Plagues in World History (24 page)

Influenza did not really come into its own as a pandemic disease until the eighteenth century, when the more rapid transport of peoples and the worldwide scope of wars began to make global outbreaks more likely. Unlike bubonic plague, 116 y Chapter 5

a rat-and flea-based disease that could follow the movements of grain and mer-chandise shipments, influenza had to wait until modern technology made human-to-human transmission across long distances possible. Also, cities now began to greatly increase in size and density, especial y in the latter half of the century with the advent of the industrial and agricultural revolutions. Pandemics are thought to have occurred in 1729–1730, 1732–1733, 1761–1762, 1781–1782, and 1788–1789, with the one in 1781–1782 particularly severe. The pandemic of 1761–1762 also coincided with the Seven Years’ War of 1756–1763, the first truly global conflict that pitted the European powers and their colonies in the Americas and India against each other. These pandemics were characterized by the high morbidity and low mortality typical of influenza, although firm figures are hard to come by. A months-long, east-to-west spread of flu across Europe, with an origin typically in Russia, was noted in this century, albeit an Asian source of the disease began to be suspected by the 1780s; flu also came to the Americas from Europe in the course of these pandemics but after a delay of as much as a year. And while this century saw more detailed and accurate diagnoses of influenza outbreaks and a more enlightened approach to the medical profession, the old ideas of the miasmatic spread of disease and of contagion still applied, and bleeding and cupping were stil the norm in terms of treatment. However, because influenza was a relatively mild disease, at least compared to plague or smal pox, that kil ed few people, invasive purgative remedies may not have been as intensive, and doctors seem to have recommended above all that their patients rest and consume nourishing foods, advice that still holds true to this day.13

The nineteenth century saw all these trends noted in the previous century continue and indeed accelerate: Travel across oceans and continents grew far swifter with the advent of steamship and railroad technologies; European colonialism and imperialism established far-flung empires in every corner of the globe; and cities and populations expanded exponentially as the industrial revolution moved into full swing. All these developments, of course, greatly favored the outbreak and spread of influenza. At the same time, exciting and unprecedented new approaches to the medical explanation and treatment of infectious diseases emerged, such as smallpox vaccination programs and the awareness and identification of various disease-causing bacteria. And yet, such advances did not really apply to influenza and may, in fact, have given doctors a false sense of superiority over the disease. In the earlier part of the century, the miasmatic rather than the germ theory and even bleeding treatments still held sway. But greater sophistication and reliability of statistics, at least in terms of excess mortality from influenza in Europe and the United States, now became available. A major influenza pandemic occurred in 1831, at the same time as cholera swept across Europe, with a second and third wave striking in 1833 and 1837, the last Influenza y 117

causing much higher mortality than in the previous outbreaks. Finally, another influenza pandemic striking in three successive waves occurred in 1889–1891, with a last gasp of a related strain possibly following in 1899–1901. Russia was once again blamed for this pandemic’s origins (hence its popular name as the “Russian flu”) although scholars now believe it came from southern China. Best estimates are that a million people or more died in Europe and the United States.

People exposed to this pandemic may have gained some immunity to the horrific outbreak of 1918, which tended to target people in the prime of life (who would have been young children in 1889), and some scholars believe that the H2N2

flu strain that circulated in the 1957 pandemic may also have been active at the end of the nineteenth century.14

We now come to the greatest influenza pandemic of them all, the one that engulfed the entire world in three waves in 1918–1919, with remarkably high morbidity
and
mortality. It has become the pandemic against which all succeeding ones are measured, especially in recent times with fears of avian flu (H5N1) and the latest pandemic of the H1N1 strain in 2009. It is certainly the “forgotten pandemic” no longer, with a plethora of narrative histories appearing on the publishing scene in the wake of Crosby’s groundbreaking study of 1976.15 But in addition to the usual anecdotes that are typically set in the United States or Europe, a lot more information is now available about the pathogenic and social impact of flu elsewhere around the globe.

