-dwelling animals that humans prize as bushmeat (humans eat the bats, too). Until recently, Ebola was considered a disease that infected humans poorly: it might be transmitted via contact with bushmeat, for example, but a person who was infected by that route would only infect a few others before the ‘outbreak’ fizzled out. That all changed in 2014, when an epidemic in West Africa revealed that Ebola had acquired the ability to pass easily between people.
It isn’t easy for, say, a virus to jump the species barrier. In fact ‘jump’ is entirely the wrong word – it would be more helpful, though still a metaphor, to think of it ‘oozing’ across. Cells are built differently in different hosts, and invading them requires different tools. Each step along the path to becoming a human disease is therefore accompanied by a specific set of molecular changes, but acquiring those changes is a very hit-and-miss affair. The virus will likely have to pass through many, many rounds of reproduction before a mutation arises that confers a useful change. But then, if the virus’s evolutionary fitness improves as a result – if by infecting humans better, it manages to produce more of itself – then natural selection will favour that change (if it doesn’t, it won’t). Other changes may follow, and their cumulative effect is that the virus moves another step along the path.
The natural reservoir of influenza is generally considered to be birds, especially waterbirds. The big giveaway that a certain species plays the role of reservoir for a certain pathogen is that it doesn’t get sick from it. The two have co-evolved for so long that the virus manages to complete its life cycle without causing too much damage to its host, and without unleashing an immune response. Ducks, for example, can be heavily infected with flu without showing any signs of disease. After the farming revolution, ducks were among the animals that humans domesticated and brought into their villages. So were pigs, which are regarded as potential intermediaries in the process by which a bird disease became a human disease, since pig cells share features of both human and bird cells. For millennia, the three lived cheek by jowl, providing flu with the ideal laboratory in which to experiment with moving between species. Flu infected humans, but probably not very well at first. Over time, however, it accumulated the molecular tools it needed to make it highly contagious, and one day there was an outbreak deserving of the name ‘epidemic’.
Epidemic here is meant in its modern sense – that is, as an increase, often sudden, in the number of cases of a given disease in a given population. An ‘endemic’ disease, in contrast, is always found in that population. A crowd disease can be both endemic and epidemic, if it is always present in a region but also produces occasional outbreaks there. This is where the definitions of the two terms become a little blurred and vary according to the disease in question. We might say, for example, that the relatively mild outbreaks of seasonal influenza that we see each winter are the endemic form of the disease, and reserve the term epidemic for when a new strain emerges, bringing a more severe form of flu in its wake – though not everybody would agree with that distinction.
We have no written accounts of the first epidemics of the first crowd diseases, but they are likely to have been very deadly (witness the 2014 epidemic of Ebola, which might yet go on to earn the title ‘crowd disease’). We know, for example, that one of the deadliest crowd diseases of all, smallpox, was present in Egypt at least 3,000 years ago, because mummies have been found with pockmarked faces, but the first written account of a (probable) smallpox epidemic doesn’t turn up until 430 BC, when a contemporary of Hippocrates, Thucydides, described corpses piled up in the temples of Athens.
When did the first flu epidemic occur? Almost certainly in the last 12,000 years, and probably in the last 5,000 – since the first cities arose, creating ideal conditions for the disease to spread. It too must have been horrific. We find this hard to understand, because today, in general, influenza is far from lethal. Yet even today, a small proportion of people come off badly each flu season. These unlucky individuals develop acute respiratory distress syndrome (ARDS): they become short of breath, their blood pressure drops, their faces take on a bluish tinge, and if they aren’t rushed to hospital they will very likely die. In a few cases, their lungs may even haemorrhage, causing them to bleed from their noses and mouths. ARDS is a glimpse of the carnage that first flu epidemic wrought.
There is no record of it (the oldest full writing system wasn’t developed until 4,500 years ago), so we don’t know when or where it happened, but Uruk in what is now Iraq might be a good candidate. Considered the largest city in the world 5,000 years ago, Uruk had around 80,000 inhabitants living inside a walled enclosure of six square kilometres – twice the area of London’s financial heart, the City. Nobody had any immunity. Nobody could help anybody else. Many would have died. Other flu epidemics must have followed, and they were probably milder: though the strains that caused them differed from that original one, and from each other, they were similar enough that the survivors gradually acquired some immunity. Influenza gradually came to look more like the disease we recognise today, though at the cost of a great many lives.
‘Against other things it is possible to obtain security,’ wrote the Greek philosopher Epicurus in the third century BC, ‘but when it comes to death we human beings all live in an unwalled city.’2 From the moment influenza became a human disease, it began to shape human history – though we had to wait for Hippocrates to write the first (probable) description of it. Even after Hippocrates, it’s hard to be sure that what is being described is influenza as we know it. Not only have concepts of epidemic and disease changed, but the disease itself has gone by different names, reflecting changing ideas about what causes it. On top of that, flu is easily confused with other respiratory diseases – most obviously the common cold, but also more serious diseases such as typhus and dengue fever, that start out with flu-like symptoms.