For example, the one part of the world that seems to have suffered the most from the pandemic was India, where recent estimates place its death toll at close to twenty million, which is nearly double the number of deaths India suffered during the Third Pandemic of plague. If we accept a figure of fifty million for flu deaths around the world, then India’s share alone would account for 40 percent of that total. The Indian experience with influenza illustrates a strong connection between the disease and poverty, since lower castes of Indian Hindu society suffered disproportionately compared to the higher castes, which was probably due to their poorer nutrition and lack of good nursing care that could have helped the body resist opportunistic bacterial infections. In addition, India shows how a place far removed from the front of World War I and not mobilizing on a grand scale for war could nonetheless suffer tragically during the pandemic. In India’s case, influenza’s spread seems to have been greatly facilitated by the railroad network installed by the British and by overcrowded conditions in the cities, while its high mortality rate (for flu) of 6 to 10 percent was perhaps owing to the failure of the monsoon rains during the summer of 1918 that made famine, instead of war, the synergistic partner of disease.16 All three factors—disease, war, and famine—were in bed together in Tanzania, a German colony in Africa that was taken over by Britain during the war and where troop and refugee movements 118 y Chapter 5

both spread the flu and pillaged agricultural lands, which then could not be re-planted as farmers succumbed to the disease, resulting in mortalities comprising 10 percent of the population.17 War likely impacted the response to influenza in India in a more indirect way, by distracting the British government from taking more effective measures against the disease, for which it was criticized by the native press. Instead, the British relied on cooperation with voluntary, nongovernmental organizations (NGOs) to provide what medical and hospitalization services were available during the epidemic, which was perhaps a lesson it learned from the outbreak of plague in Bombay in 1896. In addition, since Western medicine proved woefully ineffective in explaining or treating the disease despite being newly armed with the germ theory, native traditions of Ayurvedic and Unani medicine were favored by voluntary hospitals and other groups offering medical care, which nonetheless still faced suppression from the government under the delusion “that it had all the answers.”18

Other places in the third world, such as the Belgian Congo, Ghana, and the Dutch East Indies (present-day Indonesia), suffered mortality rates comparable to India’s. But influenza reached even isolated regions of the globe, such as the hinterlands of Alaska and the Canadian subarctic as well as islands in the South Pacific, such as Western Samoa and Tonga, where influenza acted like a “virgin soil” epidemic much as smallpox did in the New World in the sixteenth century, wiping out 50 or even 100 percent of local populations. This was not all due to native lack of prior exposure to the disease, however. A study of the influenza pandemic in the Canadian subarctic, for example, found that families stricken by the flu also suffered from lack of food and wood fuel, as they were dependent on distant supply lines to the Hudson Bay Company stores, which had collapsed with the onset of the disease; the hunger and cold that resulted certainly amplified susceptibility to the flu. In other, distant parts of the world, such as Australia, the American Samoan islands, and the city of Fairbanks, Alaska, quarantine was successful in preventing or containing outbreaks of influenza.19

Among the more sensational developments to take place in research into the influenza pandemic of 1918–1919 is the genetic recreation of the virus responsible from autopsy samples preserved at the Armed Forces Institute of Pathology in Rockville, Maryland, and in the Alaskan permafrost. The samples in question were taken from two young soldiers who died at their army bases in the United States in September 1918 and from an Inuit woman who succumbed to the pandemic in November 1918 in a village bordering the Bering Strait where all but eight of the inhabitants died. Between 1996 and 2005, a research team at the institute was able to complete the eight-gene sequence of the virus from the samples and then use it to resurrect a live 1918 virus that was then tested on laboratory mice.20 Not everyone was so enamored of this Frankenstein-like ex-Influenza y 119

periment on so lethal a viral monster,21 yet it did provide some valuable historical information. It was found that the 1918 H1N1 strain was uniquely virulent, in that it was able to rapidly reproduce inside the lungs—as much as several thousand times faster than a normal influenza virus—which in turn provoked a correspondingly uncontrolled immune response, known in modern medical parlance as a “cytokine storm.” (Cytokines are molecular substances that trigger our white blood immune cells or leukocytes to hurry to wherever the infection is located in the body, and a circular process then ensues as the immune cells produce yet more cytokines.) This only made matters worse, as the lungs began to fill up with a combination of immune cells as well as blood and fluid leaking into the alveolar sacs where tissue had been damaged. The resulting suffocation of the victim is currently called acute respiratory distress syndrome (ARDS).