Treading carefully, aware of the traps that time inserts between words, historians have nevertheless speculated that it was flu that devastated the armies of Rome and Syracuse in Sicily in 212 BC. ‘Deaths and funerals were a daily spectacle,’ wrote Livy in his History of Rome. ‘On all sides, day and night, were heard the wailings for the dead.’3 It may have been the respiratory disease that raged through Charlemagne’s troops in the ninth century AD, that he knew as febris Italica (Italian fever). Probable flu epidemics were documented in Europe in the twelfth century, but the first really reliable description of one doesn’t appear until the sixteenth century. In 1557, in the brief interlude when Mary I was on the English throne, an epidemic eliminated 6 per cent of her subjects – more Protestants than ‘Bloody Mary’, as she became known, could dream of burning at the stake.
By the sixteenth century, the age of discovery was well underway. Europeans were arriving in ships in the New World, bringing with them their newfangled diseases to which local populations had no immunity. They had no immunity because they had not been through the same harrowing but tempering cycle of epidemics of animal origin. The fauna of the New World lent itself less easily to domestication than that of the Old, and some inhabitants were still hunter-gatherers. Flu may have been the disease that travelled with Christopher Columbus on his second voyage to the New World, in 1493, and that wiped out much of the Amerindian population of the Antilles after he stopped off there. That year, the Caribbean experienced something similar to what happened, several millennia earlier, in a Eurasian city like Uruk – only this time one group was left standing: the conquistadors.
For a long time historians ignored infectious diseases as historical players, not suspecting this imbalance in their effects on different populations. Right up until the twentieth century, European historians recounting Spaniard Hernán Cortés’ astonishing David-and-Goliath conquest of the Aztec Empire in Mexico generally failed to mention that an epidemic of smallpox did most of the work for him.4 For them, flu was a mild irritant, a cross to be borne in the darker months. They didn’t grasp the fear it struck into the hearts of Native Americans, Australians or Pacific Islanders, or how closely those peoples associated it with the coming of the white man. ‘There was a firm belief among all, that of late years, since they had visits from white men, their influenza epidemics were far more frequent and fatal than they used to be,’ wrote one nineteenth-century visitor to Tanna in the Vanuatu archipelago. ‘This impression is not confined to Tanna, it is, if I mistake not, universal throughout the Pacific.’ Once the historians had realised their error, some of them started calling crowd diseases by a different name: imperial diseases.5
It was the work of palaeoclimatologists that brought that error home to them. Palaeoclimatologists try to understand what the earth’s climate was like in the past, and why, by studying such things as sediment deposits, fossils and tree rings. Finding that the world grew cooler in the late Roman era, for example, they suggest that the Plague of Justinian – a pandemic of bubonic plague that killed approximately 25 million people in Europe and Asia in the sixth century AD – led to vast tracts of farmland being abandoned and forests growing back. Trees extract carbon dioxide from the atmosphere, and this reforestation led to so much of the gas being sequestered in wood that the earth cooled (the opposite of the greenhouse effect we are witnessing today).
Similarly, the massive waves of death that Cortés, Francisco Pizarro (who conquered the Inca Empire in Peru) and Hernando de Soto (who led the first European expedition into what is now the United States) unleashed in the Americas in the sixteenth century caused a population crash that may have ushered in the Little Ice Age.6 The effect wasn’t reversed until the nineteenth century, when more Europeans arrived and began to clear the land again. The Little Ice Age was probably the last time a human disease affected the global climate, however. Though there would be other pandemics, the gradual mechanisation of farming, combined with the exponential growth of the world’s population, meant that even the deaths of tens of millions of farmers could leave no dent in the atmosphere – at least not one that palaeoclimatologists have been able to detect.
The first flu pandemic that experts agree was a pandemic – that is, an epidemic that encompassed several countries or continents – is thought to have begun in Asia in 1580, and spread to Africa, Europe and possibly America. Here, though, we have to introduce a caveat. Determining the origin and direction of spread of a flu pandemic is not easy – as we’ll see – meaning that every categorical statement regarding the source of historic flu pandemics should be taken with a pinch of salt. This is especially true since, from at least the nineteenth century, Europeans whose compatriots had once tracked lethal diseases through the New World were quick to see each new plague as blowing out of China, or the silent spaces of the Eurasian steppes.