This is precisely what was observed in numerous autopsies conducted in 1918–1919, when lungs and sometimes the entire body cavity were found to be full of a bloody, frothy liquid, which had produced some of the most dramatic and alarming symptoms of the disease, such as a blue-black cyanosis of the face and skin (the result of a failure of oxygen to reach the blood) and blood pouring from the nose and ears.22 Just such cytokine responses are nowadays produced in newly emerging viral diseases that are likewise highly fatal, such as Ebola and other hemorrhagic fevers, hantavirus pulmonary syndrome (HPS), and severe acute respiratory syndrome (SARS).23 As if this wasn’t bad enough, the 1918

virus also laid the groundwork especially well for bacterial pneumonia, which is always a danger due to its synergistic relationship with influenza.

What is still left unresolved, however, is from where exactly this atypical influenza virus originated. Researchers at the Armed Forces Institute came to the conclusion that the 1918 virus arose suddenly from a direct adaptation of avian flu to humans, rather than through an intermediary swine influenza strain, as was previously thought.24 This would increase the likelihood that the source of the 1918–1919 pandemic was China or Southeast Asia, the ancestral home of human avian flu strains since it is where the most contact between waterfowl and humans has traditionally occurred. As early as December 1917 and January 1918, a pneumonia-like disease was reported in the Shanxi province of China along the Mongolian border; it is argued that this was pneumonic plague rather than influenza, since it was diagnosed as such by Dr. Wu Liande, the man who had headed up the response to the 1910–1911 outbreak of pneumonic plague in Manchuria. However, Wu’s diagnosis of plague was contested at the time. He made it in some chaotic circumstances, since his unauthorized autopsies sparked rioting among the local population, and although bacteria were found in sputum and spleen samples, they were allegedly not
Yersinia pestis
. We have already noted that bacterial pneumonia is an opportunistic disease of influenza, and in any 120 y Chapter 5

case, the exceptional virulence of the 1918 flu pandemic would seem to mimic that of pneumonic plague. Another possibility includes Haskell County, Kansas, a small, isolated, rural community where influenza broke out suddenly in January and February 1918, well before the first soldiers came down with the flu three hundred miles away at Camp Funston in Fort Riley, Kansas, on March 4, 1918. A third alternative is that the virus originated in Etaples, France, where British soldiers stationed at a camp there came down with what was described at the time as “purulent bronchitis,” accompanied by a “heliotrope cyanosis” that was later noted in flu victims, during the winter of 1916–1917; when influenza subsequently swept over Europe during its second, deadly wave in the autumn of 1918, doctors who had performed autopsies on the earlier “bronchitis” victims became convinced they had died of the same disease that was now killing in a vast pandemic. What is more, the base camp at Etaples was supplied by food markets that included ducks, geese, chickens, and pigs, and utilized gas weap-onry that had mutagenic properties (i.e., the ability to mutate genes). However, no autopsy samples from Etaples currently survive in order to confirm the presence of the influenza virus, and some British doctors stationed there at the time were not convinced that the bronchitis was contagious, since it did not spread.25

Of course, it is always possible that the 1918–1919 pandemic of influenza had several points of origin at once.

While the latest microbiological detective work into influenza is all very impressive, there is still a role to be played by the historical context of the 1918–1919 outbreak. The most obvious component of that context is the First World War, which came to a close in November 1918 just as the terrible second wave of flu was in full swing. The fifteen million or more military and civilian deaths directly caused by the war were of course dwarfed by the worldwide totals for influenza, although if we restrict ourselves to Europe, where most of the action during the war took place, then flu mortalities would be just a fraction of the war’s impact. Certainly, influenza and World War I seemed to exist in a mutual, symbiotic relationship. After flu broke out in its first wave during the spring of 1918 among American soldiers mustering in camps across the country, it then spread to Europe as the doughboys disembarked at Brest in France. By late spring and summer, flu was playing its role in the war as the German offensive stalled at the Marne thirty-seven miles from Paris; according to the memoirs of General Eric von Ludendorff published later in 1919, the “blitzkatarrh” was to blame for the failure of German muster and morale at this turning point in the war. As the Allies began their counteroffensive in late summer and autumn, the second wave of the flu began sweeping through both sides. U.S. president Woodrow Wilson has been criticized by historians for refusing to delay troop movements in October 1918 as was urged by medical advisers; a delay could have Influenza y 121