Contemporary reports suggest that this first flu pandemic spread from north to south across Europe in six months. Rome recorded 8,000 deaths, meaning that it was literally ‘decimated’ – roughly one in ten Romans died – and some Spanish cities suffered a similar fate.7 Between 1700 and 1800 there were two flu pandemics. At the height of the second, in 1781, 30,000 people a day were falling sick in St Petersburg. By then, most people were calling the disease ‘influenza’. The name was first coined by some fourteenth-century Italians who attributed it to the pull or ‘influence’ of the stars, but it took several centuries to catch on. We retain it today, of course, though as with the descriptors ‘melancholy’ and ‘phlegmatic’, its conceptual moorings have been swept away.
It was in the nineteenth century that crowd diseases reached the zenith of their evolutionary success, and held dominion over the globe. This was the century of the Industrial Revolution, and accompanying it, the rapid expansion of cities in many parts of the world. These cities now became breeding grounds for crowd diseases, such that urban populations were unable to sustain themselves – they needed a constant influx of healthy peasants from the countryside to make up for the lives lost to infection. Wars, too, brought epidemics in their wake. Conflict makes people hungry and anxious; it uproots them, packs them into insanitary camps and requisitions their doctors. It makes them vulnerable to infection, and then it sets large numbers of them in motion so that they can carry that infection to new places. In every conflict of the eighteenth and nineteenth centuries, more lives were lost to disease than to battlefield injuries.
The nineteenth century saw two flu pandemics. The first, which erupted in 1830, is said to have ranked in severity – though not in scale – with the Spanish flu. The second, the so-called ‘Russian’ flu that began in 1889, was thought to have originated in Bokhara in Uzbekistan. It was the first to be measured, at least to some extent, since by then scientists had discovered what a powerful weapon statistics could be in the fight against disease. Thanks to the efforts of those early epidemiologists, we know that the Russian flu claimed somewhere in the region of a million lives, and that it washed over the world in three waves. A mild first wave heralded a severe second one, and the third was even milder than the first. Many cases developed into pneumonia, which was often the cause of death, and this flu didn’t only claim the elderly and the very young – as in a normal flu season – but people in their thirties and forties too. Doctors were unsettled by their observation that many patients who survived the initial attack went on to develop nervous complications, including depression. The Norwegian artist Edvard Munch may have been one of them, and some have suggested that his famous painting, The Scream, sprang from his flu-darkened thoughts. ‘One evening I was walking along a path, the city was on one side and the fjord below,’ he wrote later. ‘I felt tired and ill. I stopped and looked out over the fjord – the sun was setting, and the clouds turning blood red. I sensed a scream passing through nature; it seemed to me that I heard the scream.’8 By the time Munch wrote those words, the pandemic was over, and so was the millennia-long struggle between man and flu. In the next century, the twentieth, science would conquer the crowd diseases once and for all.
To us living in a world a hundred years older, a world in the grip of an AIDS pandemic, the idea that science would conquer infectious diseases for good seems nonsensical. But at the turn of the twentieth century many people believed it, at least in the west. The main reason for their optimism was germ theory – the insight that germs cause disease. Bacteria had been known about for a couple of centuries, ever since a Dutch lens grinder named Antony van Leeuwenhoek passed a magnifying glass over a drop of pond water and saw that it was teeming with life, but they had been regarded as a kind of harmless ectoplasm – nobody suspected that they could make people ill. Robert Koch in Germany and Louis Pasteur in France made the connection, starting in the 1850s. The discoveries of these two men are too numerous to list, but among them, Koch showed that TB, the ‘Romantic’ disease of poets and artists, was not inherited – as was widely believed – but caused by a bacterium, while Pasteur disproved the notion that living organisms could be generated spontaneously from inanimate matter.
In combination with older ideas about hygiene and sanitation, germ theory now began to turn the tide on the crowd diseases. Campaigns were launched to purify drinking water and promote cleanliness. Vaccination programmes were imposed, though not without resistance – not surprisingly, people balked at the idea that they could be protected against a disease by being injected with it – and these efforts produced concrete results. If in the wars of previous centuries, more lives had been lost to disease than to combat, that trend was now reversed. Weapons had become more lethal, but military doctors had also become better at controlling infection. Those might seem like odd grounds for claiming success, but army doctors were among the first to put germ theory into practice, and their expertise trickled down to their civilian counterparts. At the beginning of the twentieth century, cities at last became self-sustaining.
In the early decades of that century, therefore, faith in science and rationalism was high. The excitement over the discovery of the link between bacteria and disease had not yet abated, and there was a temptation to find bacteria responsible for every malaise. Ilya Mechnikov, the wild Russian ‘demon of science’ whom Pasteur had brought to his institute in Paris, even blamed them for old age. Mechnikov had won a Nobel Prize in 1908 for his discovery of phagocytosis – the mechanism by which immune cells in human blood swallow up harmful bacteria and destroy them. But he also suspected bacteria in the human intestine of releasing toxins that harden the arteries, contributing to the body’s ageing – a belief that brought a certain amount of ridicule down on his head. He became obsessed with villages in Bulgaria where people reputedly lived to be more than a hundred, attributing their longevity to the sour milk they drank – and in particular, to the ‘good’ bacteria that soured it. In the last years of his life, he drank huge quantities of sour milk, before dying in 1916 at the age of seventy-one.1 (These days, the microbes in our gut are generally considered to be either harmless, or good for us.)
Viruses, however, were still a mystery. In Latin the word virus means something like poison, or potent sap, and at the turn of the twentieth century that was exactly how people understood it. When in his 1890 novel O Cortiço (The Slum), Brazilian writer Aluísio Azevedo wrote ‘Brazil, that inferno where every budding flower and every buzzing bluebottle fly bears a lascivious virus’, a venomous secretion is probably what he had in mind. But scientists were beginning to question that definition. Were they toxins or organisms? Liquid or particle? Dead or alive? The first virus was discovered in 1892, when Russian botanist Dmitri Ivanovsky identified a virus as the cause of a disease in tobacco plants. He hadn’t seen it. What he had discovered was that the disease was caused by an infectious agent that was smaller than all known bacteria – too small to see.
In 1892, the Russian flu was raging across Europe, and it was in the same year that Ivanovsky made his discovery that a student of Koch, Richard Pfeiffer, identified the bacterium responsible for influenza. That’s right, the bacterium responsible for influenza. Pfeiffer’s bacillus, also known as Haemophilus influenzae, really exists, and it causes disease, but it does not cause flu (Pfeiffer’s error lives on in its name, like a warning to scientists, or a bad historical joke). Nobody suspected that flu could be the work of a virus, that unclassifiable thing that existed somewhere beyond the limits of observability, and they continued to not suspect it in 1918. In fact, viruses occupied only a tiny corner of the psychic universe of 1918. They hadn’t been seen, and there was no test for them. These two facts are crucial to understanding the impact of the Spanish flu. Things changed in the wake of the pandemic, as this book will explain, but it took time. When James Joyce wrote, in his thoroughly modern novel Ulysses (1922), ‘Foot and mouth disease. Known as Koch’s preparation. Serum and virus’, he probably thought of a virus in much the same way as Azevedo had.2
The disciples of Pasteur and Koch disseminated germ theory far and wide, so that it gradually displaced Galenic concepts of disease. The psychological shift that this demanded was as troubling as the one Hippocrates had provoked more than 2,000 years earlier, and people were slow to embrace it. When two waves of cholera swept London in the mid-nineteenth century, its residents blamed miasma rising from the filthy River Thames. After a brilliant piece of detective work that involved marking fatal cases of the disease on a map, a doctor called John Snow traced the source of one outbreak to a particular water pump in the city, and deduced – correctly – that water rather than air spread cholera. He published his conclusion in 1854, but it was only after the ‘Great Stink’ of 1858 – when a spell of hot weather rendered the smell of untreated sewage on the banks of the Thames overpowering – that the authorities finally commissioned an engineer, Joseph Bazalgette, to design a proper system of sewers for the city. Their reasoning? By eliminating the miasma, they would eliminate cholera too.
Germ theory also had profound implications for notions of personal responsibility when it came to disease. Hippocrates had some surprisingly modern ideas about this. People were responsible for their diseases, he believed, if they did not make lifestyle choices conducive to good health, but they could not be blamed if a disease was hereditary. Even in that case, however, they had choices. He gave the example of cheese, arguing that one should choose whether or not to eat cheese in the light of knowledge about the constitution one had inherited. ‘Cheese,’ he wrote, ‘does not harm all men alike; some can eat their fill of it without the slightest hurt, nay, those it agrees with are wonderfully strengthened thereby. Others come off badly.’3
By the Middle Ages, people had shifted most of the responsibility for disease back onto the gods, or God, and a sense of fatalism persisted for centuries, despite the rise of science. In 1838, the French writer George Sand took her tubercular lover Frédéric Chopin to the Spanish island of Majorca, hoping that the Mediterranean climate would ease the symptoms of her ‘poor melancholy angel’. She didn’t expect it to cure him, because to her mind TB was incurable. Nor did it occur to her that she could catch it from him. By then, however, ideas about what caused TB were already in flux, and when the pair arrived in Palma, they discovered that its inhabitants wanted nothing to do with them. As an outraged Sand wrote to a friend, they were asked to leave, TB ‘being extremely rare in those latitudes and, moreover, considered contagious!’4
In the nineteenth century, epidemics were still regarded – like earthquakes – as acts of God. Germ theory forced people to consider the possibility that they could control them, and this revelation brought another new set of ideas into play: the theory of evolution that Charles Darwin had introduced in his On the Origin of Species